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JMS-17-2
- Development stage
- Preclinical
- Lead developer
- Drexel University
- Modality
- Small Molecules
- Administration
- Intraperitoneal
01
Overview
JMS-17-2 is a potent and selective small-molecule antagonist of the CX3C chemokine receptor 1 (CX3CR1, also known as the fractalkine receptor) with an IC50 of 0.32 nM. Developed by researchers at Drexel University, JMS-17-2 blocks fractalkine (CX3CL1)-induced ERK phosphorylation and significantly reduces the migration of cancer cells in vitro. In preclinical animal models of metastasis, administration of JMS-17-2 impairs the lodging of circulating tumor cells (CTCs) to the skeleton and soft-tissue organs, thereby preventing metastatic seeding and reducing overall tumor burden. It is primarily being investigated for its potential therapeutic application in preventing or containing metastatic progression in breast cancer, pancreatic ductal adenocarcinoma (PDAC), and other CX3CR1-driven malignancies.
- Other names
- 5-[3-[4-(4-chlorophenyl)-1-piperidinyl]propyl]pyrrolo[1,2-a]quinoxalin-4(5H)-one5-[3-[4-(4-chlorophenyl)piperidin-1-yl]propyl]pyrrolo[1,2-a]quinoxalin-4-oneJMS 17-2JMS17-2JMS-17-2JMS 17-2 hydrochlorideJMS17-2 hydrochlorideJMS-17-2 hydrochloride
02
Targets
AKT (RAC-alpha serine/threonine-protein kinase)CX3CL1 (Fractalkine)CX3CR1 (C-X3-C motif chemokine receptor 1)MAPK3 (Mitogen-activated protein kinase 1)
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