SAN DIEGO, March 17, 2026 (GLOBE NEWSWIRE) -- BlossomHill Therapeutics, Inc., a privately-held, clinical-stage biopharmaceutical company focused on the design and development of next-generation medicines for cancer, today announced it will introduce its next-generation KRAS pipeline at the American Association for Cancer Research (AACR) Annual Meeting 2026. These two non-covalent pan-KRAS inhibitors leverage a differentiated chemical scaffold to address limitations of contemporary molecules - achieving sub-nanomolar potency and a prolonged off-rate, combined with oral bioavailability. In addition, the company will present new preclinical data supporting the continued advancement of its clinical programs BH-30643, a first-in-class, mutant-selective, macrocyclic OMNI-EGFRTM inhibitor, and BH-30236, an oral CLK inhibitor for hematologic malignancies. The AACR Annual Meeting 2026 will be held April 17-22, 2026, in San Diego.
“We are excited to share new data from across our pipeline at AACR, including new preclinical data supporting the continued advancement of our lead clinical programs BH-30643 and BH-30236, and the introduction of our novel switch II-targeting KRAS programs, one of which will be highlighted during a minisymposium,” said Jean Cui, Ph.D., Founder and Chief Executive Officer of BlossomHill Therapeutics. “KRAS remains one of the most important and historically difficult targets in oncology. Our next-generation pan-KRAS inhibitors are intentionally designed using a differentiated chemical scaffold to deliver pseudo-irreversible target engagement and improved drug-like properties we believe will translate to clinical impact. We look forward to engaging with the scientific community at the upcoming AACR meeting.”
Details of the presentations are as follows:
Title: Discovery and characterization of BH-501284: A non-covalent, pan-KRAS inhibitor for treatment of diverse KRAS-mutant tumors (#6736)
Date & Time: April 21, 2026; 2:30-4:30 p.m. PT
Session Title: Targeted Therapies
Session Type: Minisymposium
Location: San Diego Convention Center
Key Findings: BH-501284 is a potent, selective, orally available non-covalent pan-KRAS inhibitor that demonstrates picomolar binding affinity, broad activity across KRAS mutations, and durable tumor regression in non-small cell lung cancer (NSCLC), colorectal cancer (CRC) and pancreatic ductal adenocarcinoma (PDAC models). By preferentially targeting inactive KRAS and maintaining activity under growth factor-driven resistance conditions, BH-501284 may overcome key limitations of existing KRAS inhibitors.
Title: Design and discovery of BH-501242, a novel pan-KRAS on/off inhibitor targeting KRAS switch II pocket (#5120)
Date & Time: April 21, 2026; 9:00 a.m.-12:00 p.m. PT
Session Title: New Ligands and Inhibitors
Location: San Diego Convention Center, Poster Section 38
Key Findings: Preclinical data demonstrate that BH-501242, a novel pan-KRAS inhibitor targeting the switch II pocket, potently inhibits a broad range of KRAS mutations, including G12D, G12V, and G12C, with sub-nanomolar cellular activity and robust tumor regression in multiple xenograft models. Its ability to bind both active and inactive KRAS and achieve strong oral exposure supports further development as a differentiated, mutation-agnostic KRAS therapy.
Title: CLK inhibitor BH-30236 synergizes with venetoclax in anti-leukemia activity via splicing modulation in preclinical AML and CLL models (#5872)
Date & Time: April 21, 2026; 2:00-5:00 p.m. PT
Session Title: Tyrosine Kinase, Phosphatase, and Other Inhibitors
Location: San Diego Convention Center, Poster Section 18
Key Findings: BH-30236, a novel oral CLK1/2/4 inhibitor, modulates alternative splicing to induce apoptosis and suppress leukemia stem cell–associated pathways, demonstrating robust anti-leukemia activity in acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL) models. In combination with venetoclax, BH-30236 produced synergistic tumor regression, including durable, complete responses in resistant xenograft models.
Title: BH-30643, a novel macrocyclic non-covalent, mutant-selective EGFR inhibitor, addresses the resistance and potency limitations of contemporary EGFR TKIs (#5877)
Date & Time: April 21, 2026; 2:00-5:00 p.m. PT
Session Title: Tyrosine Kinase, Phosphatase, and Other Inhibitors
Location: San Diego Convention Center, Poster Section 18
Key Findings: BH-30643 is a macrocyclic, non-covalent, mutant-selective OMNI-EGFR inhibitor that uniquely overcomes T790M and C797S resistance mutations while maintaining potent activity against classical EGFR drivers and sparing wildtype EGFR. In preclinical studies, BH-30643 demonstrated prolonged suppression of tumor cell proliferation compared to osimertinib, including under growth factor-mediated resistance conditions.
About BlossomHill Therapeutics
BlossomHill Therapeutics, Inc. is a privately held, clinical-stage biopharmaceutical company focused on designing and developing next-generation targeted therapies for cancer. Founded and led by industry veteran J. Jean Cui, Ph.D., with her proven track record in oncology drug design and development – including three FDA-approved drugs – BlossomHill applies cutting-edge science to address key oncogenic drivers and improve patient outcomes in difficult-to-treat cancers. The company’s lead clinical programs include BH-30643, a first-in-class, macrocyclic, non-covalent, mutant-selective OMNI-EGFRTM inhibitor for the treatment of EGFR- or HER2-mutated non-small cell lung cancer (NSCLC), and BH-30236, a macrocyclic CLK inhibitor for the treatment of relapsed or refractory acute myeloid leukemia (R/R AML) or higher-risk myelodysplastic syndrome (HR-MDS), representing a first-in-class opportunity. BlossomHill Therapeutics is headquartered in San Diego, California and has raised a total of $257 million from leading life sciences investors. For more information, visit bhtherapeutics.com and follow us on LinkedIn and X.
Contacts:
Media:
Ashlea Kosikowski
1AB
ashlea@1abmedia.com
Investors:
Alicia Davis
1AB
alicia@1abmedia.com
