Enanta Pharmaceuticals : Presentation - Corporate Overview 39th Annual J.P. Morgan Healthcare Conference

CREATING SMALL MOLECULE DRUGS

FOR VIRAL INFECTIONS AND LIVER DISEASES

Corporate Overview

39th Annual J.P. Morgan Healthcare Conference

January 12, 2021

Forward Looking Statements Disclaimer

This presentation contains forward-looking statements concerning our business, operations and financial performance and condition, as well as our plans, objectives and expectations for our research and development programs, our business and the industry in which we operate. Any statements contained herein that are not statements of historical facts may be deemed to be forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as "aim," "anticipate," "assume," "believe," "contemplate," "continue," "could," "due," "estimate," "expect," "goal," "intend," "may," "objective," "plan," "predict," "potential," "positioned," "seek," "should," "target," "will," "would," and other similar expressions that are predictions of or indicate future events and future trends, as well as other comparable terminology. These forward-looking statements include, but are not limited to, statements about overall trends, royalty revenue trends, research and clinical development plans and prospects, liquidity and capital needs and other statements of expectations, beliefs, future plans and strategies, anticipated events or trends, and similar expressions. These forward-looking statements are based on our management's current expectations, estimates, forecasts and projections about our business and the industry in which we operate and our management's beliefs and assumptions. These forward-looking statements are not guarantees of future performance or results and involve known and unknown risks, uncertainties and other factors that are in some cases beyond our control. As a result, any or all of our forward-looking statements in this presentation may turn out to be inaccurate.

Please refer to the risk factors described or referred to in "Risk Factors" in Enanta's most recent Quarterly Report on Form 10-Q, and other periodic reports filed with the Securities and Exchange Commission. Enanta cautions investors not to place undue reliance on the forward-looking statements contained in this presentation. These statements speak only as of the date of this presentation, and Enanta undertakes no obligation to update or revise these statements, except as may be required by law.

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A Unique Approach to Drug Discovery

Using a proven, chemistry-driven approach to develop best-in-class small molecule drugs for virology and liver disease

Robust Clinical Stage Pipeline

RSV: Phase 2b in adult patients (RSVP)

Phase 2b in adult stem cell transplant patients (RSVPTx) Phase 2 in pediatric patients (RSVPEDs)

NASH: Phase 2b (ARGON-2)

Phase 1 (Follow-on FXR agonist) HBV: Two Phase 1b studies (core inhibitor)

Proven Track Record of Success

Strong Balance Sheet

Glecaprevir - HCV protease inhibitor in MAVYRET®/MAVIRET® $122M in fiscal 2020 royalties on HCV regimens

Strong balance sheet and royalties to fund robust pipeline $419M in cash at 9/30/20

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Our Therapeutic Focus

RSV hMPV

COVID-19HBV

HCV NASH

Leveraging our core strength in Hepatitis C to become a leader in oral treatments for viral infections and liver diseases

Several new therapeutic areas with goal of building multiple approaches in each

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Enanta Pipeline

PRODUCT CANDIDATE	DISCOVERY PRECLINICAL	PHASE 1	PHASE 2	PHASE 3	MARKET

Glecaprevir-containingpan-genotypic2-DAA combo

EDP-938EDP-938EDP-938

EDP-514EDP-514EDP-721

RSVP

RSVPEDs in Q1 2021

RSVTx

Viremic HBV patients

NUC-suppressed HBV patients

EDP-305

EDP-297

ARGON-2

* Fixed-dose combination contains glecaprevir and AbbVie's NS5A inhibitor, pibrentasvir. Marketed as MAVYRET (U.S.) and MAVIRET (ex-U.S.)

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Our Therapeutic Focus

RSV hMPV

COVID-19HBV

HCV NASH

Leveraging our core strength in Hepatitis C to become a leader in oral treatments for viral infections and liver diseases

Several new therapeutic areas with goal of building multiple approaches in each

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Respiratory Syncytial Virus (RSV)

Causes severe lung infections, including bronchiolitis (infection of small airways in the lungs) and pneumonia (an infection of the lungs). No safe and effective treatments.

