On July 17, 2025 Ajax Therapeutics, Inc. and Schrödinger, Inc. (Nasdaq: SDGR) reported an expansion of their exclusive research collaboration to include a new Janus kinase (JAK) target (Press release, Ajax Therapeutics, JUL 17, 2025, View Source [SID1234654434]). The partnership was established in 2019 with a goal of leveraging Schrödinger’s advanced computational platform and Ajax’s structural biology insights to develop a pipeline of novel molecules, with a focus on JAK inhibitors. Ajax’s lead candidate from the collaboration, AJ1-11095, is a potential first-in-class Type II JAK2 inhibitor currently being evaluated in a Phase 1 clinical study for the treatment of myelofibrosis.
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"We’re excited to expand our longstanding research collaboration with Schrödinger," stated Martin Vogelbaum, chief executive officer of Ajax Therapeutics. "Given our teams’ history of success in creating more selective and potent JAK2 inhibitors, we expect to take a similar approach to this new JAK target with the goal of generating a new class of inhibitors that extend beyond oncology indications to include inflammatory and autoimmune disorders."
"Our collaboration with Ajax and the progress of AJ1-11095 demonstrates the power of combining our world-leading computational platform at scale with Ajax’s novel structural biology insights," stated Ramy Farid, Ph.D., chief executive officer of Schrödinger. "We are really pleased with the progress our teams have made over the course of this partnership, and we look forward to working with the Ajax team on this new JAK family target."
Abnormal JAK signaling is a key driver in myeloproliferative neoplasms, including myelofibrosis, as well as in inflammatory and autoimmune diseases. In collaboration with Schrödinger, Ajax is leveraging advanced computational methods and structural biology insights to develop next-generation inhibitors with the potential for greater selectivity and deeper, more durable responses compared to existing JAK inhibitors.
Under the terms of the amended agreement, Ajax and Schrödinger will collaborate on the discovery of the development candidate, and Ajax will be responsible for clinical development and commercialization. Schrödinger is eligible to receive discovery and development milestones similar to the terms of the original agreement. Schrödinger is also eligible to receive sales milestones and single-digit royalties on net sales of any products emerging from the additional target.
In 2024, Ajax completed an oversubscribed $95 million Series C financing, in which Schrödinger participated as a continuing investor. Schrödinger was a co-founder of Ajax and maintains an equity stake in the company.
About AJ1-11095
AJ1-11095 was designed using structure-based drug design and computational methods at scale to selectively bind the Type II conformation of the JAK2 kinase to provide greater efficacy with disease modification compared to all currently approved JAK2 inhibitors, including ruxolitinib, which bind the Type I conformation of JAK2. AJ1-11095 has been shown in preclinical studies to reverse marrow fibrosis, reduce mutant allele burden, and maintain efficacy against MPN cells that become resistant to chronic Type I JAK2 inhibition. AJ1-11095 is currently in a Phase I study for patients with MF who have been failed by a Type1 JAK2 inhibitor. Further details about the study can be found at www.clinicaltrials.gov.