Antisense Therapeutics Limited announced that the ATL1102 Phase II non-ambulant DMD patient plasma protein data was presented on September 24, 2021 at the 26th International Annual Congress of the World Muscle Society in the late breaking news poster titled "ATL1102 treatment in non-ambulant boys with DMD modulates Latent TGF-beta-binding protein 4, and thrombospondin-1, two disease genetic modifiers of ambulant DMD, and CXCL16". ATL1102 was assessed in an open label Phase II study in adolescent non-ambulant patients with DMD demonstrating highly promising trial results. Planned as part of the Phase II study, a large-scale protein analysis (known as a proteomics analysis) of retained blood plasma samples from the non-ambulant DMD patients treated with ATL1102 was undertaken to identify the proteins affected so as to provide further insight into the mode of action and biological activity of ATL1102. At the end of the 24 week dosing period, ATL1102 treated patients demonstrated a statistically significant mean reduction in Thrombospondin-1 (-49%), and increases in LTBP4 (20.7%), soluble CXCL16 (29.9%), and VCAM-1 (18.0%) compared to baseline levels (FDR p-value <0.0005). The ATL1102 induced positive LTBP4 increases and TSP-1 decreases in plasma indicates that ATL1102 modifies the levels of two proteins involved in modifying the rate of loss of ambulation (LoA) in DMD. LTBP4 sequesters TGF- to keep it latent and TSP-1 activates latent TGF- with LTBP4 and TSP-1 both involved in the fibrotic process in DMD. An inherited minor form of the TSP-1 gene with reduced expression of TSP-1 has been reported as being protective against loss of ambulation in DMD. A rare recessive inherited form of the LTBP4 gene in 12% of patients with greater levels is associated with milder DMD providing 1-2 years delayed loss of ambulation. ATL1102's effect in increasing blood levels of (i) soluble VCAM-1 (sVCAM-1), a CD49d ligand, is supportive of ATL1102's antisense mechanism of action in reducing CD49d to reduce sVCAM-1 bound to CD49d, and in reducing inflammation, and (ii) soluble CXCL16, a chemokine with a role in muscle regeneration, appears to align with the positive effects on muscle structure observed under MRI in the ATL1102 Phase II trial. These plasma proteins were increased such that they approached the median levels seen in an external control dataset of healthy adults, supporting the beneficial nature of the outcomes in ATL1102 treated DMD patients. The protein changes observed in the plasma of the ATL1102 treated non ambulant DMD patients in the Phase II study is also consistent with the drug's positive effects on muscle function and strength reported in the ATL1102 Phase II trial. Analysis of the plasma protein data is ongoing in order to further elucidate ATL1102's biological effects and to position the drug's development in disease settings. The Company will continue to report on any material developments from this ongoing data analysis and associated commercial opportunities. Based on the positive outcomes from the protein analysis reported above, Australian Provisional Patent Application No. 2021903024 was filed 20 September 2021 with claims covering applications of ATL1102 in new potential disease settings including diabetic, respiratory and age-related diseases to support the Company's future commercial and partnering plans for ATL1102.