Higher risk populations for severe illness include:

• Premature babies
• Older adults, especially those 65 years and older
• People with chronic lung disease or certain heart problems
• People with weakened immune systems (e.g. HIV, organ transplant, chemotherapy)

RSV at a Glance

	Children < 5 years	Adults > 65 years
	33M global cases
	3M global hospitalizations	177K US hospitalizations
	120K global deaths	14K US deaths
	2.1M US outpatient visits

Sources: Hall CB, Weinberg GA, Iwane MK, Blumkin AK, Edwards KM, et al. The burden of respiratory syncytial virus infection in young children.New Engl J Med. 2009;360(6):588-98.; Falsey AR, Hennessey PA, Formica MA, Cox C, Walsh EE.Respiratory syncytial virus infection in elderly andhigh-riskadults.New Engl J Med. 2005;352(17):1749-59.; Shi et al.Global, regional, and national disease burden estimates of acute lower respiratory infections due to respiratory syncytial virus in young children in 2015: a systematic review and modelling study.Lancet. 2017 Sep 2; 390(10098): 946-958.

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EDP-938:N-Protein Inhibitor for RSV

• EDP-938is the only N-inhibitor under clinical evaluation
• • Non-fusionapproach directly targets viral replication vs. entry
  • Granted Fast Track Designation by FDA
• Strong preclinical virological profile:
• • Nanomolar inhibitor of both RSV-A and RSV-B activity
  • Maintained antiviral potency across all clinical isolates tested
  • Demonstrated high-barrier to resistance in vitro
  • Synergy with other drug mechanisms (e.g. fusion and L inhibitors)
  • Active against virus variants resistant to other mechanisms
  • Robust in vivo efficacy data

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EDP-938 Development Program

Phase 1 Results

• Safe and well tolerated, no SAEs, AEs were mild
• At Phase 2 doses, mean trough levels 30x higher than EC90 of EDP- 938 against RSV-infected human cells

Phase 2a Challenge Study Results

• Primary and key secondary efficacy endpoints were achieved (p<0.001) at both dose levels after 5 days of dosing
• • Primary endpoint: Reduction in area under the curve (AUC) viral load in the intent-to-treat-infected population (ITT-I)
  • Secondary endpoint: Reduction in Total Symptom Score (TSS)
• Mean Ctrough concentrations were approximately >20-40x higher than EC90
• Well tolerated with safety profiles similar to placebo
• Consistent profile observed in >250 subjects exposed to EDP-938 for up to 7 days in Phase 1 and Phase 2a

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Robust Antiviral Effect

Rapid and Sustained Reduction in Viral Load in Both Active Arms Compared to Placebo (71%, 74% ↓ AUC; P<0.001)

Days After First Dose

Dosing Period

First Dose

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Robust Symptom Reduction

Rapid and Sustained Attenuation of RSV Symptoms in Both Active Arms Compared to Placebo (68%, 74% ↓ AUC; P<0.001)

Days After First Dose

Dosing Period

First Dose

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RSVP - A Phase 2b Study of EDP-938 in Adult Outpatients with RSV

Double-Blinded

Treatment Phase

5 days

•

Placebo (QD)

~70 Adults		9 Day Follow-up
(≤75yo)
	EDP-938 800 mg (QD)*

•

Day 1

Day 5

Day 14

Primary Objective:

Effect of EDP-938 on progression of RSV infection by assessment of clinical symptoms measured over the 14-day study period

Secondary Objective:

Antiviral efficacy, safety and PK of EDP-938

*Equivalent to 600mg suspension dosage form used in challenge study

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Enanta is Prepared for When RSV Returns

• Current RSV season in Northern Hemisphere has not begun due to continuing COVID-19 mitigation measures
• Modeling predicts large future outbreaks of RSV1
• • Caused by an increase in susceptible RSV population, resulting from ongoing mitigation measures
  • Assuming measures are reduced, a peak in infections are projected for the next RSV seasons
• Enanta is ready to move quicky upon RSV re-emergence
• • Number of clinical sites more than doubled with expansion in EU and Asia-Pacific (total of ~150 sites globally)
• Updated guidance will be provided once RSV becomes prevalent again

