CYTOKINETICS INC MANAGEMENT'S DISCUSSION AND ANALYSIS OF FINANCIAL CONDITION AND RESULTS OF OPERATIONS (form 10-Q)

This discussion and analysis should be read in conjunction with our financial
statements and accompanying notes included elsewhere in this report. Operating
results are not necessarily indicative of results that may occur in future
periods.

This report contains forward-looking statements indicating expectations about
future performance and other forward-looking statements within the meaning of
Section 27A of the Securities Act of 1933, as amended (the "Securities Act"),
Section 21E of the Securities Exchange Act of 1934, as amended (the "Exchange
Act"), and the Private Securities Litigation Reform Act of 1995, that involve
risks and uncertainties. We intend that such statements be protected by the safe
harbor created thereby. Forward-looking statements involve risks and
uncertainties and our actual results and the timing of events may differ
significantly from the results discussed in the forward-looking statements.
Examples of such forward-looking statements include, but are not limited to,
statements about or relating to:

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guidance concerning revenues, research and development expenses and general and administrative expenses for 2022;

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the sufficiency of existing resources to fund our operations for at least the next 12 months;

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our capital requirements and needs for additional financing;

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our expectations as to our cash utilization for 2022 and in any subsequent period;

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the initiation, design, conduct, enrollment, progress, timing and scope of
clinical trials and development activities for our drug candidates conducted by
ourselves or our partners, including the anticipated timing for initiation of
clinical trials, including SEQUOIA-HCM, our ongoing Phase 3 clinical trial of
aficamten in patients with symptomatic obstructive hypertrophic cardiomyopathy
and COURAGE-ALS, our ongoing Phase 3 clinical trial of reldesemtiv in patients
with amyotrophic lateral sclerosis, anticipated rates of enrollment for clinical
trials and anticipated timing of results becoming available or being announced
from clinical trials;

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the results from the clinical trials, the non-clinical studies and chemistry, manufacturing, and controls activities of our drug candidates and other compounds, and the significance and utility of such results; anticipated interactions with regulatory authorities;

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our and our partners' plans or ability to conduct the continued research and development of our drug candidates and other compounds;

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the timing and likelihood of regulatory approval for omecamtiv mecarbil or any of our other drug candidates;

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our expected roles in research, development or commercialization under our strategic alliances with our partners and collaborators;

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the properties and potential benefits of, and the potential market opportunities for, our drug candidates and other compounds, including the potential indications for which they may be developed;

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the sufficiency of the clinical trials conducted with our drug candidates to demonstrate that they are safe and efficacious;

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our receipt of milestone payments, royalties, reimbursements and other funds from current or future partners under strategic alliances;

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our ability to continue to identify additional potential drug candidates that may be suitable for clinical development;

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market acceptance of our drugs;

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changes in third party healthcare coverage and reimbursement policies;

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our plans or ability to commercialize drugs, with or without a partner, including our intention to develop sales and marketing capabilities;

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the focus, scope and size of our research and development activities and programs;

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the utility of our focus on the biology of muscle function, and our ability to leverage our experience in muscle contractility to other muscle functions;

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our ability to protect our intellectual property and to avoid infringing the intellectual property rights of others;

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future payments and other obligations under loan, lease, and revenue interest agreements and the convertible notes;

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potential competitors and competitive products;

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retaining key personnel and recruiting additional key personnel;

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the potential impact of recent accounting pronouncements on our financial position or results of operations; and

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the continuing impact of the COVID-19 pandemic on our research and development activities and business operations.

Such forward-looking statements involve risks and uncertainties, including, but not limited to:

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decisions by Ji Xing Pharmaceuticals Limited with respect to the timing, design
and conduct of development and commercialization activities for aficamten or
omecamtiv mecarbil in the People's Republic of China (including the Hong Kong
SAR and Macau SAR) and Taiwan;

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our ability to meet any of the conditions for disbursement and our receipt of any loan disbursements under the Development Funding Loan Agreement, dated January 7, 2022, between us and Royalty Pharma Development Funding, LLC;

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our ability to meet any of the conditions for disbursement of additional sale
proceeds under the Revenue Participation Right Purchase Agreement, dated January
7, 2022, between us and Royalty Pharma Investments 2019 ICAV;

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decisions by FDA or other regulatory authorities to approve our new drug
application for omecamtiv mecarbil by February 28, 2023 (target PDUFA action
date) or otherwise, or to condition such approval on the approval of a dosage
selection test for the personalized dose optimization of omecamtiv mecarbil in
patients, our ability or the ability of any third party to develop or
commercialize such a dosage selection test, or the timing, prospects, process or
likelihood of the approval of such a dosage selection test;

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our ability to enroll patients in our clinical trials by any particular date;

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our ability to complete our clinical trials by any particular date;

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our ability to enter into strategic partnership agreements for any of our programs on acceptable terms and conditions or in accordance with our planned timelines;

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our ability to obtain additional financing on acceptable terms, if at all;

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our receipt of funds and access to other resources under our current or future strategic alliances, in the development, testing, manufacturing or commercialization of our drug candidates or slower than anticipated patient enrollment, in our or partners' clinical trials, or in the manufacture and supply of clinical trial materials;

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failure by our contract research organizations, contract manufacturing organizations and other vendors to properly fulfill their obligations or otherwise perform as expected;

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results from non-clinical studies that may adversely impact the timing or the further development of our drug candidates and other compounds;

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the possibility the FDA or foreign regulatory agencies may delay or limit our or our partners' ability to conduct clinical trials or may delay or withhold approvals for the manufacture and sale of our products;

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changing standards of care and the introduction of products by competitors or
alternative therapies for the treatment of indications we target that may limit
the commercial potential of our drug candidates;

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difficulties or delays in achieving market access, reimbursement and favorable
drug pricing for our drug candidates and the potential impacts of health care
reform;

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changes in laws and regulations applicable to drug development, commercialization or reimbursement;

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the uncertainty of protection for our intellectual property, whether in the form of patents, trade secrets or otherwise;

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potential infringement or misuse by us of the intellectual property rights of third parties;

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activities and decisions of, and market conditions affecting, current and future strategic partners;

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accrual information provided by and performance of our contract research organizations, contract manufacturing organizations, and other vendors;

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potential ownership changes under Internal Revenue Code Section 382; and

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the timeliness and accuracy of information filed with the U.S. Securities and Exchange Commission by third parties.

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In addition, such statements are subject to the risks and uncertainties
discussed in the "Risk Factors" section and elsewhere in this document. Such
statements speak only as of the date on which they are made, and, except as
required by law, we undertake no obligation to update any forward-looking
statement to reflect events or circumstances after the date on which the
statement is made or to reflect the occurrence of unanticipated events. New
factors emerge from time to time, and it is not possible for us to predict which
factors will arise. In addition, we cannot assess the impact of each factor on
our business or the extent to which any factor, or combination of factors, may
cause actual results to differ materially from those contained in any
forward-looking statements.

Business

When used in this report, unless otherwise indicated, "Cytokinetics," "Company,"
"we," "our" and "us" refers to Cytokinetics, Incorporated. CYTOKINETICS, and our
logo used alone and with the mark CYTOKINETICS, are registered service marks and
trademarks of Cytokinetics. Other service marks, trademarks and trade names
referred to in this report are the property of their respective owners.

Overview

We are a late-stage biopharmaceutical company focused on discovering, developing
and commercializing first-in-class muscle activators and next-in-class muscle
inhibitors as potential treatments for debilitating diseases in which muscle
performance is compromised and/or declining. We have discovered and are
developing muscle-directed investigational medicines that may potentially
improve the health span of people with devastating cardiovascular and
neuromuscular diseases of impaired muscle function. Our research and development
activities relating to the biology of muscle function have evolved from our
knowledge and expertise regarding the cytoskeleton, a complex biological
infrastructure that plays a fundamental role within every human cell. As a
leader in muscle biology and the mechanics of muscle performance, we are
developing small molecule drug candidates specifically engineered to impact
muscle function and contractility.

Our clinical-stage drug candidates are: omecamtiv mecarbil, a novel cardiac myosin activator, CK-136 (formerly known as AMG 594), a novel cardiac troponin activator, reldesemtiv, a novel fast skeletal muscle troponin activator ("FSTA"), aficamten, a novel cardiac myosin inhibitor, and CK-3772271 ("CK-271"), our second novel cardiac myosin inhibitor.

Omecamtiv mecarbil is being evaluated for the potential treatment of heart
failure. We previously announced positive results from GALACTIC-HF (Global
Approach to Lowering Adverse Cardiac Outcomes Through Improving Contractility in
Heart Failure), a Phase 3 cardiovascular outcomes clinical trial of omecamtiv
mecarbil in heart failure. On February 4, 2022, we announced the United States
Food and Drug Administration ("FDA") had accepted for filing our new drug
application ("NDA") for omecamtiv mecarbil for treatment of heart failure with
reduced ejection fraction ("HFrEF").

CK-136 was discovered under our joint research program with Amgen Inc. ("Amgen"). In collaboration with us, Amgen conducted a randomized, placebo-controlled, double-blind, single and multiple ascending dose, single-center Phase 1 study to assess the safety and tolerability, pharmacokinetics and pharmacodynamics of CK-136 in healthy subjects.

Aficamten is a novel, oral, small molecule cardiac myosin inhibitor. Aficamten
arose from an extensive chemical optimization program conducted with attention
to therapeutic index and pharmacokinetic properties that may translate into
next-in-class potential in clinical development. Aficamten was designed to
reduce the hypercontractility that is associated with hypertrophic
cardiomyopathy ("HCM").

Aficamten is being evaluated in patients with symptomatic, obstructive HCM
("oHCM"). Following the results from Cohorts 1, 2 and 3 of REDWOOD-HCM
(Randomized Evaluation of Dosing With CK-274 in Obstructive Outflow Disease in
HCM), a Phase 2 multicenter, randomized, placebo-controlled, double-blind,
dose-finding clinical trial of aficamten, we are conducting SEQUOIA-HCM (Safety,
Efficacy, and Quantitative Understanding of Obstruction Impact of Aficamten in
HCM), the ongoing Phase 3 randomized, placebo-controlled, double-blind,
multi-center clinical trial designed to evaluate aficamten in patients with
symptomatic oHCM on background medical therapy for 24 weeks, and Cohort 4 of
REDWOOD-HCM to, inter alia, determine the safety and tolerability of aficamten
in patients with non-obstructive HCM ("nHCM").

CK-271 is our second novel, oral, small molecule cardiac myosin inhibitor.
CK-271 produces reversible dose and plasma concentration-dependent reductions in
cardiac contractility without affecting heart rate in preclinical models. CK-271
reduces compensatory cardiac hypertrophy and cardiac fibrosis in preclinical
models of HCM and heart failure with preserved ejection fraction.

Reldesemtiv selectively activates the fast skeletal muscle troponin complex in
the sarcomere by increasing its sensitivity to calcium, leading to an increase
in skeletal muscle contractility. Reldesemtiv is being evaluated for treatment
in patients with amyotrophic lateral sclerosis ("ALS") in our ongoing Phase 3
clinical trial, COURAGE-ALS (Clinical Outcomes Using Reldesemtiv on ALSFRS-R in
a Global Evaluation in ALS).

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Our research continues to drive innovation and leadership in muscle biology. All
of our drug candidates have arisen from our cytoskeletal research activities.
Our focus on the biology of the cytoskeleton distinguishes us from other
biopharmaceutical companies, and potentially positions us to discover and
develop novel therapeutics that may be useful for the treatment of severe
diseases and medical conditions. Each of our drug candidates has a novel
mechanism of action compared to currently marketed drugs, which we believe
validates our focus on the cytoskeleton as a productive area for drug discovery
and development. We intend to leverage our experience in muscle contractility to
expand our current pipeline and expect to identify additional potential drug
candidates that may be suitable for clinical development.

Research and Development Programs

Our long-standing interest in the cytoskeleton has led us to focus our research
and development activities on the biology of muscle function and, in particular,
small molecule modulation of muscle contractility. We believe that our expertise
in the modulation of muscle contractility is an important differentiator for us.
Our preclinical and clinical experience in muscle contractility may position us
to discover and develop additional novel therapies that have the potential to
improve the health of patients with severe and debilitating diseases or medical
conditions.

