AMB-104 leverages the validated target engagement of the Company’s CSF1R monoclonal antibody built into an antibody-drug conjugate (ADC) to deliver a tumor-killing payload to treat AML.
Therapeutic area
Acute myeloid leukemia (AML)
Program safety
Validated linker-payload
and target binder
First-in-class
Only agent targeting
CSF1R for AML
Next milestone
IND-enabling studies and submission
AML and unmet needs
AML is a rapidly progressing tumor that develops when at least 20% of the bone marrow cells consist of immature white blood cells (“leukemia blasts”), leading to bone marrow failure to produce healthy blood cells.
Despite available treatments, including intensive chemotherapy or venetoclax-based combinations, approximately 20-40% of newly diagnosed patients do not achieve complete recovery and more than 50% relapse within 3 years.
For relapse or refractory AML patients, some targeted therapies can be used, but a significant number of patients have no actionable biomarkers. As a result, AML remains a devastating disease in need of more efficacious and safer therapies.
AMB-104 ADC for the treatment of AML
CSF1R is overexpressed across different segments of the AML patient population including both newly diagnosed patients and Relapse/Refractory patients. AMB-104 leverages the overexpression of CSF1R to target AML cancer cells with a proven cytotoxic payload and has broad application for use across a range of AML patient populations.
The development of AMB-104 for AML is supported by a robust preclinical data package that includes, among other things, confirmed overexpression of CSF1R on AML patient samples, efficient internalization into AML cells, and robust in vitro and in vivo efficacy data.
AmMax's antibody targeting CSF1R
- Clinically validated target engagement.
- Proven strong binding affinity and internalization in AML cells.
Proven linker with exatecan as payload
- Linker-payload has been tested in multiple Phase 1/2 clinical studies.
- Exatecan (cytotoxic payload) efficacy has been clinically validated.