Sources: 1.www.pnas.org/cgi/doi/10.1073/pnas.20131821172.https://www.cdc.gov/surveillance/nrevss/rsv/natl-trend.html;

Detection of RSV in the US in 20202

					5000
			600		4000
			400		3000
Antigen			PCR
	200		2000
					1000

Jan	April	Dec

RSVP Clinical Trial Sites

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Two Additional Phase 2 Clinical Trials: RSVTx and RSVPEDs

Double-Blinded Treatment Phase

Planned for Q1 2021

~90 subjects

Age 28 days - 24 months Dosed in 4 age cohorts

5 days

Part 1: MAD in 4 age

cohorts

Part 2: Selected dose from Part 1 across 4 age cohorts

9 Day Follow-up

• Primary Objective, Part 1: Safety and PK of EDP-938
• Primary Objective, Part 2: Antiviral activity of EDP-938

Day 1	Day 5	Day 14

				Double-Blinded Treatment Phase
Initiated in Q4 2020	21 days
~200 adult HCT recipients				Placebo (QD)
						28 Day Follow-up
Age 18 - 75 years
			800 mg (QD)
		Day 1	Day 21 Day 28	Day 49

• Primary Objective: Effect of EDP-938on development of LRTC in HCT subjects with acute RSV URTI
• Secondary Objectives: Viral load, progression to respiratory failure or all-causemortality, PRO, PK and safety

LRTC: lower respiratory tract complication; HCR: hematopoietic cell transplant; URTI: upper respiratory tract infection; PRO: patient reported outcomes; PK: pharmacokinetics

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.

RSV L-Protein Inhibitor

• Enanta's newest RSV program
• RSV L-protein is a viral RNA-dependent RNA polymerase that contains multiple enzyme activities required for RSV replication
• Novel RSV L-protein inhibitor leads have nanomolar potency against RSV-A and RSV-B
• Not expected to have cross resistance to other classes of inhibitors
• • Potential to be used alone or in combination with other RSV mechanisms, such as EDP-938

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Human Metapneumovirus (hMPV)

Important cause of respiratory tract infections (RTIs), particularly in children, the elderly and immunocompromised individuals

• Paramyxovirus closely related
hMPV at a Glance
to RSV

• • hMPV replication dependent on several viral proteins that form a multiprotein complex in cells
  • Multiple potential targets for hMPV drug discovery
• No approved vaccine or therapeutics available
• Enanta nanomolar hMPV inhibitor leads under active optimization

Serious respiratory infections can occur in children under 5 years old

Second most common cause of lower RTIs in children (behind RSV)

Reinfection with hMPV occurs throughout life

Source: Epidemiology of Human Metapneumovirus; Jeffrey S. Kahn; Clinical Microbiology Reviews Jul 2006, 19 (3) 546-557; DOI: 10.1128/CMR.00014-06;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1539100/

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SARS-CoV-2(COVID-19)

Caused by respiratory infection of a new highly pathogenic coronavirus, SARS-CoV-2

• SARS-CoV-2belongs to coronaviridae, a family of enveloped RNA viruses that includes SARS-CoV and MERS-CoV
• Despite vaccine and therapeutic progress, need an oral treatment for those infected with SARS-CoV-2, and potentially for mutated virus, or for future coronaviruses
• Enanta is leveraging years of antiviral drug discovery expertise to identify direct-acting antivirals
• • Discovery efforts on multiple targets utilizing a combination of screening and drug design
  • Potent molecules currently undergoing lead optimization

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Our Therapeutic Focus

RSV hMPV

COVID-19HBV

HCV NASH

Leveraging our core strength in Hepatitis C to become a leader in oral treatments for viral infections and liver diseases

Several new therapeutic areas with goal of building multiple approaches in each

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Hepatitis B Virus (HBV)

Potentially life-threatening liver infection caused by the hepatitis B virus

Current treatments rarely give true cures

• Interferon is ~10% effective, but with side effects
• Reverse-transcriptaseinhibitors effective at reducing viral load, but low cure rates (1% or lower) and treatment for life to improve cirrhosis or hepatocellular carcinoma (HCC) outcomes