Small molecules that affect muscle contractility may have several applications
for a variety of serious diseases and medical conditions. For example, heart
failure is a disease often characterized by impaired cardiac muscle
contractility which may be treated by modulating the contractility of cardiac
muscle. Similarly, certain diseases and medical conditions associated with
muscle weakness may be amenable to treatment by enhancing the contractility of
skeletal muscle. Because the modulation of the contractility of different types
of muscle, such as cardiac and skeletal muscle, may be relevant to multiple
diseases or medical conditions, we believe we can leverage our expertise in
these areas to more efficiently discover and develop potential drug candidates
that modulate the applicable muscle type for multiple indications.

We segment our research and development activities related to muscle contractility by our cardiac muscle contractility program and our skeletal muscle contractility program. We also conduct research and development on novel treatments for disorders involving muscle function beyond muscle contractility.

Our research and development expenses for the three months ended June 30, 2022
and 2021 were $57.1 million and $36.4 million, respectively, and $103.1 million
and $68.0 million for the six months ended June 30, 2022 and 2021, respectively.

Cardiac Muscle Program

Our cardiac muscle contractility program is focused on the cardiac sarcomere,
the basic unit of muscle contraction in the heart. The cardiac sarcomere is a
highly ordered cytoskeletal structure composed of cardiac myosin, actin and a
set of regulatory proteins. Cardiac myosin is the cytoskeletal motor protein in
the cardiac muscle cell. It is directly responsible for converting chemical
energy into the mechanical force, resulting in cardiac muscle contraction. Our
most advanced cardiac program is based on the hypothesis that activators of
cardiac myosin may address certain adverse properties of existing positive
inotropic agents. Current positive inotropic agents, such as beta-adrenergic
receptor agonists or inhibitors of phosphodiesterase activity, increase the
concentration of intracellular calcium, thereby increasing cardiac sarcomere
contractility. The effect on calcium levels, however, also has been linked to
potentially life-threatening side effects. In contrast, our novel cardiac myosin
activators work by a mechanism that directly stimulates the activity of the
cardiac myosin motor protein, without increasing the intracellular calcium
concentration. They accelerate the rate-limiting step of the myosin enzymatic
cycle and shift it in favor of the force-producing state. Rather than increasing
the velocity of cardiac contraction, this mechanism instead lengthens the
systolic ejection time, which results in increased cardiac function in a
potentially more oxygen-efficient manner.

Our earlier stage cardiac program is based on the hypothesis that inhibitors of
hyperdynamic contraction and obstruction of left ventricular blood flow may
counteract the pathologic effects of mutations in the sarcomere that lead to
hypertrophic cardiomyopathies. A targeted oral therapy addressing this disease
etiology may improve symptoms, exercise capacity and potentially slow disease
progression.

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Amgen Strategic Alliance

Our now terminated strategic alliance with Amgen to discover, develop, and
commercialize novel small molecule therapeutics designed to activate cardiac
muscle, including omecamtiv mecarbil, for the potential treatment of heart
failure was governed by the collaboration and option agreement dated December
29, 2006, as amended (the "Amgen Agreement"). Prior to the effective termination
of the Amgen Agreement, Amgen had exclusive, worldwide rights to develop and
commercialize omecamtiv mecarbil and related compounds subject to our specified
development and commercial participation rights. Amgen also entered an alliance
with Les Laboratoires Servier and Institut de Recherches Internationales Servier
("Servier") for exclusive commercialization rights for omecamtiv mecarbil in
Europe as well as the Commonwealth of Independent States ("CIS"), including
Russia; Servier has contributed funding for development and provides strategic
support to the program.

On November 23, 2020, we announced that Amgen had elected to terminate the Amgen
Agreement and thereby end its collaboration with Cytokinetics, and intended to
transition development and commercialization rights for omecamtiv mecarbil and
CK-136 to Cytokinetics.

On December 23, 2020, we announced that Amgen notified us that Servier elected
to terminate the sublicense agreement between Amgen and Servier for the
development and commercialization of omecamtiv mecarbil in Europe and the
Commonwealth of Independent States, including Russia (the "Servier Agreement").
The termination was effective as of March 18, 2021, at which time all
development, commercialization and other rights with respect to omecamtiv
mecarbil previously granted by Amgen to Servier reverted to Amgen.

The termination of the Amgen Agreement was effective May 20, 2021, at which time
worldwide rights related to the development and commercialization of omecamtiv
mecarbil and CK-136 reverted to Cytokinetics. Cytokinetics and Amgen have
entered into several agreements to facilitate the transition of the programs for
omecamtiv mecarbil and CK-136 to Cytokinetics.

As a result of the termination of the Amgen Agreement and Servier Agreement, we
are evaluating a wide range of corporate development strategies for potential
co-development, co-commercialization and licensing deals in relation to
omecamtiv mecarbil and our other drug candidates in order to mitigate the cost
effects of these terminations and to enhance our commercial capabilities.

In 2017, we entered into a Royalty Purchase Agreement (the "RP OM RPA") with RPI
Finance Trust ("RPFT"). Under the RP OM RPA, Cytokinetics sold a portion of its
right to receive royalties from Amgen on future net sales of omecamtiv mecarbil
to RPFT for a one-time payment of $90 million. The RP OM RPA provides for the
sale of a royalty to RPFT of 4.5% on worldwide net sales of omecamtiv mecarbil,
subject to a potential increase of up to an additional 1% under certain
circumstances. As a result of the termination of the Amgen Agreement and
pursuant to our obligations under the RP OM RPA, we and RPFT entered into
Amendment No. 1 to Royalty Purchase Agreement, dated January 7, 2022 to preserve
RPFT's rights under the RP OM RPA by providing for direct payments by us to RPFT
of 4.5% of our and our affiliates' and licensees' worldwide net sales of
omecamtiv mecarbil, subject to a potential increase of up to an additional 1%
under certain circumstances (if the FDA approves omecamtiv mecarbil on its
target PDUFA date of February 28, 2023, the royalty owed to RPFT will be 5.1% of
worldwide net sales of omecamtiv mecarbil).

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Omecamtiv mecarbil

Our lead drug candidate from our cardiac contractility program is omecamtiv
mecarbil, a novel cardiac myosin activator. We are developing omecamtiv mecarbil
as a potential treatment across the continuum of care in heart failure both for
use in the hospital setting and for use in the outpatient setting.

Omecamtiv mecarbil: Clinical Development

GALACTIC-HF: GALACTIC-HF is a Phase 3 cardiovascular outcomes clinical trial of
omecamtiv mecarbil which was conducted by Amgen, in collaboration with
Cytokinetics. The primary objective of this double-blind, randomized,
placebo-controlled multicenter clinical trial is to determine if treatment with
omecamtiv mecarbil when added to standard of care is superior to standard of
care plus placebo in reducing the risk of cardiovascular death or heart failure
events in patients with high risk chronic heart failure and reduced ejection
fraction. GALACTIC-HF was conducted under a Special Protocol Assessment ("SPA")
with the FDA. GALACTIC-HF completed enrollment in mid-2019, having enrolled
8,256 symptomatic chronic heart failure patients with reduced ejection fraction
in over 1,000 sites in 35 countries who were either currently hospitalized for a
primary reason of heart failure or had had a hospitalization or admission to an
emergency room for heart failure within one year prior to screening. Patients
were randomized to either placebo or omecamtiv mecarbil with dose titration up
to a maximum dose of 50 mg twice daily based on the plasma concentration of
omecamtiv mecarbil after initiation of drug therapy. The primary endpoint is a
composite of time to cardiovascular death or first heart failure event,
whichever occurs first, with heart failure event defined as hospitalization,
emergency room visit, or urgent unscheduled clinic visit for heart failure.
Secondary endpoints include time to cardiovascular death; patient reported
outcomes as measured by the Kansas City Cardiomyopathy Questionnaire Total
Symptom Score; time to first heart failure hospitalization; and time to
all-cause death.

On October 8, 2020 we announced the topline results from GALACTIC-HF and on
November 13, 2020 we announced the primary results from GALACTIC-HF. The results
of GALACTIC-HF show that after a median duration of follow-up of 21.8 months,
the trial demonstrated a statistically significant effect of treatment with
omecamtiv mecarbil to reduce risk of the primary composite endpoint of
cardiovascular ("CV") death or heart failure events (heart failure
hospitalization and other urgent treatment for heart failure) compared to
placebo in patients treated with standard of care. A first primary endpoint
event occurred in 1,523 of 4,120 patients (37.0%) in the omecamtiv mecarbil
group and in 1,607 of 4,112 patients (39.1%) in the placebo group (hazard ratio,
0.92; 95% confidence interval [CI] 0.86, 0.99; p=0.025). This effect was
observed without evidence of an increase in the overall rates of myocardial
ischemic events, ventricular arrhythmias or death from cardiovascular or all
causes.

The statistically significant reduction in the composite of heart failure events
or CV deaths, without significant imbalances in the overall incidence of adverse
events across treatment arms, was observed in one of the broadest and most
diverse range of patients enrolled in a contemporary heart failure trial.
GALACTIC-HF included both inpatients and outpatients, and with a high
representation of participants with moderate to severe heart failure symptoms as
well as lower ejection fraction, systolic blood pressure and renal function.

No reduction in the secondary endpoint of time to CV death was observed. Death
from cardiovascular causes occurred in 808 (19.6%) patients treated with
omecamtiv mecarbil and 798 patients (19.4%) assigned to placebo (hazard ratio,
1.01; 95% CI, 0.92 to 1.11; p=0.86). The pre-specified analysis of change from
baseline to week 24 in the KCCQ total symptom score by randomization setting
(inpatient mean difference [95% CI]: 2.50 [0.54, 4.46], outpatient mean
difference: -0.46 [-1.40, 0.48], joint P = 0.028) did not meet the significance
threshold of P=0.002 based upon the multiplicity control testing procedure. No
other secondary endpoints were met in accordance with the prespecified
statistical analysis.

The effect of omecamtiv mecarbil was consistent across most prespecified
subgroups and with a potentially greater treatment effect suggested in patients
with a lower left ventricular ejection fraction ("LVEF") (LVEF ?28%, n=>4,000,
hazard ratio, 0.84; 95% CI 0.77, 0.92; interaction p=0.003). Omecamtiv mecarbil
also significantly decreased NT-proBNP concentrations by 10% (95% CI 6-14%) at
Week 24 compared to placebo.

The overall safety profile of omecamtiv mecarbil in GALACTIC-HF appeared to be
consistent with data from previous trials. Adverse events and treatment
discontinuation of study drug were balanced between the treatment arms. In
general, the overall rates of myocardial ischemia, ventricular arrhythmias and
death were similar between treatment and placebo groups. Additionally, there was
no significant difference in the change in systolic blood pressure between
baseline and at 24 or 48 weeks between the omecamtiv mecarbil and placebo
groups. There was a small but significant decrease in heart rate in participants
assigned to omecamtiv mecarbil compared to placebo at both timepoints. Median
cardiac troponin I concentration increased 4 ng/L (95% CI 3-5; limit of
detection, 6 ng/L) from baseline with omecamtiv mecarbil compared to placebo.

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In December 2020, we announced additional results from GALACTIC-HF. These
results of GALACTIC-HF showed that the effect of omecamtiv mecarbil on the
primary composite endpoint in GALACTIC-HF was consistent across most
prespecified subgroups and with a potentially greater treatment effect suggested
in patients with a lower LVEF (LVEF ?28%, n=4,456, hazard ratio, 0.84; 95% CI
0.77, 0.92; interaction p=0.003). Supplemental analyses of this lower ejection
fraction subgroup in GALACTIC-HF showed that this potentially greater treatment
effect in patients who received omecamtiv mecarbil was consistently observed in
patients with characteristics that may indicate advanced heart failure status,
such as being hospitalized within the last 3 months (HR 0.83, 95% CI 0.74 -
0.93, p=0.001), having New York Association Class III or IV heart failure (HR
0.80, 95% CI 0.71 - 0.90, p<0.001), higher N-terminal-pro brain natriuretic
peptide levels (HR 0.77, 95% CI 0.69 - 0.87, p<0.001), and lower blood pressures
(HR 0.81, 95% CI 0.70 - 0.92, p=0.002). The absolute risk reductions (ARR)
ranged from 5.2% to 8.1% in these subgroups as compared to the ARR of 2.1%
observed in the overall population.

Additionally, a supplemental analysis of the continuous relationship between
ejection fraction and the hazard ratio for the primary composite endpoint in
GALACTIC-HF suggested a potentially stronger treatment effect of omecamtiv
mecarbil in patients with increasingly lower ejection fractions.

