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evofosfamide + sunitinib
- Development stage
- Phase 2
- Lead developer
- Merck KGaA
- Modality
- Peptide-Drug Conjugates → Peptide Conjugates → Peptides, Small Molecules
- Administration
- Intravenous, Oral
01
Overview
Evofosfamide (formerly known as TH-302) is a hypoxia-activated prodrug designed to target tumor cells in low oxygen environments. Upon activation in hypoxic regions of tumors, it releases bromo-isophosphoramide mustard, a DNA alkylator that induces selective tumor cell death. Sunitinib is an oral small molecule inhibitor of multiple receptor tyrosine kinases (RTKs), including those for platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR), leading to reduced tumor vascularization and increased cancer cell apoptosis. The combination has been investigated for synergistic anti-tumor effects, particularly in renal cell carcinoma and pancreatic neuroendocrine tumors (panNETs). Preclinical studies suggest that sunitinib-induced hypoxia may enhance the activation of evofosfamide within tumors[1][2][3][4][5][6].
- Other names
- TH-302 + sunitinibevofosfamide + sunitinib
02
Targets
CSF1R (Macrophage colony-stimulating factor receptor)DNAFLT3 (Fms related receptor tyrosine kinase 3)KIT (c-KIT proto-oncogene receptor tyrosine kinase)PDGFRA (Platelet-derived growth factor receptor alpha)PDGFRB (Platelet-derived growth factor receptor beta)RET (Rearranged during transfection receptor tyrosine kinase)VEGFR-1 (Vascular endothelial growth factor receptor 1)VEGFR2 (Vascular endothelial growth factor receptor 2)VEGFR4 (Vascular endothelial growth factor Receptor-3)RTKs (Receptor Tyrosine Kinases)
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