Prelude Therapeutics Presents Data at the 2025 ASH Annual Meeting from its Myeloproliferative Neoplasm (MPN) Programs

First disclosure of PRT12396, a JAK2V617F-selective JH2 inhibitor demonstrates disease modifying potential in myeloproliferative neoplasms

PRT12396 has completed GLP toxicology studies and is on track for IND filing in the first quarter 2026

First disclosure of a mutant calreticulin (mCALR) targeted degrader antibody conjugate (DAC) with a novel CDK9 degrader payload

JAK2V617F and mCALR are the two primary driver mutations responsible for disease progression and poor prognosis in the majority of MPN patients

WILMINGTON, Del., Dec. 06, 2025 (GLOBE NEWSWIRE) -- Prelude Therapeutics Incorporated (Nasdaq: PRLD) (“Prelude” or the “Company”), a precision oncology company, presented earlier today the first preclinical data on its JAK2V617F mutant selective JH2 inhibitors and additional preclinical data from its mCALR-targeted degrader antibody conjugate (DAC) discovery program. Both oral presentations took place at the American Society of Hematology (ASH) 67^th Annual Meeting in Orlando, FL. These presentations can be found at Publications - Prelude Therapeutics.

“Since JAK2V617F was first identified as a major driver mutation in JAK2 enzyme in myeloproliferative neoplasms two decades ago, our industry has been searching for an inhibitor that can selectively target the mutant JAK2 enzyme without disrupting normal JAK2 function” stated Kris Vaddi, Ph.D., Chief Executive Officer of Prelude. “We are proud to have made significant advances in the discovery of such molecules and to share preclinical data demonstrating that our lead candidate meaningfully differentiates between mutant and wild-type JAK2 and potentially overcomes dose-limiting toxicities associated with current therapies. This work underscores the potential for a disease-modifying approach beyond what is achievable with today’s JAK2 inhibitors, and we look forward to advancing this molecule into the clinic in early 2026.”

Continued Vaddi, “Beyond JAK2, mCALR is the other most common driver mutation in MPNs. Clinical data with an mCALR-directed antibody has now demonstrated meaningful therapeutic benefit for patients. Our degrader antibody conjugate (DAC) approach is designed to build on this validation by delivering a disease-relevant payload, such as our highly potent CDK9 degrader, directly to mCALR-positive cells. We believe this innovative strategy offers a differentiated, and potentially even more efficacious approach as we seek to advance the next wave of disease-modifying therapies for MPN patients. We were pleased to share these initial results from both programs today at ASH.”