In May 2021, at the American College of Cardiology 70th Annual Scientific
Session, we announced data from a secondary analysis of GALACTIC-HF assessing
the effect of omecamtiv mecarbil on clinical outcomes in relationship to patient
baseline ejection fraction. The analysis evaluated the effect of patient
treatment with omecamtiv mecarbil based on quartiles of baseline EF defined as
EF ?22%, EF 23-28%, EF 29-32% and EF ?33% as well as considering baseline EF as
a continuous variable. The incidence of the primary outcome of first heart
failure event or cardiovascular death increased with decreasing ejection
fraction; in the lowest LVEF quartile (EF ?22%) the incidence (35.6 per 100
patient-years) was almost 80% greater than in the highest EF quartile (EF ?33%;
20 per 100 patient-years). Treatment with omecamtiv mecarbil demonstrated a 15%
(HR 0.85; 95% CI 0.74-0.97; p = 0.016) and 17% (HR 0.83; 95% CI 0.73-0.95; p =
0.005) relative risk reduction in the lower two quartiles, respectively,
compared to no difference in the upper two quartiles.

Analysis of ejection fraction as a continuous variable demonstrated a
progressively larger treatment effect of omecamtiv mecarbil with decreasing
ejection fraction. Accordingly, the absolute treatment effect on the primary
composite endpoint also increased between the patients treated with placebo and
omecamtiv mecarbil as baseline ejection fraction decreased such that in the
lowest ejection fraction quartile, there was an absolute reduction of 7.4 events
per 100 patient-years, with a number-needed-to-treat of 11.8 patients necessary
to prevent an event over three years.

In June 2021, at the European Society of Cardiology-Heart Failure Congress, we
announced additional analyses from GALACTIC-HF demonstrating patients with
atrial fibrillation or flutter have increased treatment effect with omecamtiv
mecarbil; patients with higher baseline NT-proBNP have increased treatment
effect with omecamtiv mecarbil; and patients with severe heart failure have
increased treatment effect with omecamtiv mecarbil.

In September 2021, we announced that additional results from GALACTIC-HF
assessing the effect of omecamtiv mecarbil in Black patients with HFrEF were
presented in a late breaking clinical trial session at the HFSA Annual
Scientific Meeting. Specifically, it was presented that of the 8,256 patients
enrolled in the trial, 562 were Black (6.8%) and 285 were randomized to receive
treatment with omecamtiv mecarbil. Among Black patients, treatment with
omecamtiv mecarbil resulted in a trend towards reduction in the primary endpoint
by 18% (HR=0.82, 95% CI 0.64-1.04), corresponding to a reduction in the primary
event rate of 7.7/100 patient-years with a number-needed-to-treat of 13
patients. This result, like the overall study results, was driven primarily by a
reduction in HF hospitalizations (HR=0.80) and HF events (HR=0.82), with no
effect on cardiovascular mortality (HR=1.03). There were no significant
differences in adverse events in Black patients between the groups treated with
omecamtiv mecarbil and placebo.

In April 2022, we announced that additional data from GALACTIC-HF were presented
at the American College of Cardiology 71st Annual Scientific Session, including
a healthcare resource utilization analysis and an analysis of the effect of
treatment with omecamtiv mecarbil in hospitalized patients compared outpatients.
Specifically, an analysis was presented indicating that treatment with omecamtiv
mecarbil led to a 19% cost reduction per patient among the patient subgroup with
ejection fraction less than 30% and were without atrial fibrillation and being
treated with digoxin. In addition, an analysis was presented indicating that the
rate of the primary outcome in GALACTIC-HF was higher in hospitalized patients
in the placebo group (38.3/100 person-years [PY]) than in outpatients (23.1/100
PY) with an adjusted hazard ratio (HR) of 1.21 (95% CI 1.12, 1.31). There was a
stepwise gradient in risk, with those randomized as outpatients in the placebo
group within 3 months of a heart failure event at the highest risk (26.6/100
patient years (PY)) as compared with those 9-12 months post-event (19.0/100 PY)
with an adjusted hazard ratio (HR) of 1.20 (95% CI 1.01, 1.42), p for trend =
0.008). The effect of omecamtiv mecarbil versus placebo on the primary outcome
was similar in hospitalized patients (HR 0.89, 95% CI 0.78, 1.01) and
outpatients (HR 0.94, 95% CI 0.86, 1.02), indicating that omecamtiv mecarbil
similarly reduced the risk of the primary outcome both when initiated in
hospitalized patients and in outpatients. In both hospitalized patients and
outpatients, the initiation of omecamtiv mecarbil was safe and well tolerated.
Treatment-emergent serious adverse events occurred more frequently in patients
randomized during hospitalization but did not differ significantly between the
treatment groups.

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In May 2022, we announced the results from two additional analyses of omecamtiv
mecarbil from GALACTIC-HF were presented in Late-Breaking Science Sessions at
Heart Failure 2022, an International Congress of the European Society of
Cardiology. The analysis from GALACTIC-HF related to low blood pressure has been
simultaneously published in the European Heart Journal.

Specifically, an analysis was presented indicating that in patients with low
blood pressure, there was a greater treatment effect from omecamtiv mecarbil on
the primary composite endpoint of cardiovascular death or first heart failure
event than in patients without low blood pressure such that there was an
absolute risk reduction of 9.8 events per 100 patient-years (hazard ratio, 0.81;
95% confidence interval [CI] 0.70, 0.94; interaction p=0.051). Patients with low
blood pressure treated with omecamtiv mecarbil also experienced improvements in
blood pressure over time as did those treated with placebo. Additionally, the
incidence of treatment-emergent serious adverse events in patients with low
blood pressure who received omecamtiv mecarbil (RR 0.88; 95% CI 0.82, 0.95;
p<0.001) and adjudicated first stroke (RR 0.31; 95% CI 0.12, 0.79; p=0.009) was
lower compared to placebo.

The second analysis presented on the impact of tricuspid regurgitation (TR) on
the effectiveness of omecamtiv mecarbil. The analysis indicated that patients
with moderate/severe TR in GALACTIC-HF experienced higher rates of the primary
composite endpoint, cardiovascular death, all-cause death and heart failure
events. The impact of moderate/severe TR on heart failure events was more
pronounced in outpatients and in patients with higher LVEF, lower NT-proBNP and
lower eGFR. The treatment effect of omecamtiv mecarbil on the primary outcome
was consistent across patients with no TR, mild TR and moderate/severe TR such
that baseline TR did not modify the treatment effect (interaction p=0.91).

METEORIC-HF: On February 15, 2022, we announced topline results and on April 3,
2022, we announced the full results from METEORIC-HF (Multicenter Exercise
Tolerance Evaluation of Omecamtiv Mecarbil Related to Increased Contractility in
Heart Failure), a Phase 3 clinical trial of omecamtiv mecarbil in patients with
HFrEF, were presented at the American College of Cardiology 71st Annual
Scientific Session. METEORIC-HF evaluated the effect of treatment with omecamtiv
mecarbil compared to placebo on exercise capacity as determined by
cardiopulmonary exercise testing ("CPET") following 20 weeks of treatment in
patients with HFrEF receiving standard of care therapy. The trial completed
enrollment of 276 patients in June 2021. There was no effect on the primary
endpoint, which was the change in peak oxygen uptake (pVO2) on CPET from
baseline to Week 20 in patients treated with omecamtiv mecarbil compared to
placebo. Adverse events, including major cardiac events, were similar between
the treatment arms and the safety profile of omecamtiv mecarbil in METEORIC-HF
was consistent with prior clinical trials including GALACTIC-HF.

Omecamtiv mecarbil: New Drug Application

On February 4, 2022, we announced that the FDA had accepted and filed our NDA
for omecamtiv mecarbil for the treatment of HFrEF. The FDA assigned the NDA a
standard review with a Prescription Drug User Fee Act ("PDUFA") target action
date of November 30, 2022. The FDA also indicated, at that time, that it was not
currently planning to hold an advisory committee meeting to discuss the NDA. On
May 17, 2022, we announced that the Company recently participated in a mid-cycle
communication meeting with the FDA and was informed that the FDA was planning to
convene an advisory committee meeting to discuss the NDA. On June 17, 2022, we
announced that, in response to a request from the FDA, the Company provided
additional pharmacokinetic analyses of omecamtiv mecarbil related to its NDA and
after an initial review of the Company's submission, the FDA communicated that
the additional data provided constituted a major amendment to the NDA and
extended the PDUFA target action date by three (3) months to February 28, 2023
to provide time for a full review of the submission. On June 24, 2022, we
announced that the FDA had informed the Company that the previously announced
meeting of the Cardiovascular and Renal Drugs Advisory Committee to review the
NDA for omecamtiv mecarbil is currently scheduled for December 13, 2022.

Omecamtiv mecarbil: Microgenics Immunoassay Development

Amgen and Microgenics Corporation ("Microgenics") were parties to that certain
Collaborative Development and Commercialization Agreement, dated July 26, 2012
(as amended from time to time, the "Assay Agreement"), for the development of an
antibody-based immunoassay (the "Microgenics OM Assay") used for the in vitro
measurement of concentrations of omecamtiv mecarbil in human blood and other
bodily fluids, as well as related calibrator and controls, based on immunoassay
technologies developed by Microgenics and its affiliates suitable for
application on automated chemistry analyzers. The Microgenics OM Assay was
intended to ensure personalized dose optimization of omecamtiv mecarbil in
patients being treated. The Microgenics OM Assay was utilized in both
GALACTIC-HF and METEORIC-HF to enable optimal dose titration in patients. We
have been informed by Amgen that the Assay Agreement terminated
contemporaneously with the termination of the Amgen Agreement. Consequently, we
are pursuing the development and/or usage of alternative dosage selection tests
to the Microgenics OM Assay to be used for personalized dose optimization of
omecamtiv mecarbil if required by FDA or other regulatory authorities in order
to obtain marketing approval of omecamtiv mecarbil.

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Omecamtiv mecarbil: Ji Xing Strategic Alliance

On December 20, 2021, we entered into License and Collaboration Agreement with
Ji Xing (the "Ji Xing OM License Agreement"), pursuant to which we granted to Ji
Xing an exclusive license to develop and commercialize omecamtiv mecarbil in the
People's Republic of China (including the Hong Kong and Macau SARs) ("China")
and Taiwan. Under the terms of the Ji Xing OM License Agreement, we are the
beneficiary of a nonrefundable $50.0 million payment obligation from Ji Xing
comprised of a $40.0 million payment as consideration for the rights granted by
us to Ji Xing and $10.0 million attributable to our having submitted to FDA an
NDA for omecamtiv mecarbil. We may be eligible to receive from Ji Xing
additional payments totaling up to $330.0 million for the achievement of certain
commercial milestone events in connection to omecamtiv mecarbil. In addition, Ji
Xing will pay us tiered royalties in the mid-teens to the low twenties range on
the net sales of pharmaceutical products containing omecamtiv mecarbil in China
and Taiwan, subject to certain reductions for generic competition, patent
expiration and payments for licenses to third party patents. The Ji Xing OM
License Agreement, unless terminated earlier, will continue on a
market-by-market basis until expiration of the relevant royalty term.

CK-136

CK-136 is a novel, selective, oral, small molecule cardiac troponin activator
which was discovered under our joint research program with Amgen. In preclinical
models, CK-136 increases myocardial contractility by binding to cardiac troponin
through an allosteric mechanism that sensitizes the cardiac sarcomere to
calcium, facilitating more actin-myosin cross bridge formation during each
cardiac cycle thereby resulting in increased myocardial contractility. Similar
to cardiac myosin activation, preclinical research has shown that cardiac
troponin activation does not change the calcium transient of cardiac myocytes.

CK-136: Clinical Development

In collaboration with Cytokinetics, Amgen conducted a randomized,
placebo-controlled, double-blind, single and multiple ascending dose,
single-center Phase 1 study to assess the safety and tolerability,
pharmacokinetics and pharmacodynamics of CK-136 in healthy subjects. As a result
of the effective termination of the Amgen Agreement on May 20, 2021, worldwide
rights related to the development and commercialization of CK-136 reverted to
Cytokinetics, and Cytokinetics and Amgen have entered into several agreements to
facilitate the transition of the program for CK-136 to Cytokinetics.

In 2020, we announced that preclinical data were presented at the Keystone
Symposium "Charting a New Course for Heart Failure: From Discovery to Data,"
demonstrating that CK-136 selectively increases calcium sensitivity of cardiac
muscle fibers and increases cardiac contractility.