HBV at a Glance

US	850K - 2M people
US, Japan,
Major	~4.9M people
EU Populations
Worldwide	~290M people

Estimated 15-25% of patients with chronic HBV infection will develop chronic liver diseases

including cirrhosis, HCC or liver decompensation

Sources: WHO, CDC, Datamonitor

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HBV Core Inhibitor EDP-514 Summary

• A novel core inhibitor that displays potent anti-HBV activity at multiple points in the HBV lifecycle

In vitro • Potent anti-HBV activity in HBV expressing stable cell lines

• Capable of preventing the establishment of cccDNA
• Potent pan-genotypic activity

In vivo • Favorable tolerability and pharmacokinetic profile

• Over 4-log reduction in HBV viral titers with 12 weeks of treatment in a chimeric liver mouse model

Fast Track designation by FDA

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EDP-514 is Efficacious in the Humanized Liver Mouse Model

• uPA/SCID mice were infected with genotype C HBV and dosed with EDP-514 for 12 weeks

						Treatment						Follow-up
						(Day 0-83)						(Day 84-112)
(copies/mL)	1.0E+09
1.0E+08
Level	1.0E+07
HBV DNA	1.0E+06
1.0E+05
Serum	1.0E+04
0	7	14	21	28	35	42	49	56	63	70	77	84	91	98	105	112
									Days

Max. Viral DNA Log

Reduction at Day 77

Vehicle Control	-0.04
Entecavir Control	-2.21
EDP-514 25 mg/kg BID	-2.99
EDP-514 50 mg/kg BID	-3.61
EDP-514 75 mg/kg BID	-3.95
EDP-514 100 mg/kg BID	-4.43

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EDP-514 Clinical Development Program

Phase 1 Study

Phase 1b Study

Part 1 Complete

• Healthy volunteer SAD/MAD study evaluated safety, tolerability and PK
• Generally safe and well tolerated over dose range for up to 14 days
• • All reported TEAEs of mild severity
• PK profile supportive of once daily dosing with no food effect

Part 2 Ongoing

• NUC-suppressedpatients
• Evaluating safety, tolerability, PK and antiviral activity over 28 days
• 24 patients randomized to receive one of three multiple ascending doses of EDP-514 or placebo
• Preliminary data anticipated in 2Q 2021

Ongoing

• Viremic chronic HBV subjects not currently on therapy
• Evaluating the safety, tolerability, PK and antiviral activity over 28 days
• 24 patients randomized to receive one of three multiple ascending doses of EDP-514 or placebo
• Preliminary data anticipated in 2Q 2021

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EDP-721: HBV RNA Destabilizer

• Small molecules that cause destabilization and ultimate degradation of HBV RNAs
• • Result in reduction of HBsAg and other viral proteins in whole cell systems and animal models
  • Potential to complement or replace injectable (siRNA/ASO) with oral agents
• EDP-721is an oral small molecule HBV RNA destabilizer with a robust preclinical profile
• • Sub-nanomolarpotency in vitro; dose dependent HBsAg reductions in vivo
  • HBV pan-genomic activity; additive to synergistic activity with nucleosides and core inhibitors
• EDP-721in combination with other agents may lead to a functional cure

-

-

-

High levels of HBsAg suppress immune responses through multiple mechanisms EDP-721 reduces HBsAg derived from both integrated viral DNA and cccDNA Sustained loss of HBsAg is regarded as a core component of a functional cure for HBV

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Combination Regimen: Potential for Functional Cure

• Combination of multiple antiviral agents can block different points in the HBV life cycle
• Potential to drive rapid and deep suppression of viral replication (EDP-514 + NUC) and suppression of sAg production (EDP-721)
• All-oralregimen of EDP-514,EDP-721, NUC has potential to lead to a functional cure for HBV

		Integrated			EDP-721
		cccDNA	DNA
			eAg		EDP-514
Uncoating & Import	rcDNA			sAg		NUC
Repair
			Transcription	X		Reverse
				Core	Assembly	Transcription
			pgRNA	Translation
			sAg	Pol
		X
		Nucleus			Recycling

