Edgewood Oncology is a clinical‑stage biotech developing BTX‑A51, a small‑molecule multi‑kinase inhibitor that co‑targets CK1α, CDK7 and CDK9 to suppress MDM2 and MCL‑1 transcription, thereby restoring p53‑mediated apoptosis. The drug is being evaluated in Phase 2 trials for relapsed/refractory acute myeloid leukemia, high‑risk myelodysplastic syndrome, and genetically defined solid tumors such as GATA3‑mutant breast cancer, offering a safety profile that avoids the toxicities of direct MDM2 or MCL‑1 inhibitors.
Funding
$20M raised to dateRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.
Founders
Product
Problem
Patients with relapsed or refractory acute myeloid leukemia, high‑risk myelodysplastic syndrome, GATA3‑mutant breast cancer, and other genetically defined solid tumors have limited therapeutic options, often due to resistance mechanisms involving MDM2 and MCL‑1 that suppress p53‑mediated apoptosis.
Solution
Edgewood Oncology is developing BTX‑A51, a novel small‑molecule multi‑kinase inhibitor that simultaneously targets CK1α, CDK7 and CDK9. By co‑inhibiting these kinases, BTX‑A51 reduces transcription of MDM2 and MCL‑1 at super‑enhancers, leading to p53 accumulation and activation of programmed cell death. The indirect inhibition of MDM2 avoids the dose‑limiting toxicities seen with direct MDM2 inhibitors, while transcriptional suppression of MCL‑1 circumvents cardiotoxicity associated with direct MCL‑1 inhibitors. Early Phase 1 data show a favorable safety profile and evidence of antileukemic activity, supporting further evaluation in Phase 2 studies for both hematologic malignancies and genetically defined solid tumors.
Target Audience
Primary customers are pharmaceutical developers and clinical research organizations focusing on therapies for relapsed/refractory acute myeloid leukemia, high‑risk myelodysplastic syndrome, and genetically defined solid tumors such as GATA3‑mutant breast cancer.
Features
- Multi‑specific inhibition of CK1α, CDK7 and CDK9 to disrupt super‑enhancer‑driven transcription of oncogenic survival genes
- Indirect down‑regulation of MDM2, leading to p53 stabilization and apoptosis without classic MDM2‑inhibitor toxicities
- Transcriptional suppression of MCL‑1, reducing resistance mechanisms in AML and solid tumors while avoiding cardiotoxicity
- Demonstrated preclinical efficacy in AML, liposarcoma, and GATA3‑mutant breast cancer models
- Phase 1b clinical data showing favorable safety, complete remissions with incomplete count recovery (CRi) in relapsed/refractory AML, and a wide therapeutic window
- Ongoing Phase 2a trials evaluating BTX‑A51 as monotherapy and in combination with azacitidine for AML and as targeted therapy for ER⁺/HER2⁻ breast cancer