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In October 2021, we announced that preclinical data relating to the discovery
and optimization of CK-136 were presented at the 2021 Medicinal Chemistry Gordon
Research Conference in West Dover, VT. The data presented described the primary
research objectives related to CK-136 including the identification of initial
hit compounds and subsequent chemical optimization as well as preclinical
characterization in biochemical assays, cardiac myocytes, and in vivo models of
cardiac function. An initial cardiac troponin activator identified in screening
was shown in a reconstituted sarcomere assay to selectively activate the cardiac
troponin complex. Importantly, it did not inhibit phosphodiesterase 3 (PDE-3)
and showed no effect on the cardiomyocyte calcium transient, indicating its
selectivity. The optimization of the initial hit compound that led to CK-136
focused to maximizing the therapeutic window and its pharmacokinetic profile as
could result in favorable increases in cardiac function. Preclinical studies
demonstrated that the pharmacodynamic range for CK-136 was larger than that
associated with omecamtiv mecarbil in similar preclinical models. Additionally,
CK-136 demonstrated a pharmacokinetic profile and a projected human half-life
that should enable once or twice daily dosing. These preclinical data suggest
that CK-136 is a selective cardiac troponin activator with a favorable
pharmacodynamic window associated with substantial increases in cardiac
contractility, representing a potential approach to augmenting cardiac
contractility in diseases characterized by reduced cardiac function.

Aficamten

Aficamten is a novel, oral, small molecule cardiac myosin inhibitor that our
company scientists discovered. Aficamten arose from an extensive chemical
optimization program conducted with attention to therapeutic index and
pharmacokinetic properties that may translate into next-in-class potential in
clinical development. Aficamten was purposely designed to reduce the
hypercontractility that is associated with HCM. In preclinical models, aficamten
reduces myocardial contractility by binding directly to cardiac myosin at a
distinct and selective allosteric binding site, thereby preventing myosin from
entering a force producing state. Aficamten reduces the number of active
actin-myosin cross bridges during each cardiac cycle and consequently reduces
myocardial contractility. This mechanism of action may be therapeutically
effective in conditions characterized by excessive hypercontractility, such as
HCM. The preclinical pharmacokinetics of aficamten were characterized evaluated
and optimized for potential rapid onset, ease of titration and rapid symptom
relief in the clinical setting. The initial focus of the development program for
aficamten will include an extensive characterization of its
pharmacokinetics/pharmacodynamic ("PK/PD") relationship as has been a hallmark
of Cytokinetics' industry-leading development programs in muscle pharmacology.
The overall development program will assess the potential of aficamten to
improve exercise capacity and relieve symptoms in patients with hyperdynamic
ventricular contraction due to HCM.

Aficamten: Clinical Development

We conducted a Phase 1 double-blind, randomized, placebo-controlled, multi-part,
single and multiple ascending dose clinical trial of aficamten to assess the
safety and tolerability, pharmacokinetics and pharmacodynamics of aficamten in
healthy subjects. In September 2019 we presented data from the Phase 1 study of
aficamten at the HFSA 23rd Annual Scientific Meeting in Philadelphia. The study
met its primary and secondary objectives to assess the safety and tolerability
of single and multiple oral doses of aficamten, describe the pharmacokinetics of
aficamten and its pharmacodynamic effects as measured by echocardiography, as
well as to characterize the PK/PD relationship with regards to cardiac function.
These data support the advancement of aficamten into a Phase 2 clinical trial in
patients with oHCM (REDWOOD-HCM), which started in the first quarter of 2020.

In January 2021, we announced that the FDA granted orphan drug designation to aficamten for the treatment of symptomatic HCM.

In May 2021, we announced that the first site had been activated to enroll
patients in REDWOOD-HCM OLE, an open-label extension clinical study designed to
assess the long-term safety and tolerability of aficamten in patients with
symptomatic oHCM. Eligible patients have completed participation in REDWOOD-HCM,
the Phase 2 clinical trial of aficamten.

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In July 2021, we announced positive topline results of Cohorts 1 and 2 of
REDWOOD-HCM. Specifically, results from Cohorts 1 and 2 of REDWOOD-HCM
demonstrated that treatment with aficamten for 10 weeks resulted in
statistically significant reductions from baseline compared to placebo in the
average resting left ventricular outflow tract pressure gradient ("LVOT-G")
(p=0.0003, p=0.0004, Cohort 1 and Cohort 2, respectively) and the average
post-Valsalva LVOT-G (p=0.001, p<0.0001, Cohort 1 and Cohort 2, respectively).
The majority of patients treated with aficamten (78.6% in Cohort 1 and 92.9% in
Cohort 2) achieved the target goal of treatment, defined as resting gradient <30
mmHg and post-Valsalva gradient <50 mmHg at Week 10 compared to placebo (7.7%).
Reductions in LVOT-G occurred within two weeks of initiating treatment with
aficamten, were maximized within two to six weeks of the start of dose
titration, and were sustained until the end of treatment at 10 weeks. The
observed reductions in LVOT-G were dose dependent, with patients achieving
greater reductions of LVOT-G with increasing doses of aficamten. Treatment with
aficamten in REDWOOD-HCM was generally well tolerated. The incidence of adverse
events was similar between treatment arms. No serious adverse events were
attributed to aficamten and no treatment interruptions occurred on aficamten. No
new cases of atrial fibrillation in patients treated with aficamten were
reported. In this dose-range finding trial, one patient experienced a transient
decrease in LVEF that required dose adjustment but not dose interruption. LVEF
returned to baseline within two weeks after the end of treatment in both
cohorts, which was consistent with the reversibility of LVEF decreases that were
similarly observed in healthy participants in the Phase 1 study of aficamten.

In September 2021, we announced that the primary results of REDWOOD-HCM were presented in a late breaking clinical trial session at the HFSA Annual Scientific Meeting.

Reductions in LVOT-G occurred within two weeks of initiating treatment with
aficamten, were maximized within two to six weeks of the start of dose titration
and were sustained until the end of treatment at 10 weeks. Reversibility of the
pharmacodynamic effect of aficamten was seen after a two-week washout, with
resting LVOT-G, post-Valsalva LVOT-G, NT-proBNP and LVEF returning to baseline
values. The observed reductions in LVOT-G were dose dependent, with patients
achieving greater reductions of LVOT-G with increasing doses of aficamten. Over
the 10-week study period, patients treated with aficamten in both Cohort 1 and
Cohort 2 also experienced statistically significant reductions in NT-proBNP
(p=0.003). Treatment with aficamten was also associated with an improvement in
heart failure functional class as measured by New York Heart Association (NYHA)
class. Improvement by at least one class was achieved by 31% in the placebo
group, 43% of patients in Cohort 1 (p>0.1) and 64% of patients in Cohort 2
(p=0.08).

In October 2021, we announced the design of SEQUOIA-HCM. SEQUOIA-HCM is a Phase
3 randomized, placebo-controlled, double-blind, multi-center clinical trial
designed to evaluate aficamten in patients with symptomatic oHCM on background
medical therapy for 24 weeks. The primary objective is to assess the effect of
aficamten on change in peak oxygen uptake (pVO2) measured by CPET from baseline
to week 24. Secondary objectives include change in Kansas City Cardiomyopathy
Questionnaire (KCCQ) score from baseline to week 12 and week 24, the proportion
of patients with ?1 class improvement in NYHA functional class from baseline to
week 12 and week 24, change in post-Valsalva left ventricular outflow tract
gradient (LVOT-G) to week 12 and week 24, the proportion of patients with
post-Valsalva LVOT-G <30 mmHg, and change in total workload during CPET to week
24.

SEQUOIA-HCM is open for enrollment and is expected to enroll 270 patients,
randomized on a 1:1 basis to receive aficamten or placebo in addition to
standard-of-care treatment. Each patient will receive up to four escalating
doses of aficamten or placebo based on echocardiographic guidance alone. At
screening, patients enrolled in SEQUOIA-HCM must have a resting LVOT-G ?30 mmHg,
post-Valsalva peak LVOT-G ?50 mmHg, and be NYHA Class II or III. Patients
receiving aficamten will begin with 5 mg dosed once daily. At weeks 2, 4 and 6
patients will receive an echocardiogram to determine if they will be up-titrated
to escalating doses of 10, 15 or 20 mg. Dose escalation will occur only if a
patient has a post-Valsalva LVOT-G ?30 mmHg and a biplane LVEF ?55%. Patients
who do not meet escalation criteria will continue to receive their current dose
or may be down-titrated if appropriate.

In December 2021, we announced that the FDA granted Breakthrough Therapy Designation for aficamten for the treatment of oHCM.

On February 1, 2022, we announced positive topline results from Cohort 3 of
REDWOOD-HCM and on April 2, 2022, we announced that the full results were
presented at the American College of Cardiology 71st Annual Scientific Session.
Cohort 3 of REDWOOD-HCM enrolled patients with symptomatic oHCM and a resting or
post-Valsalva LVOT-G of ?50 mmHg whose background therapy included disopyramide
and in the majority a beta-adrenergic blocker. All patients received up to three
escalating doses of aficamten once daily (5, 10, 15 mg), titrated based on
echocardiographic guidance. The doses employed were the same as those used in
Cohort 1 of REDWOOD-HCM. Overall treatment duration was 10 weeks with a 4-week
follow up period after the last dose. In total, thirteen patients were enrolled
and all patients completed the study on treatment.

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Results from Cohort 3 demonstrated a substantial reduction in the mean (± SD)
resting LVOT-G (from 50 ± 25 at baseline to 24 ± 17 mmHg at Week 10) and
Valsalva LVOT-G (from 78 ± 27 to 50 ± 25 mmHg). For the resting LVOT-G, the
least square mean difference (± SE) for the change from baseline to Week 10 was
-28 ± 3.2 mmHg (p < 0.0001) and for the Valsalva LVOT-G was -27 ± 5.9 mmHg (p =
0.0002). The relief of obstruction was accompanied by a modest reduction in LVEF
(from 74 ± 7% at baseline to 69 ± 7% at Week 10). For LVEF, the least square
mean difference (± SE) for the change from baseline to Week 10 was -4.8 ± 1.9%
(p = 0.018). There were no patients who experienced a reduction in LVEF below
the prespecified safety threshold of 50%.

Treatment with aficamten resulted in 6 of the 13 patients (46%) experiencing a
complete hemodynamic response by Week 10, with the remaining 7 (54%) still
eligible for dose escalation to the highest dose of aficamten (20 mg) employed
in SEQUOIA-HCM, the Phase 3 trial. Eleven of 13 patients (85%) experienced
improvement in NYHA class by at least one class. In addition to hemodynamic and
functional capacity improvements, patients also experienced a significant
improvement in NT-proBNP and trended to lower hs-troponin I. The safety and
tolerability of aficamten were consistent with prior experience in REDWOOD-HCM
with no dose interruptions or treatment discontinuations and no serious adverse
events. Coadministration of aficamten along with disopyramide and beta-blockers
or calcium-channel blockers did not result in any significant
electrocardiographic changes including in the QT-interval, or in blood pressure
or heart rate.

On March 2, 2022, we announced the opening of enrollment in Cohort 4 of
REDWOOD-HCM. Cohort 4 will enroll, in an open label fashion, 30-40 patients with
symptomatic non-obstructive HCM ("nHCM") receiving background medical therapy.
At screening, patients must have a LVEF of ?60%, an elevated NT-proBNP >300
pg/mL, and must not have resting or post-Valsalva LVOT gradients (<30 mmHg in
each case). The primary objective is to determine the safety and tolerability of
aficamten in patients with nHCM. Other objectives include the effect of
aficamten on LVEF, NYHA Functional Class and cardiac biomarkers. All patients
will receive up to three escalating doses of aficamten, with doses being
adjusted based on echocardiography according to LVEF alone. Cohort 4 will employ
doses of 5, 10 and 15 mg once daily. Overall treatment duration will be 10 weeks
with a 4-week follow up period after the last dose.