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EDP-721In Vivo Activity

• Dose dependent decrease in HBsAg observed with EDP-721 in AAV-HBV mouse model

	7			AAV-HBV HBsAg Levels
	6							Vehicle
IU/mL	5							EDP-721 0.1 mg/kg QD
HBsAg
4							EDP-721 1 mg/kg QD
10
Log								EDP-721 10 mg/kg QD
	3
	2
	0	2	4	6	8	10	12	14

Day Post Treatment

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Efficacy of Anti-HBsAg Agents in AAV-HBV Mouse Model

	Agent	Modality	Route of Admin.	Dose (mg/kg)	HBsAg Log Drop
	@ d14
	EDP-721	Small Molecule	PO	10	~3
	VIR-22181	siRNA	SC	9	~3
	AB-7292	siRNA	SC	3	~2.5
	ARB-14672	siRNA	IV	0.3	~1
	ALG-1250973	siRNA	SC	5	~1
	ALG-0205724	ASO	SC	10	~1.5
	PAPD5/7 ASO5	ASO	SC	5	~1.5

Sources: 1 EASL 2020 SAT426; 2 EASL 2018 O2646; 3 Jeffries 2020; 4 AASL 2020 O84; 5 AASLD 2019 P704

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Our Therapeutic Focus

RSV hMPV

COVID-19HBV

HCV NASH

Leveraging our core strength in Hepatitis C to become a leader in oral treatments for viral infections and liver diseases

Several new therapeutic areas with goal of building multiple approaches in each

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Non-Alcoholic Steatohepatitis (NASH)

Leading cause of liver disease in western countries

• Associated with metabolic syndrome, diabetes and hypertension
• Dramatically increases risk of cirrhosis, liver failure and hepatocellular carcinoma
• By 2030 NASH will be the most frequent reason for liver transplants in the U.S.

Stages

of Liver

Damage

Sources:American Liver Foundation,GlobalLiver.org

NASH at a Glance

	US	2.5 - 16.3M people
	Worldwide	115M people
	Worldwide in
	357M people
	2030

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EDP-305: A Potent FXR Receptor Agonist

Farnesoid X Receptor (FXR)

• Nuclear hormone receptor
• Main regulator of bile acid levels in liver and small intestine
• Responds to bile acids by regulating transcription of key enzymes and transporters
• FXR agonists ameliorate pathologies in NASH models, including fibrosis
• Clinical validation of FXR agonist in NASH with 6-ECDCA (OCA)

EDP-305

• Non-bileacid
• Designed to take advantage of increased binding interactions with the receptor
• Highly selective for FXR vs other nuclear receptors
• Potent and differentiated effects on FXR- dependent gene expression vs OCA in preclinical models
• Robust efficacy seen in multiple fibrosis and NASH models
• Granted Fast Track Designation by FDA

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EDP-305ARGON-1 Study Summary

Endpoints Met at Week 12 Using 2.5 mg Dose

Primary Endpoint:

ALT change

Secondary Endpoint:

Liver fat by MRI-PDFF

• Strong target engagement as shown by decrease in C4, and increase in FGF-19 and ALP
• Robust reduction in marker of liver injury (GGT)
• Generally safe for up to 12 weeks
• • Majority of treatment emergent adverse events were mild to moderate
  • Incidence of treatment discontinuation
    due to pruritus: 1.8% for 1 mg and 20.8% for 2.5 mg
  • Associated with small numeric absolute changes in lipids

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EDP-305:ARGON-2 Phase 2b Study

Treatment Duration

• 340 biopsy-proven NASH with fibrosis patients

72 weeks

Placebo (QD)

EDP-305 1.5 mg (QD)

EDP-305 2.0 mg (QD)

Day 1 Week 12

Internal Interim

Analysis

Primary Endpoint:

Improvement of fibrosis without worsening of NASH and/or NASH resolution without worsening of fibrosis

Week 72

• Includes 12-week internal interim analysis by mid-2021 (to generate dose information more quickly for potential combinations), as well as a prespecified powered IA when ~40% of subjects reach week 72 biopsy
• Two doses selected to provide strong target engagement and a balanced profile in terms of efficacy and tolerability
• • 1.5 mg dose: designed to demonstrate stronger biomarker signals of efficacy than seen at 1.0 mg
  • 2.0 mg dose: designed to demonstrate less pruritus than seen at 2.5 mg

