On March 5, 2026 Atavistik Bio, a biotechnology company discovering the next generation of selective allosteric therapeutics, reported the closing of a $40 million extension to its Series B financing from new investor RA Capital Management, bringing the total round proceeds to $160 million. RA Capital joins other top-tier investors who participated in the Series B round, including Nextech Invest, The Column Group, Lux Capital and Regeneron Ventures, as previously announced in December 2025. Atavistik Bio will use the proceeds from the upsized Series B financing to fund clinical development of ATV-1601, a potential best-in-class AKT1-selective oral inhibitor for HHT, and its JAK2 V617F mutant-selective inhibitor program for MPNs through clinical proof of concept.
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"We’re excited to welcome RA Capital as an investor in Atavistik Bio. Our Series B round, backed by a highly respected syndicate, reflects strong belief in our selective allosteric programs and our focus to advance meaningful therapies for patients with severe diseases," said Bryan Stuart, Chief Executive Officer at Atavistik Bio. "This additional funding further strengthens our ability to accelerate the development of best-in-class therapies designed to deliver superior efficacy, improved tolerability profiles, and potentially transformative outcomes for patients."
"We are pleased to support Atavistik Bio in this next phase of growth as the company is at the forefront of developing transformative therapies for HHT and MPNs," said Nandita Shangari, PhD, Managing Director at RA Capital Management. "Atavistik Bio’s highly experienced team and a pipeline of high-quality programs targeting significant unmet need, position the company to create meaningful value."
About Hereditary Hemorrhagic Telangiectasia (HHT), AKT1 Inhibition and ATV-1601
HHT is a severe inherited bleeding disorder that affects more than 1.6 million people globally, with no approved therapies currently available. This condition often leads to frequent bleeding episodes and vascular shunts, resulting in chronic anemia, multiorgan damage, and life-threatening complications. AKT1 hyperactivation is a hallmark of HHT and has been shown to drive the vascular pathology of HHT. Selectively inhibiting AKT1, the primary AKT isoform and driver of abnormal endothelial growth implicated in HHT, offers a novel and potentially disease-modifying therapeutic approach for this difficult disease. Although there has been substantial investment in pan-AKT inhibitors, their use is limited by AKT2-driven toxicities, most notably hyperglycemia, which impact tolerability and restrict their use for chronic dosing. ATV-1601 is an oral allosteric inhibitor that selectively inhibits AKT1.
ATV-1601 was evaluated in a Phase 1 oncology study, and demonstrated a favorable safety profile, validating its differentiated selectivity profile that addresses key limitations of pan-AKT inhibitors. Development efforts will now focus on advancing ATV-1601 in HHT.
About Myeloproliferative Neoplasms (MPNs) and Selective Targeting of the JAK2 V617F Mutation
MPNs are a group of rare chronic blood cancers for which current treatment options are limited. The JAK2 V617F mutation is the most common driver mutation in patients living with MPNs, affecting approximately 95% of patients with polycythemia vera, 60% of patients with essential thrombocythemia, and 55% of patients with myelofibrosis. Approved pan-JAK inhibitors, such as ruxolitinib, provide symptom relief, but non-selectively inhibit both mutant and wild-type JAK2. This limits the ability to reduce JAK2 V617F mutant allele burden and can disrupt normal blood cell production regulated by wild-type JAK2, contributing to adverse events and treatment discontinuation. Selectively targeting the JAK2 V617F mutation has the potential to reduce mutant allele burden, preserve normal bone marrow function, and have a disease modifying impact that will substantially improve long term outcomes for patients with MPNs.
(Press release, Atavistik Bio, MAR 5, 2026, View Source [SID1234663321])