On May 23, 2022, we announced positive data relating to aficamten from
REDWOOD-HCM OLE were presented in Late-Breaking Science Sessions at Heart
Failure 2022, an International Congress of the European Society of Cardiology.
Specifically, data from 38 patients enrolled in REDWOOD-HCM OLE were presented,
including 30 patients treated for 12 weeks and 19 patients treated for 24 weeks.
The data showed that treatment with aficamten was associated with substantial
reductions in the average resting LVOT-G (mean change from baseline (SD) = -32.6
(28) mmHg, p<0.0001 at 12 weeks, -32.8 (32.3) mmHg, p=0.0003 at 24 weeks) and
Valsalva LVOT-G (-42.7 (38.7) mmHg, p<0.0001 at 12 weeks, -51.1 (35.3) mmHg,
p<0.0001 at 24 weeks). These reductions started to occur within two weeks of
treatment, were sustained through 24 weeks of treatment, and were achieved with
only modest decreases in the average LVEF (-3.2 (4.2) %, p=0.0038 at 24 weeks).
Compared to baseline (47% Class II, 53% Class III), New York Heart Association
(NYHA) Functional Class was improved in the majority of patients (p<0.0001 for
improvement by one or more NYHA class), and no patients had a worsening of NYHA
Class. At 12 weeks, 72% of patients improved by one class and 7% improved by two
classes; at 24 weeks 61% of patients improved by one class and 17% improved by
two classes. For patients reaching Week 24, 56% were Class I and 39% were Class
II. There were also significant improvements in cardiac biomarkers including
NTpro-BNP (reduction of 70% from baseline, p<0.001) and cardiac troponin (20%
reduction, p=0.002). Treatment with aficamten was well-tolerated with one
temporary discontinuation due to LVEF <50% and one temporary down-titration,
neither related to drug. Both patients remain on treatment with aficamten.

On June 13, 2022, we announced that additional data from a new analysis of
REDWOOD-HCM relating to the effect of treatment with aficamten on measures of
cardiac structure and function were presented at the American Society of
Echocardiography (ASE) 33rd Annual Scientific Sessions. Specifically, the new
analysis investigated changes from baseline in echocardiographic measures of
cardiac structure and function after 10 weeks of treatment with aficamten
compared with placebo. At baseline, all patients (n=41) enrolled in Cohorts 1
and 2 of REDWOOD-HCM had severe left ventricular outflow tract (LVOT)
obstruction, 88% had associated systolic anterior motion (SAM) of the mitral
valve, and 90% had mitral regurgitation. SAM occurs when the mitral valve
leaflet gets pushed against the interventricular septum during systole,
resulting in obstruction of the LVOT and mitral regurgitation.

Measures of cardiac structure, diastolic and mitral valve function improved at
Week 10 in patients treated with aficamten. There was a significant reduction in
left atrial volume index (p<0.01) and a trend towards a reduction in left
ventricular hypertrophy (left ventricular mass index; p=0.06). Treatment with
aficamten also resulted in improved ventricular relaxation and filling, as
indicated by a reduction in lateral E/e' (p<0.01) and an increase in lateral e'
(p<0.05). Additionally, treatment with aficamten improved mitral valve dynamics
as noted by a reduction in the proportion of patients with SAM (placebo: 92.3%
at baseline to 75.0% at Week 10; aficamten: 85.7% at baseline to 35.7% at Week
10; p=0.038 for comparison to placebo) and a trend towards a reduction in those
with eccentric mitral regurgitation (placebo: 25.0% at baseline to 33.3% at Week
10; aficamten: 42.9% at baseline to 7.1% at Week 10; p=0.055 for comparison to
placebo) at Week 10. Together, these data point to evidence of early signs of
improved cardiac function and structure and improved mitral valve dynamics after
a 10-week treatment period with aficamten.

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Ji Xing Strategic Alliance

On July 14, 2020, we entered into a certain License and Collaboration Agreement
with Ji Xing (the "Ji Xing Aficamten License Agreement"), pursuant to which we
granted to Ji Xing an exclusive license to develop and commercialize aficamten
in China and Taiwan. Under the terms of the Ji Xing Aficamten License Agreement,
we received from Ji Xing an upfront payment of $25.0 million. We may be eligible
to receive from Ji Xing milestone payments totaling up to $200.0 million for the
achievement of certain development and commercial milestone events in connection
to aficamten in the field of oHCM, and/or nHCM and other indications. In
addition, Ji Xing will pay us tiered royalties in the low-to-high teens range on
the net sales of pharmaceutical products containing aficamten in China and
Taiwan, subject to certain reductions for generic competition, patent expiration
and payments for licenses to third party patents. The Ji Xing Aficamten License
Agreement, unless terminated earlier, will continue on a market-by-market basis
until expiration of the relevant royalty term.

CK-271

In 2020, we completed our planned Phase 1, single-dose pharmacokinetic
evaluation and tolerability assessments of CK-271 in healthy volunteers and
determined it to be suitable for further development. The primary objective of
this Phase 1 placebo-controlled, single ascending dose clinical study in healthy
adults was to assess the safety and tolerability of CK-271. The secondary
objective was to evaluate the pharmacokinetic profile of CK-271 following single
oral ascending doses. The study design included three cohorts, with 8 adults per
cohort randomized (6:2) in a blinded fashion to CK-271 or placebo. Dose
escalation decisions were made after review of the available safety,
pharmacokinetic, and echocardiography data. We are evaluating its potential for
its further development in connection with our plans to conduct a broad
development program for our cardiac myosin inhibitor(s) in HCM and potentially
other indications.

Skeletal Muscle Contractility Program

Our skeletal muscle contractility program is focused on the activation of the
skeletal sarcomere, the basic unit of skeletal muscle contraction. The skeletal
sarcomere is a highly ordered cytoskeletal structure composed of skeletal muscle
myosin, actin, and a set of regulatory proteins, which include the troponins and
tropomyosin. This program leverages our expertise developed in our ongoing
discovery and development of cardiac sarcomere activators, including the cardiac
myosin activator, omecamtiv mecarbil.

We believe that our skeletal sarcomere activators may lead to new therapeutic
options for diseases and medical conditions associated with neuromuscular
dysfunction and potentially also conditions associated with aging and muscle
weakness and wasting. The clinical effects of muscle weakness and wasting,
fatigue and loss of mobility can range from decreased quality of life to, in
some instances, life-threatening complications. By directly improving skeletal
muscle function, a small molecule activator of the skeletal sarcomere
potentially could enhance functional performance and quality of life in patients
suffering from diseases or medical conditions associated with skeletal muscle
weakness or wasting, such as ALS, spinal muscular atrophy ("SMA"), chronic
obstructive pulmonary disease ("COPD") or sarcopenia (general frailty associated
with aging).

Astellas Strategic Alliance

Our strategic alliance with Astellas to advance novel therapies for diseases and
medical conditions associated with muscle impairment and weakness commenced in
2013 under the License and Collaboration Agreement, dated June 21, 2013 between
the parties (the "Astellas Agreement"). Initially we exclusively licensed to
Astellas rights to co-develop and potentially co-commercialize reldesemtiv and
other FSTAs in non-neuromuscular indications and to develop and commercialize
other novel mechanism skeletal muscle activators in all indications, subject to
certain Cytokinetics' development and commercialization rights. Subsequently, in
2014, we and Astellas expanded the strategic alliance to include certain
neuromuscular indications, including SMA, for reldesemtiv and other FSTAs and to
advance reldesemtiv into Phase 2 clinical development, initially in SMA. In
2016, we and Astellas further expanded the strategic alliance to include the
development of reldesemtiv for the potential treatment of ALS, as well as the
possible development in ALS of other FSTAs previously licensed by us to
Astellas.

In April 2020, Cytokinetics and Astellas entered into two agreements, which,
taken together, amend and restate our research, development and
commercialization collaboration with Astellas under the Astellas Agreement, as
set out below.

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Cytokinetics and Astellas signed a Fast Skeletal Regulatory Activator Agreement
dated April 23, 2020 (the "Astellas FSRA Agreement"). As a result of the
Astellas FSRA Agreement, Cytokinetics will now have exclusive control and
responsibility for Cytokinetics' future development and commercialization of
reldesemtiv, CK-601 and other fast skeletal regulatory activator (collectively
"FSRA") compounds and products, and accordingly, Astellas agreed to terminate
its license to all FSRA compounds and related products. Under the Astellas FSRA
Agreement, Astellas agreed to pay one-third of the out-of-pocket clinical
development costs which may be incurred in connection with Cytokinetics' Phase 3
clinical trial of reldesemtiv in ALS up to a maximum contribution by Astellas of
$12 million. In addition, Astellas agreed to non-cash contributions to
Cytokinetics, which include the transfer of its existing inventories of active
pharmaceutical ingredient of reldesemtiv and CK-601. Astellas also agreed to the
continued conduct of ongoing stability studies pertaining to such existing
inventories of active pharmaceutical ingredient, at Astellas' cost. In exchange,
Cytokinetics will pay Astellas a low- to mid- single digit royalty on sales of
reldesemtiv in the United States, Canada, United Kingdom and the European Union
until the later of (i) ten years following the first commercial sale of such
product in a major market country, or (ii) December 31, 2034, subject to certain
royalty reduction provisions. Cytokinetics would not owe Astellas royalties on
sales of reldesemtiv in any other country, or on the sale of any FSRA compounds
or related products other than reldesemtiv.

Cytokinetics and Astellas also signed that certain License and Collaboration
Agreement for Other Skeletal Sarcomere Activators, dated April 23, 2020 (the
"Astellas OSSA Agreement"). The Astellas OSSA Agreement is an amendment and
restatement of the Astellas Agreement and removes the FSRA compounds and related
products from the collaboration.

Under the Astellas OSSA Agreement, Astellas extended the joint research program
at Cytokinetics focused on the discovery of additional next-generation skeletal
muscle activators (other than FSRAs) through December 31, 2020, with a minimum
of fifteen (15) research FTE's being supported by Astellas. The parties
subsequently agreed to extend this joint research program through March 31,
2021, with up to five (5) research FTE's at Cytokinetics being supported by
Astellas.

On April 27, 2021, we received written notice of termination from Astellas of the Astellas OSSA Agreement. The effective date of the termination of the Astellas OSSA Agreement was November 1, 2021.

Under the terms of the Astellas OSSA Agreement, Astellas received exclusive
rights to co-develop and commercialize skeletal sarcomere activators (other than
FSRA compounds and products) in all indications, subject to certain development
and commercialization rights of Cytokinetics; Cytokinetics had the right to
co-promote and conduct certain commercial activities in the U.S., Canada and/or
Europe under agreed scenarios. If development candidates were identified and
advanced in clinical research, the Astellas OSSA Agreement contained provisions
related to shared development roles between Cytokinetics and Astellas, and
opportunities for Cytokinetics to co-invest and/or co-promote under certain
conditions. In the case of development candidates taken forward solely by
Astellas, Cytokinetics would have received development and regulatory milestones
of $25 to $35 million per product, up to $250 million for all products, except
under certain scenarios, commercial milestones of up to $200 million, and
royalties that ranged from a mid-single digit level to low double-digits. In the
event of co-investment by Cytokinetics and approvals in certain indications,
Cytokinetics would have received royalties ranging from mid-to-high double
digits (not to exceed an incremental rate in the mid-twenties).

Pursuant to the terms of the Astellas OSSA Agreement, upon the effective date of
the termination, all licenses and other rights granted to Astellas under the
Astellas OSSA Agreement terminated.

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Reldesemtiv

Reldesemtiv selectively activates the fast skeletal muscle troponin complex in
the sarcomere by increasing its sensitivity to calcium, leading to an increase
in skeletal muscle contractility. Reldesemtiv has demonstrated pharmacological
activity in preclinical models and evidence of potentially clinically relevant
pharmacodynamic effects in humans. The FDA granted reldesemtiv orphan drug
designation for the potential treatment of SMA in 2017 and for the potential
treatment of ALS in 2019. The European Medicines Agency ("EMA") granted orphan
medicinal product designation to reldesemtiv for the potential treatment of SMA
in July 2019 and for the potential treatment of ALS in March 2020.

Reldesemtiv: Clinical Development

SMA: In 2018, we announced data from a hypothesis-generating, Phase 2
double-blind, randomized, placebo-controlled clinical study in patients with SMA
which was designed to determine potential pharmacodynamic effects of a
suspension formulation of reldesemtiv following 8 weeks of oral dosing in each
of two cohorts of 36 patients with Type II, Type III, or Type IV disease.
Secondary objectives were to evaluate the safety, tolerability and
pharmacokinetics of reldesemtiv. The study showed statistically significant
concentration-dependent increases in changes from baseline in Six Minute Walk
Distance ("6MWD"), a sub-maximal exercise test of aerobic capacity and
endurance. The study also showed statistically significant increases for Maximal
Expiratory Pressure ("MEP"), a measure of strength of respiratory muscles. Other
assessments, including the Hammersmith Functional Motor Score - Extended,
Revised Upper Limb Module, Timed Up-and-Go, Forced Vital Capacity, and the SMA
Health Index ("SMA-HI"), a patient reported outcome measure ("PROM") developed
to comply with FDA standards for PROMs, did not demonstrate differences between
reldesemtiv versus placebo. Adverse events were similar between groups receiving
reldesemtiv and placebo.

