23 Nov

Entitlement Offer Closing Date Extended

______________________________________________________________________________________________________ LEVEL 1, 14 WALLACE AVENUE, TOORAK VIC 3142 AUSTRALIA TEL . +61 (3) 9827 8999 FAX +61 3 9859 7701 WEB WWW.ANTISENSE.COM.AU ANTISENSE THERAPEUTICS LIMITED ABN 41 095 060 745 ASX Announcement 23 November 2021 Entitlement Offer Closing Date Extended • Closing date extended to 17 December 2021 for non-renounceable entitlement offer The Board of Directors of Antisense Therapeutics Limited [ASX:ANP | US OTC:ATHJY | FSE:AWY], (the Company) today announced that the Closing Date for the non-renounceable entitlement offer to raise up to $16.8 million (“Entitlement Offer”), has been extended to 17 December 2021. The Company has become aware that many shareholders who receive their documents via mail may have still not received their Offer Documents as of 22 November 2021, due to current postal service operating constraints. Given the timing proximity to the Company’s upcoming Annual General Meeting to be held on 15 December 2021, the Board has resolved to extend the Offer Period to 5pm (Melbourne time) on 17 December 2021. Key Dates Event Date* (Australian Eastern Daylight Saving Time) Annual General Meeting 15 December 2021 Entitlement Offer closes 5.00pm on 17 December 2021 Allotment of New Shares and New Options 22 December 2021 Commencement of trading of New Shares on ASX 23 December 2021 Dispatch of holding statements 24 December 2021 * The timetable is indicative only and subject to change. The Company retains the discretion, subject to the ASX Listing Rules and the Corporations Act, to alter any or all of these key dates at its discretion (generally or in particular cases), without prior notice, including extending the Closing Date or to withdraw the Offers without prior notice. Applicants are encouraged to submit their Application Forms (if applicable) as soon as possible. This announcement has been authorised for release by the Board For more information please contact : Antisense Therapeutics Investment Enquiries Mark Diamond Gennadi Koutchin Managing Director XEC Partners +61 (0)3 9827 8999 gkoutchin@xecpartners.com.au www.antisense.com.au 1300 932 037 ______________________________________________________________________________________________________ ANTISENSE THERAPEUTICS LIMITED ABN 41 095 060 745 About Antisense Therapeutics Limited [ASX: ANP | US OTC: ATHJY | FSE: AWY] is an Australian publicly listed biotechnology company, developing and commercializing antisense pharmaceuticals for large unmet markets in rare diseases. The products are in-licensed from Ionis Pharmaceuticals Inc. (NASDAQ: IONS), an established leader in antisense drug development. The Company is developing ATL1102, an antisense inhibitor of the CD49d receptor, for Duchenne muscular dystrophy (DMD) patients and recently reported highly promising Phase II trial results. ATL1102 has also successfully completed a Phase II efficacy and safety trial, significantly reducing the number of brain lesions in patients with relapsing-remitting multiple sclerosis (RRMS). The Company has a second drug, ATL1103 designed to block GHr production that successfully reduced blood IGF-I levels in Phase II clinical trials in patients with the growth disorder acromegaly. About ATL1102 ATL1102 is an antisense inhibitor of CD49d, a subunit of VLA-4 (Very Late Antigen-4). Antisense inhibition of VLA-4 expression has demonstrated activity in a number of animal models of inflammatory disease including asthma and MS with the MS animal data having been published in a peer reviewed scientific journal. ATL1102 was shown to be highly effective in reducing MS lesions in a Phase IIa clinical trial in patients with RR- MS. The ATL1102 Phase IIa clinical data has been published in the medical Journal Neurology (Limmroth, V. et al Neurology, 2014; 83(20): 1780-1788). About DMD Duchenne Muscular Dystrophy (DMD) is an X-linked disease that affects 1 in 3600 to 6000 live male births (Bushby et al , 2010). DMD occurs as a result of mutations in the dystrophin gene which causes a substantial reduction in or absence of the dystrophin protein. Children with DMD have dystrophin deficient muscles and are susceptible to contraction induced injury to muscle that triggers the immune system which exacerbates muscle damage as summarized in a publication co-authored by the Director of the FDA CDER (Rosenberg et al, 2015). Ongoing deterioration in muscle strength affects lower limbs leading to impaired mobility, and also affects upper limbs, leading to further loss of function and self-care ability. The need for wheelchair use can occur in early teenage years for patients on corticosteroids with a mean age of 13, with respiratory, cardiac, cognitive dysfunction also emerging. Patients with a greater number of immune T cells expressing high levels of CD49d have more severe and progressive disease and are non-ambulant by the age of 10 despite being on corticosteroid treatment (Pinto Mariz et al, 2015). With no intervention, the mean age of life is approximately 19 years. The management of the inflammation associated with DMD is currently addressed via the use of corticosteroids, however they are acknowledged as providing insufficient efficacy and are associated with significant side effects. As a consequence, there is an acknowledged high need for new therapeutic approaches for the treatment of inflammation associated with DMD. Rosenberg AS, Puig M, Nagaraju K, et al . Immune-mediated pathology in Duchenne muscular dystrophy. Sci Transl Med 2015, 7: 299rv4. Bushby et al for the DMD Care Consideration Working Group/ Diagnosis and management of Duchenne muscular dystrophy, part 1 Lancet Neurol. 2010 Jan;9(1):77-93 and part 2 Lancet Neurol. 2010 Feb;9(2):177-89 . Pinto-Mariz F, Carvalho LR, Araújo AQC, et al . CD49d is a disease progression biomarker and a potential target for immunotherapy in Duchenne muscular dystrophy. Skeletal Muscle 2015, 5: 45-55.
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