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EDP-297: A Potent and Differentiated Follow-on FXR Agonist

• EDP-297preclinical profile shows:
• • High target-tissuedistribution (liver and intestine) vs plasma and skin
  • Potency greater than that published on any FXR agonist in clinical development today
• A highly potent andhighly targeted FXR agonist may allow for lower doses and reduced drug levels at non-targeted tissues
• • Potential to reduce pruritus unless pruritus is FXR-mediated by FXR receptors in liver or intestine
• Initiated Phase 1 study in 3Q 2020; data expected in 2Q 2021

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EDP-297: Highly Potent with Excellent Target Tissue Distribution

			FXR FL	Dose	Intestine /	Liver /
	Compound	Activation	Plasma	Plasma
	(mouse, po)
			EC50 (nM)	@ 4 hrs ~ Tmax
	OCA	Bile Acid	1301	10 mg/kg	160	26
	cilofexor	Non-Bile Acid	412	1 mg/kg	0.6	0.9
	EDP-305	Non-Bile Acid	8	1 mg/kg	7	15
	tropifexor	Non-Bile Acid	0.43	1 mg/kg	0.8	8
	EDP-2974	Non-Bile Acid	<0.1	1 mg/kg	265	75

Enanta data except where noted:

1. EC50 = 99 nM reported by Intercept
2. Gilead data. Trauner et al Hepatology 2019
3. EC50 = 0.26 nM reported by Novartis. Tully et al J. Med. Chem., 2019
4. EDP-297is undetectable in mouse skin

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Our Therapeutic Focus

RSV hMPV

COVID-19HBV

HCV NASH

Leveraging our core strength in Hepatitis C to become a leader in oral treatments for viral infections and liver diseases

Several new therapeutic areas with goal of building multiple approaches in each

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Glecaprevir - Our Licensed Protease Inhibitor for Hepatitis C Virus

	Product		Regimen		Enanta Asset		Economics*
			2-DAA (ABBV)		glecaprevir (PI)		Double-digit royalty on 50%
					of net sales

Glecaprevir Sales	Royalty Rate
(50% of MAVYRET net sales)	(annual)
$2.5B	20%

17%

$1.0B

Calendar 2020 HCV Royalties

Q4 $TBD

Q3 $23.6M

Q2 $18.7M

$750M

14%

Q1 $27.6M

$500M

12%

10%

*Enanta also receives royalties on paritaprevir sales (30% of Viekira 3DAA sales, same tiers)

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Financial Highlights

	($ In millions)		Fiscal Year Ended	Fiscal Quarter Ended
		Sept. 30, 2020	Sept. 30, 2020
	Total Revenues	$122.5	$23.6
	R&D Expenses	$136.8	$36.7
	G&A Expenses	$27.4	$6.7
	Net Income (Loss)	$(36.2)	$(29.3)
	Net Income (Loss) per
	$(1.81)	$(1.46)
	Diluted Common Share
	Balance Sheet
	Cash, Cash Equivalents	$419.3	$419.3
	and Marketable Securities

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Key Catalysts 2021

Virology

NASH

RSV N-InhibitorEDP-938

• Initiated RSVTx in 4Q 2020  Initiate RSVPEDs in Q1 2021
   Resume recruitment for RSVP when RSV returns

hMPV, SARS-CoV-2 and RSV L-inhibitor

• Nominate two clinical development candidates

HBV Core Inhibitor EDP-514 and RNA Destabilizer EDP-721

• EDP-514Phase 1b in viremic HBV patients; preliminary data anticipated in 2Q 2021
• EDP-514Phase 1b in NUC-suppressed HBV patients; preliminary data anticipated in 2Q 2021
• Initiate Phase 1 with EDP-721 in mid-2021

FXR Agonists EDP-305 and EDP-297

• ARGON-2Phase 2b in NASH ongoing; 12-week interim analysis in mid-2021
• Phase 1 with EDP-297(follow-on FXR) ongoing with data expected in 2Q 2021
• Advance non-FXR compounds for NASH

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