Additional results presented in 2018 showed sustained increases in 6MWD and MEP
four weeks after discontinuation of study drug (i.e., follow-up). A post-hoc
analysis also showed that changes from baseline in the 6MWD at 450 mg twice
daily were significantly correlated with changes from baseline on certain
domains of the SMA-HI intended to reflect improved endurance, especially Fatigue
and Activity Participation. Decreases in SMA-HI scores reflect reduced disease
burden as measured by that PROM, suggesting that as 6MWD increased, disease
burden assessed by that domain of the SMA-HI was reduced.

In 2019, we announced that we received feedback from the FDA that the 6MWD is an
acceptable primary efficacy endpoint for a potential registration program for
reldesemtiv in patients with SMA who have maintained ambulatory function. The
FDA also recommended adding a global function scale as a secondary endpoint.

In 2019, we announced that data from two preclinical studies of reldesemtiv showed that the addition of reldesemtiv to treatment with SMN upregulators (nusinersen and SMN-C1, an analogue to risdiplam) significantly increased muscle force in a mouse model of SMA.

ALS: In collaboration with Astellas, we conducted FORTITUDE-ALS (Functional
Outcomes in a Randomized Trial of Investigational Treatment with CK-2127107 to
Understand Decline in Endpoints - in ALS). This Phase 2 trial enrolled 458
eligible ALS patients who were randomized (1:1:1:1) to receive either 150 mg,
300 mg or 450 mg of reldesemtiv or placebo dosed orally twice daily for 12
weeks. The primary efficacy endpoint of FORTITUDE-ALS was the change from
baseline in the percent predicted slow vital capacity ("SVC") at 12 weeks.
Secondary endpoints included slope of the change from baseline in the mega-score
of muscle strength measured by hand held dynamometry and handgrip dynamometry in
patients on reldesemtiv; change from baseline in the ALS Functional Rating Scale
- Revised ("ALSFRS-R"); incidence and severity of treatment-emergent adverse
events; and plasma concentrations of reldesemtiv at the sampled time points
during the study. Exploratory endpoints measured included the effect of
reldesemtiv versus placebo on self-assessments of respiratory function made at
home by the patient with help as needed by the caregiver; disease progression
through quantitative measurement of speech production characteristics over time;
disease progression through quantitative measurement of handwriting abilities
over time; and the change from baseline in quality of life (as measured by the
ALS Assessment Questionnaire-5) in patients on reldesemtiv.

In 2019, we announced results of FORTITUDE-ALS. FORTITUDE-ALS did not achieve
statistical significance for a pre-specified dose-response relationship in its
primary endpoint of change from baseline in SVC after 12 weeks of dosing
(p=0.11). Similar analyses of ALSFRS-R and slope of the Muscle Strength
Mega-Score yielded p-values of 0.09 and 0.31, respectively. However, patients on
all dose groups of reldesemtiv declined numerically less than patients on
placebo for SVC and ALSFRS-R, with larger differences emerging over time.

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While the dose-response analyses for the primary and secondary endpoints did not
achieve statistical significance at the level of 0.05, in a post-hoc analysis
pooling the doses together, patients who received reldesemtiv in FORTITUDE-ALS
declined less than patients who received placebo. The trial showed numerical
effects favoring reldesemtiv across dose levels and timepoints with clinically
meaningful magnitudes of effect observed at 12 weeks for the primary and
secondary endpoints. The differences between reldesemtiv and placebo in SVC and
ALSFRS-R total score observed after 12 weeks of treatment were still evident at
follow-up, four weeks after the last dose of study drug.

The incidence of early treatment discontinuations, serious adverse events and
clinical adverse events in FORTITUDE-ALS were similar between placebo and active
treatment arms. The most common clinical adverse effects in the trial included
fatigue, nausea and headache. The leading cause for early termination from
FORTITUDE-ALS for patients who received placebo was progressive disease; the
leading cause for early termination for patients who received reldesemtiv was a
decline in cystatin C based estimated glomerular filtration rate ("eGFR"), a
measure of renal function. Elevations in transaminases and declines in cystatin
C eGFR were dose-related.

In 2019, post-hoc analyses from FORTITUDE-ALS were presented. The analyses
demonstrated that, in the combined middle and faster progressing tertiles of
patients, the decline in the ALSFRS-R total score from baseline to week 12 in
patients who received any dose of reldesemtiv was significantly smaller than the
decline on placebo, while no significant difference between reldesemtiv and
placebo was observed in slower progressing patients.

In 2019, we presented subgroup analyses of FORTITUDE-ALS showing that the effect
of reldesemtiv on patients with ALS was similar whether or not patients were
also receiving Radicava® (edaravone) and/or Rilutek® (riluzole).

In December 2020, we announced that additional post-hoc analyses from
FORTITUDE-ALS evaluating how baseline patient characteristics impacted the
effect of treatment with reldesemtiv versus placebo. When patients were divided
into faster, middle and slower progressing tertiles based on pre-study ALSFRS-R
progression rates, the middle and fastest progressing tertiles of patients
combined showed a 27% difference at 12 weeks between patients receiving
reldesemtiv versus placebo (1.15 ALSFRS-R points, p=0.011), compared to 18% (0.4
points; p=0.43) in the slowest progressing tertile. In general, patients with a
longer symptom duration were slower progressors; 59% of those with SD >24 months
were in the slowest tertile. Most patients who were minimally affected with an
ALSFRS-R ?45 at baseline were also slow progressors. In comparing the treatment
effect of slow progressing patients with symptoms ?24 months and a baseline
ALSFRS-R score of ?44 to the original primary analysis population, the effect
size and statistical significance increased, despite reducing the number of
analyzed patients. In an analysis of the total study population (n=458),
combining all patients who received reldesemtiv and comparing to those who
received placebo, the change from baseline to week 12 in the ALSFRS-R total
score showed a least square mean (LSM) difference of 0.87 (p=0.013). However,
limiting the analysis population to patients with symptoms ?24 months and a
baseline ALSFRS-R score of ?44 (n=272), the LSM difference was 1.84 (p=0.0002).
Together, these post-hoc analyses indicate that the impact of treatment with
reldesemtiv was more apparent in patients with faster pre-study rates of
progression, which include patients with short symptom duration and lower
baseline ALSFRS-R scores.

Also in December 2020, we announced the design of COURAGE-ALS, the Phase 3
clinical trial of reldesemtiv in patients with ALS, which is currently open for
enrollment. COURAGE-ALS is expected to enroll approximately 555 patients with
ALS. Patients will be randomized 2:1 to receive 300 mg of reldesemtiv or
matching placebo dosed orally twice daily for 24 weeks, followed by a 24-week
period in which all patients will receive 300 mg of reldesemtiv twice daily.
Eligible patients will be within the first two years of their first symptom of
muscle weakness, have a vital capacity of ?65% predicted, and a screening
ALSFRS-R ?44. Patients currently taking stable doses of Radicava® (edaravone)
and/or Rilutek® (riluzole) will be permitted and randomization stratified
accordingly. The primary efficacy endpoint will be change from baseline to 24
weeks in ALSFRS-R. Secondary endpoints include combined assessment of ALSFRS-R
total score; time to onset of respiratory insufficiency and survival time up to
week 24 using a joint rank test; change from baseline to 24 weeks for vital
capacity; ALSAQ-40; and bilateral handgrip strength. Two unblinded interim
analyses by the Data Monitoring Committee are planned. The first will assess for
futility, 12 weeks after approximately one-third or more of the planned sample
size is randomized. A second interim analysis will also assess for futility, and
there will be an option for a fixed increase in total enrollment if necessary to
augment the statistical power of the trial. This Phase 3 clinical trial design
builds on insights gained from FORTITUDE-ALS, further exploring the hypothesis
that fast skeletal muscle activation with reldesemtiv may be an important
therapeutic strategy in ALS.

In August 2021, we announced that COURAGE-ALS was opened to enrollment, and enrollment is currently ongoing.

In June 2022, we announced the start of COURAGE-ALS OLE, an open-label extension
clinical study designed to assess the long-term safety and tolerability of
reldesemtiv in people with ALS. Patients will be eligible for COURAGE-ALS OLE
after completing their participation in COURAGE-ALS.

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Next Generation Fast Skeletal Muscle Troponin Activators

In 2018, we announced the advancement of CK-601, a next-generation FSTA, into
IND-enabling studies, which triggered a $2.0 million milestone payment from
Astellas to us. CK-601 was designed in a joint research program conducted by the
companies' scientists to have different pharmacokinetics and physicochemical
properties than reldesemtiv which may inform its development for the treatment
of diseases and conditions associated with both neuromuscular and
non-neuromuscular etiology and pathogenesis.

Ongoing Research in Skeletal Muscle Activators

We are conducting translational research in preclinical models of disease and
muscle function with FSTAs to explore the potential clinical applications of
this novel mechanism in diseases or conditions associated with skeletal muscle
dysfunction.

Beyond Muscle Contractility

We developed preclinical expertise in the mechanics of skeletal, cardiac and
smooth muscle that extends from proteins to tissues to intact animal models. Our
translational research in muscle contractility has enabled us to better
understand the potential impact of small molecule compounds that increase
skeletal or cardiac muscle contractility and to apply those findings to the
further evaluation of our drug candidates in clinical populations. In addition
to contractility, other major functions of muscle play a role in certain
diseases that could benefit from novel mechanism treatments. Accordingly, our
knowledge of muscle contractility may serve as an entry point to the discovery
of novel treatments for disorders involving muscle functions other than muscle
contractility. We are leveraging our current understandings of muscle biology to
investigate new ways of modulating these other aspects of muscle function for
other potential therapeutic applications.

COVID-19 Business Update

We are continuing to closely monitor the impact of the global COVID-19 pandemic
on our business and continue to take proactive efforts designed to protect the
health and safety of our employees, patients, study investigators and clinical
research staff, and to maintain business continuity. We believe that the
measures we are implementing are appropriate and are helping to reduce the
transmission of COVID-19, and we will continue to monitor and seek to comply
with guidance from governmental authorities and adjust our activities as
appropriate.

Based on guidance issued by federal, state and local authorities, we
transitioned to a remote work model for a vast majority of our employees
effective March 16, 2020, while maintaining certain essential in-person
laboratory functions in order to advance key research and development
initiatives, supported by the implementation of updated onsite procedures. We
subsequently implemented a voluntary return to work for our employees subject to
precautionary measures such as mandatory temperature checks for those employees
that work on site from time to time. In March 2022, we transitioned to a hybrid
work model, where the vast majority of our local employees will be required to
work onsite for at least 3 days per week. We will continue to monitor the
evolution of the pandemic and take appropriate precautionary actions in
accordance with applicable laws and guidelines.

In the conduct of our business activities, we are also taking actions designed
to protect the safety of patients and healthcare professionals. For patients
already enrolled in our clinical trials, we and our partners are working closely
with study investigators and clinical trial site staff to continue treatment in
compliance with trial protocols and to uphold trial integrity, while working to
observe government and institutional guidelines designed to safeguard the health
and safety of patients and site staff.

While the potential economic impact brought by, and the duration of, the
COVID-19 pandemic may be difficult to assess or predict, the pandemic could
result in significant and prolonged disruption of global financial markets,
reducing our ability to access capital, which could in the future negatively
affect our liquidity. In addition, a recession or market correction resulting
from the spread of COVID-19 could materially affect our business and the value
of our common stock.

While we expect the COVID-19 pandemic to continue to affect our business
operations, the extent of the impact on our clinical development and regulatory
efforts and the value of and market for our common stock will depend on future
developments that are highly uncertain and cannot be predicted with confidence
at this time, such as the ultimate duration of the pandemic, travel
restrictions, quarantines, social distancing and business closure requirements
in the U.S. and in other countries, and the effectiveness of actions taken
globally to contain and treat COVID-19. For additional information about risks
and uncertainties related to the COVID-19 pandemic that may impact our business,
our financial condition and our results of operations, see the section titled
"Risk Factors" under Part II, Item 1A in this Quarterly Report on Form 10-Q.

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Critical Accounting Policies and Significant Estimates

The accounting policies that we consider to be our most critical (i.e., those
that are most important to the portrayal of our financial condition and results
of operations and that require our most difficult, subjective or complex
judgments), the effects of those accounting policies applied and the judgments
made in their application are summarized in "Item 7 - Management's Discussion
and Analysis of Financial Condition and Results of Operations - Critical
Accounting Policies and Significant Estimates" in our Annual Report on Form 10-K
for the fiscal year ended December 31, 2021.

