Currently, cancer therapy trial-and-error methodology is inefficient and unsustainable. Oncology is the worst therapeutic area for drug trial success; only 3.4% of drugs that enter phase I end up being FDA approved, and 57% fail due to poor drug efficacy in trials. Building tools that may aid in predicting an individual’s response to a specific therapy may help in reducing costs, guesswork, and importantly improve the outcome of patients and accelerate new drug development.
Moma Therapeutics Inc. has reported preclinical results on MOMA-313, a potent and selective DNA polymerase θ (POLθ) inhibitor under development for the treatment of homologous recombinant (HR)-deficient cancers.
The development of covalent KRAS G12C inhibitors has represented a significant advance for non-small-cell lung cancer treatment, but other mutations such as KRAS G13C/D still lack effective treatments.
Researchers from Zymeworks Inc. presented preclinical data for the novel glypican-3 (GPC3)-targeting antibody-drug conjugate (ADC), ZW-251, being developed as an anticancer agent.
Researchers from Immunome Inc. and Zentalis Pharmaceuticals Inc. presented preclinical data for IM-1021, a novel tyrosine kinase-like orphan receptor 1 (ROR1)-targeted antibody-drug conjugate with a new topoisomerase 1 (TOP1) linker payload, being developed for the treatment of solid tumors and B-cell malignancies.
AKT1 E17K is the most frequent gain of function mutation of the AKT1 gene. This mutation promotes pathologic localization of AKT1 to the plasma membrane and has been shown to induce leukemia in mice. Current options for AKT1 E17K-driven tumors are limited.
Wee1 and PKMYT1 are two kinases involved in DNA damage repair. The former is located in the nucleus and the latter in the endoplasmic reticulum. Several selective inhibitors of Wee1 or PKMYT1 have been tested in the clinical setting as monotherapy or in combination with other drugs.
Currently, cancer therapy trial-and-error methodology is inefficient and unsustainable. Oncology is the worst therapeutic area for drug trial success; only 3.4% of drugs that enter phase I end up being FDA approved, and 57% fail due to poor drug efficacy in trials. Building tools that may aid in predicting an individual’s response to a specific therapy may help in reducing costs, guesswork, and importantly improve the outcome of patients and accelerate new drug development.
FMS‐like tyrosine kinase 3 (FLT3) is a type III receptor tyrosine kinase validated as a therapeutic target for acute myeloid leukemia (AML) and regarded as an indicator of poor prognosis. Unfortunately, current FLT3 inhibitors, such as midostaurin, quizartinib or gilteritinib, often lead to myelosuppression or cardiovascular toxicity.