Our discussion and analysis of our financial condition and results of operations
are based on our financial statements, which have been prepared in accordance
with accounting principles generally accepted in the United States. The
preparation of these financial statements requires us to make estimates and
judgments that affect the reported amounts of assets, liabilities and expenses
and related disclosure of contingent assets and liabilities. We review our
estimates on an ongoing basis. We base our estimates on historical experience
and on various other assumptions that we believe to be reasonable under the
circumstances. Actual results may differ from these estimates under different
assumptions or conditions.

Recent Accounting Pronouncements

See Note 1, "Recent Accounting Pronouncements" in the Notes to Unaudited
Condensed Consolidated Financial Statements for a discussion of recently adopted
accounting pronouncements and accounting pronouncements not yet adopted, and
their expected impact on our financial position and results of operations.

Results of Operations

Revenues

Our revenues since inception were primarily from our strategic alliances. Under
our now terminated collaboration agreements with Amgen and Astellas, namely the
Amgen Agreement and the Astellas OSSA Agreement, we received payments including
upfront license fees, reimbursements of internal costs of certain FTEs and costs
to support research and development programs, and milestone payments. We have
not generated any revenue from commercial product sales to date.

Revenues for the three and six months ended June 30, 2022 and 2021, were as follows (in thousands):

                                  Three Months Ended                                        Six Months Ended
                                                                    Increase                                                 Increase
                           June 30, 2022       June 30, 2021       (Decrease)       June 30, 2022       June 30, 2021       (Decrease)
Research and
development revenues      $           968     $         2,843     $     (1,875 )   $         2,116     $         9,391     $     (7,275 )
Milestone revenues                  1,000                   -            1,000               1,000                   -            1,000
Realization of revenue             87,000                   -           87,000              87,000                   -           87,000
participation right
purchase agreement
Total revenues            $        88,968     $         2,843     $     86,125     $        90,116     $         9,391     $     80,725


Research and development revenues for the three and six months ended June 30,
2022 were from Astellas for reimbursements under the Astellas FSRA Agreement and
in 2021 were from Astellas and Amgen under the Amgen Agreement.

Co-funding under the Astellas FSRA Agreement for the conduct of COURAGE-ALS will continue until the $12.0 million cap is reached.

During the three and six months ended June 30, 2022, we recognized milestone revenues under the Research Collaboration Agreement, dated August 24, 2012, between us and MyoKardia, Inc.

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During the three and six months ended June 30, 2022, we recognized revenues of
$87.0 million related to the 2020 RTW Royalty Purchase Agreement. In July 2020,
we sold our right to receive certain payments on the net sales of products
containing the compound mavacamten, a cardiac myosin inhibitor (the "Mavacamten
Royalty"), under the Research Collaboration Agreement, dated August 24, 2012,
between us and MyoKardia, Inc. The RTW Royalty Purchase Agreement transaction
closed on November 13, 2020. On March 31, 2021, RTW Royalty Holdings assigned
its rights and obligations under the RTW Royalty Purchase Agreement to its
affiliate, RTW Investments ICAV for RTW Fund 1 ("RTW ICAV"). We understand that
on April 18, 2022, RTW ICAV and MyoKardia, Inc. entered into agreements, which
purported to assign all of RTW ICAV's rights, title and interest to the
Mavacamten Royalty to MyoKardia, Inc., and on April 25, 2022, we entered into a
tripartite agreement with RTW ICAV and MyoKardia, Inc. acknowledging the release
and discharge of any further obligations by us or MyoKardia, Inc. in connection
to the Mavacamten Royalty. As a result of the full extinguishment of the
Mavacamten Royalty, we recognized revenue of $87.0 million.

Research and Development Expenses

We incur research and development expenses associated with both partnered and our own research activities.

Research and development expenses related to any development we elect to fund
consist primarily of employee compensation, supplies and materials, costs for
consultants and contract research and manufacturing, facilities costs and
depreciation of equipment.

Research and development expenses by program for the three and six months ended June 30, 2022 and 2021, were as follows (in thousands):

                                  Three Months Ended                                      Six Months Ended
                           June 30, 2022       June 30, 2021       Increase       June 30, 2022       June 30, 2021       Increase
Cardiac muscle
contractility             $        27,664     $        26,175     $    1,489     $        53,151     $        42,412     $   10,739
Skeletal muscle
contractility                      14,841               3,094         11,747              26,300              11,450         14,850
All other research
programs                           14,621               7,174          7,447              23,610              14,142          9,468
Total research and
development expenses      $        57,126     $        36,443     $   20,683     $       103,061     $        68,004     $   35,057


Research and development expenses for the three and six months ended June 30,
2022 increased by $20.7 million and $35.1 million from the three and six months
ended June 30, 2021, respectively, primarily due to higher expenses for our
clinical development activities for COURAGE-ALS, for our cardiac muscle
inhibitor programs, and for early research activities.

We continue to develop reldesemtiv to treat ALS and we recently announced that
COURAGE-ALS, the Phase 3 clinical trial of reldesemtiv in patients with ALS, is
open to enrollment. We may also continue to develop reldesemtiv to treat SMA.
Under the Astellas FSRA Agreement, Astellas has agreed to pay one-third of the
out-of-pocket clinical development costs which may be incurred in connection
with Cytokinetics' Phase 3 clinical trial, COURAGE-ALS, of reldesemtiv in ALS up
to a maximum contribution by Astellas of $12.0 million.

Under our now terminated strategic alliance with Amgen, Amgen was responsible
for the development of omecamtiv mecarbil until the effective termination of the
Amgen Agreement, which occurred on May 20, 2021. Following the effective
termination of the Amgen Agreement, we continued the Phase 3 development of
omecamtiv mecarbil for the potential treatment of heart failure, at our own
cost. We expect to continue the development of aficamten to assess the potential
of aficamten to improve exercise capacity and relieve symptoms in patients with
hyperdynamic ventricular contraction due to HCM. Under our strategic alliances
with Ji Xing, Ji Xing is responsible for the development of aficamten and
omecamtiv mecarbil in China and Taiwan, and we may be entitled to receive
milestone payments upon the achievement of certain development and commercial
milestones.

Clinical development timelines, the likelihood of success and total completion
costs vary significantly for each drug candidate and are difficult to estimate.
We anticipate that we will determine on an ongoing basis which research and
development programs to pursue and how much funding to direct to each program,
taking into account the potential scientific and clinical success of each drug
candidate. The lengthy process of seeking regulatory approvals and subsequent
compliance with applicable regulations requires the expenditure of substantial
resources. Any failure by us to obtain and maintain, or any delay in obtaining,
regulatory approvals could cause our research and development expenditures to
increase and, in turn, could have a material adverse effect on our results of
operations.

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General and Administrative Expenses

General and administrative expenses consist primarily of compensation for
employees in executive and administrative functions, including, but not limited
to, finance, human resources, legal, business and commercial development and
strategic planning. Other significant costs include facilities costs, consulting
costs and professional fees for accounting and legal services, including legal
services associated with obtaining and maintaining patents and regulatory
compliance.

General and administrative expenses by program for the three and six months ended June 30, 2022 and 2021, were as follows (in thousands):

                                  Three Months Ended                                   Six Months Ended
                                                                                 June 30,
                           June 30, 2022       June 30, 2021       Increase        2022         June 30, 2021       Increase

Total general and
administrative expenses   $        42,716     $        21,197     $   21,519     $  75,786     $        36,795     $   38,991


General and administrative expenses for the three and six months ended June 30,
2022 increased by $21.5 million and $39.0 million from the three and six months
ended June 30, 2021, respectively, primarily due to higher outside service spend
in anticipation of the potential commercial launch of omecamtiv mecarbil, an
increase in personnel related costs including stock-based compensation and
facilities expense related to the Oyster Point Lease in the first half of 2022.

We expect that general and administrative expenses will fluctuate in the future, depending in part on the timing of and investments in commercial readiness.

Interest expense

Interest expense for the three and six months ended June 30, 2022 and 2021, were as follows (in thousands):

                                   Three Months Ended                                        Six Months Ended
                                                                     Increase                                                 Increase
                           June 30, 2022        June 30, 2021       (Decrease)       June 30, 2022       June 30, 2021       (Decrease)
Term loan                 $         1,178      $         1,205     $       

(27 ) $ 2,325 $ 2,401 $ (76 ) Convertible notes

                   1,544                2,839           (1,295 )             3,069               5,604           (2,535 )
Other                                  85                   29               56                 159                  56              103

Total interest expense $ 2,807 $ 4,073 $ (1,266 ) $ 5,553 $ 8,061 $ (2,508 )

Interest expense for the three and six months ended June 30, 2022 consists of
interest expense related to the RP Loan Agreement between the Company and RPDF,
dated January 7, 2022, interest expense related to the 2026 Notes, and interest
expense related to the finance leases. Commensurate with our entry into the RP
Loan Agreement, we terminated the Term Loan Agreement with Silicon Valley Bank
and Oxford Finance LLC and repaid all amounts outstanding thereunder in January
2022.

Loss on extinguishment of debt

As a result of the termination of the Term Loan Agreement and the repayment to
the Lenders, during the six months ended June 30, 2022, we recorded a loss of
$2.7 million in loss on debt extinguishment in the condensed consolidated
statements of operations and comprehensive loss, consisting of the premium on
debt repayments and the write-off of the remaining term loan fees and debt
issuance costs.

Non-cash interest expense on liabilities related to revenue participation right purchase agreements

Non-cash interest expense results from the accretion of our liabilities to RPFT
and RP ICAV related to the sale of future royalties under the RP OM RPA and RP
Aficamten RPA, respectively.

On January 7, 2022, we entered into the RP Aficamten RPA with RPI ICAV. Pursuant
to the RP Aficamten RPA, RPI ICAV purchased the right to receive a percentage of
net sales equal to 4.5% for annual worldwide net sales of pharmaceutical
products containing aficamten up to $1 billion and 3.5% for annual worldwide net
sales of pharmaceutical products containing aficamten in excess of $1 billion,
subject to reduction in certain circumstances (the "RP Aficamten Liability").
The carrying amount of the RP Aficamten Liability is based on our estimate of
the future royalties to be paid to RPI ICAV over the life of the arrangement as
discounted using an imputed rate of interest. The imputed rate of interest on
the unamortized portion of the RP Aficamten Liability was approximately 11.7% as
of June 30, 2022.

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In 2021, we updated our analyses of RP OM RPA to reflect our current assumptions
resulting from ongoing market research in the U.S. and to reflect other
adjustments in connection with our anticipated commercialization. Our estimates
regarding the amount of future royalty payments decreased and the time periods
within which we anticipated that such payments will be due changed. Each of
these adjustments is accounted for on a prospective basis in our liability
calculation and resulted in a decline in our imputed interest rate and noncash
interest expenses from 15% and $22.7 million in 2020 to 10% and $12.9 million in
2021, respectively. In 2021, the change in estimate had no impact on revenue and
reduced the net loss by $11.5 million. The change in accounting estimate reduced
the net loss per share by $0.15 in 2021.

We review our assumptions on a regular basis and our estimates may change in the future as we refine and reassess our assumptions.

Non-cash interest expense on liability related to the RP OM RPA and RP Aficamten
RPA for the three and six months ended June 30, 2022 and 2021, were as follows
(in thousands):

                                   Three Months Ended                                      Six Months Ended
                           June 30, 2022        June 30, 2021       Increase       June 30, 2022       June 30, 2021       Increase
RP OM Liability           $         4,429      $         2,871     $    1,558     $         8,707     $         5,666     $    3,041
RP Aficamten Liability              2,574                    -          2,574               4,860                   -          4,860
Total non-cash interest
expense recognized        $         7,003      $         2,871     $    4,132     $        13,567     $         5,666     $    7,901

Interest and Other Income, net

Interest and other income, net for the three and six months ended June 30, 2022
and 2021 consisted primarily of interest income generated from our cash, cash
equivalents and investments.

Liquidity and Capital Resources

Our cash, cash equivalents and investments and a summary of our borrowings and working capital is summarized as follows:

                                                 June 30, 2022        December 31, 2021
Financial assets:
Cash and cash equivalents                      $          93,631     $           112,666
Short-term investments                                   492,395                 358,972
Long-term investments                                     10,668                 152,050
Total cash, cash equivalents and marketable
securities                                     $         596,694     $           623,688
Borrowings:
Term loan, net                                 $          62,344     $            47,367
Convertible notes, net                                   134,674                  95,471
Total borrowings                               $         197,018     $           142,838
Working capital:
Current assets                                 $         602,250     $           535,672
Current liabilities                                       66,843                  71,860
Working capital                                $         535,407     $           463,812


The following table shows a summary of our cash flows for the periods set forth
below:

                                                          Six Months Ended
                                                 June 30, 2022         June 30, 2021
Net cash used in operating activities          $        (117,286 )   $         (59,015 )
Net cash provided by investing activities                    989            

13,605

Net cash provided by (used in) financing                  97,262
activities                                                                        (421 )
                                               $         (19,035 )   $         (45,831 )




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Sources and Uses of Cash

We have funded our operations and capital expenditures with proceeds primarily
from private and public sales of our equity securities, a royalty monetization
agreement, strategic alliances, long-term debt, other financings and interest on
investments. We have generated significant operating losses since our inception.
Our expenditures are primarily related to research and development activities.

Net cash used in operating activities of $117.3 million in the six months ended
June 30, 2022 which include a net loss of $109.3 million was largely due to
ongoing research and development activities, general and administrative expenses
to support those activities, offset by collection of receivables primarily from
our 2021 RTW Transactions. Net loss for the six months ended June 30, 2022
included, among other items: non-cash stock-based compensation, non-cash
interest expense related to sale of future royalties and non-cash interest
expense related to debt.

Net cash provided by investing activities of $1.0 million in the six months ended June 30, 2022 was primarily due to purchases of investments and property and equipment offset by proceeds from maturity of investments.

Net cash provided by financing activities of $97.3 million in the six months
ended June 30, 2022 was primarily due to $149.6 million of net proceeds related
to RP Aficamten RPA and the RP Loan Agreement and offset by the repayment of
amounts owed under our Term Loan Agreement and stock-based activities.

2021 Ji Xing and RTW Transactions

On December 20, 2021, we entered into the Ji Xing OM License Agreement, pursuant
to which we granted to Ji Xing an exclusive license to develop and commercialize
omecamtiv mecarbil in China and Taiwan. Under the terms of the Ji Xing OM
License Agreement, we are the beneficiary of a nonrefundable $50.0 million
payment obligation from Ji Xing comprised of a $40.0 million payment as
consideration for the rights granted by us to Ji Xing and $10.0 million
attributable to our having submitted to FDA an NDA for omecamtiv mecarbil. We
may be eligible to receive from Ji Xing additional payments totaling up to
$330.0 million for the achievement of certain commercial milestone events in
connection to omecamtiv mecarbil. In addition, Ji Xing will pay us tiered
royalties in the mid-teens to the low twenties range on the net sales of
pharmaceutical products containing omecamtiv mecarbil in China and Taiwan,
subject to certain reductions for generic competition, patent expiration and
payments for licenses to third party patents. The Ji Xing OM License Agreement,
unless terminated earlier, will continue on a market-by-market basis until
expiration of the relevant royalty term.

In addition to the Ji Xing OM License Agreement, we entered into common stock
purchase agreements with each of RTW Master Fund, Ltd., RTW Innovation Master
Fund, Ltd. and RTW Venture Fund Limited (collectively, the "RTW Investors"),
pursuant to which we sold and issued an aggregate of 0.5 million shares of our
common stock at a price per share of $39.125 and an aggregate purchase price of
$20.0 million.

2022 Royalty Pharma Transactions

On January 7, 2022, we announced that we had entered into that certain
Development Funding Loan Agreement (the "RP Loan Agreement") and the Revenue
Participation Right Purchase Agreement (the "RP Aficamten RPA") with Royalty
Pharma Development Funding, LLC ("RPDF") and Royalty Pharma Investments 2019
ICAV ("RPI ICAV") respectively, each of which were at the time of our entry into
such agreements affiliated with Royalty Pharma International plc.

Under the RP Loan Agreement, we are entitled to receive up to $300.0 million in term loans, $50.0 million of which was disbursed to us on closing and the remaining $250.0 million available to us upon our satisfaction of customary disbursement conditions and certain development conditions by specific deadlines, as follows:

•

$50.0 million of tranche 2 term loans during the one year period following the receipt on or prior to December 31, 2022 of marketing approval from FDA of omecamtiv mecarbil;

•

$25.0 million of tranche 3 term loans during the one year period following the
commercial availability of a diagnostic test measuring levels of omecamtiv
mecarbil to support the final FDA label language applicable to such drug,
subject to such commercial availability and the conditions to the tranche 2 term
loans having occurred on or prior to December 31, 2022;

•

$75.0 million of tranche 4 term loans during the one year period following the
receipt on or prior to September 30, 2024 of positive results from SEQUOIA-HCM,
the Phase 3 trial for aficamten; and

•

$100.0 million of tranche 5 term loans during the one year period following the
acceptance by the FDA on or prior to March 31, 2025 of an NDA for aficamten,
subject to the conditions to the tranche 4 term loans having occurred on or
prior to September 30, 2024.


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The FDA's recent postponement of the PDUFA target action date for our NDA for
omecamtiv mecarbil to February 28, 2023 may have an adverse impact on our
ability to meet the tranche 2 and tranche 3 conditions for disbursement under
the RP Loan Agreement.

Each term loan under the RP Loan Agreement matures on the 10 year anniversary of
the funding date for such term loan and is repayable in quarterly installments
of principal, interest and fees commencing on the last business day of the
seventh full calendar quarter following the calendar quarter of the applicable
funding date for such term loan, with the aggregate amount payable in respect of
each term loan (including interest and other applicable fees) equal to 190% of
the principal amount of the term loan (such amount with respect to each term
loan, "Final Payment Amount").

We may prepay the term loans in full (but not in part) at any time at our option
by paying an amount equal to the unpaid portion of Final Payment Amount for the
outstanding term loans under the RP Loan Agreement; provided that if the
conditions for either the tranche 4 term loans or the tranche 5 term loans have
been met, we must have borrowed at least $50 million principal amount of the
tranche 4 or 5 term loans. In addition, the term loans under the RP Loan
Agreement are repayable in full at the option of either us or the lender in an
amount equal to the unpaid portion of Final Payment Amount for the outstanding
term loans upon a change of control of Cytokinetics.

In addition, on January 7, 2022, we entered into the RP Aficamten RPA with RPI
ICAV, pursuant to which RPI ICAV purchased rights to certain revenue streams
from net sales of pharmaceutical products containing aficamten by us, our
affiliates and our licensees in exchange for up to $150.0 million in
consideration, $50.0 million of which was paid on the closing date, $50.0
million of which was paid to us on March 10, 2022 following the initiation of
the first pivotal trial in oHCM for aficamten and $50.0 million of which is
payable following the initiation of the first pivotal clinical trial in nHCM for
aficamten. The RP Aficamten ARPA also provides that the parties will negotiate
terms for additional funding if we achieve proof of concept results in certain
other indications for aficamten, with a reduction in the applicable royalty if
we and RPI ICAV fail to agree on such terms in certain circumstances.

Pursuant to the RP Aficamten RPA, RPI ICAV purchased the right to receive a percentage of net sales equal to 4.5% for annual worldwide net sales of pharmaceutical products containing aficamten up to $1 billion and 3.5% for annual worldwide net sales of pharmaceutical products containing aficamten in excess of $1 billion, subject to reduction in certain circumstances.

Commensurate with our entry into the RP Loan Agreement and RP Aficamten RPA, we terminated the Term Loan Agreement with the Lenders and repaid all amounts outstanding thereunder.

In future periods, we expect to incur substantial costs as we continue to expand
our research programs and related research and development activities. We expect
to incur significant research and development expenses as we advance the
research and development of compounds from our other muscle biology programs
through research to candidate selection to clinical development. We may also
incur significant sales and marketing expenses if and when one or more of our
drug candidates receive regulatory approvals, and in anticipation of regulatory
approval of one of our drug candidates.

Our future capital uses and requirements depend on numerous factors. These factors include, but are not limited to, the following:

•

the initiation, progress, timing, scope and completion of preclinical research,
non-clinical development, chemistry, manufacturing, and controls ("CMC"), and
clinical trials for our drug candidates and other compounds;

•

the time and costs involved in obtaining regulatory approvals;

•

the jurisdictions in which we are granted regulatory approvals and thus are able to successfully launch our products for commercial sale;

•

delays that may be caused by requirements of regulatory agencies;

•

our level of funding for the development of current or future drug candidates;

•

the number of drug candidates we pursue and the stage of development that they are in;

•

the costs involved in filing and prosecuting patent applications and enforcing or defending patent claims;

•

our ability to establish and maintain selected strategic alliances required for the development of drug candidates and commercialization of our potential drugs;

•

our plans or ability to expand our drug development capabilities, including our capabilities to conduct clinical trials for our drug candidates;

•

our plans or ability to engage third-party manufacturers for our drug candidates and potential drugs;

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•

our plans or ability to build or access sales and marketing capabilities and to achieve market acceptance for potential drugs;

•

the expansion and advancement of our research programs;

•

the hiring of additional employees and consultants;

•

the acquisition of technologies, products and other business opportunities that require financial commitments; and

•

our revenues, if any, from successful development of our drug candidates and commercialization of potential drugs

•

the cost of additional construction to expand our headquarters in South San Francisco and in relation to our newly leased office facilities in Radnor, Pennsylvania;

•

As we advance commercialization plans for omecamtiv mecarbil, which we believe
will importantly lay a strong foundation for commercialization of aficamten and
the expansion of our cardiovascular franchise, we anticipate that our spending
would increase, but we are also studying comparable company best practices and
building a fit-for-purpose commercial organization.

As a result of Amgen's and Servier's elections to terminate the Amgen Agreement
and the Servier Agreement respectively, we will dedicate resources to ensure the
transition of the programs related to omecamtiv mecarbil and aficamten to us.
Finally, notwithstanding the expansion of our collaboration with Ji Xing to
include omecamtiv mecarbil in December 2021 and our recent financing
transactions with entities affiliated with Royalty Pharma International plc in
January 2022, we plan to continue to evaluate a wide range of corporate
development strategies for potential co-development, co-commercialization and
licensing deals in relation to omecamtiv mecarbil and our other drug candidates
in order to mitigate the cost effects of the termination of the Amgen Agreement
and Servier Agreement and enhance our commercial capabilities. These cost
effects of termination include forfeiture of potential milestone payments from
Amgen to us, as well as additional costs to us relating to clinical studies,
regulatory filing, and commercialization of omecamtiv mecarbil.

We have incurred an accumulated deficit of $1,306.3 million since inception and
there can be no assurance that we will attain profitability. We are subject to
risks common to clinical-stage companies including, but not limited to,
development of new drug candidates, dependence on key personnel, and the ability
to obtain additional capital as needed to fund our future plans. Our liquidity
will be impaired if sufficient additional capital is not available on terms
acceptable to us, if at all. Until we achieve profitable operations, we intend
to continue to fund operations through payments from strategic collaborations,
additional sales of equity securities, grants and other financings. We have
never generated revenues from commercial sales of our drugs and may not have
drugs to market for at least several years, if ever. Our success is dependent on
our ability to obtain additional capital by entering into new strategic
collaborations and/or through financings, and ultimately on our and our
collaborators' ability to successfully develop and market one or more of our
drug candidates. We cannot be certain that sufficient funds will be available
from such collaborators or financings when needed or on satisfactory terms.
Additionally, there can be no assurance that any of our drug candidates will be
accepted in the marketplace or that any future products can be developed or
manufactured at an acceptable cost. These factors could have a material adverse
effect on our future financial results, financial position and cash flows.

Based on the current status of our development plans, we believe that our
existing cash and cash equivalents, investments and interest earned on
investments will be sufficient to meet our projected operating requirements for
at least the next 12 months. If, at any time, our prospects for internally
financing our research and development programs decline, we may decide to reduce
research and development expenses by delaying, discontinuing or reducing our
funding of development of one or more of our drug candidates or of other
research and development programs. Alternatively, we might raise funds through
strategic relationships, public or private financings or other arrangements.
There can be no assurance that funding, if needed, will be available on
attractive terms, or at all, or in accordance with our planned timelines.
Furthermore, financing obtained through future strategic relationships may
require us to forego certain commercialization and other rights to our drug
candidates. Similarly, any additional equity financing may be dilutive to
stockholders and debt financing, if available, may involve restrictive
covenants. Our failure to raise capital as and when needed could have a negative
impact on our financial condition and our ability to pursue our business
strategy.

Off-Balance Sheet Arrangements

We are not party to any off-balance sheet arrangements that have, or are reasonably likely to have, a material current or future effect on our financial condition, revenues or expenses, results of operations, liquidity, capital expenditures or capital resources.

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