csf-1r-in-1

CSF1R-IN-1 is a CSF1R inhibitor with an IC50 of 0.5 nM.

Cediranib (AZD2171) (AZD2171) is a highly potent (IC50 < 1 nmol L) ATP-competitive inhibitor of recombinant KDR tyrosine kinase in vitro, also inhibits Flt1 4 (IC50: 5 nM ≤3 nM), similar activity against PDGFRβ and c-Kit, selective more for VEGFR than PDGFR-α (36-fold), CSF-1R (110-fold), and Flt3 (1000-fold) in HUVEC cells.

c-Fms-IN-10, a derivative of thieno [3,2-d] pyrimidine, is a kinase inhibitor of FMS (Colony-stimulating factor-1 receptor, CSF-1R; IC50: 2 nM) with anti-tumor activity.

c-Fms-IN-8 is a colony-stimulating factor-1 receptor (CSF-1R, c-FMS) Type II inhibitor (IC50: 9.1 nM). It is compound 4a in the reference.

CSF1R-IN-2 is an oral-active SRC, MET and c-FMS inhibitor (IC50s: 0.12 nM, 0.14 nM and 0.76 nM for SRC, MET and c-FMS respectively).

CSF1R-IN-26 (Compound III-1) is an inhibitor of CSF-1R with an IC50 of 20.07 nM. It promotes the polarization of M2 macrophages to M1 macrophages, inducing apoptosis in MC-38 cancer cells. CSF1R-IN-26 inhibits the activation of the AKT/ERK/STAT3 signaling pathways, remodels the tumor immune microenvironment, and exhibits antitumor activity in mouse models. In SD rats, CSF1R-IN-26 demonstrates favorable pharmacokinetic properties, with a half-life of 1.86 hours and an oral bioavailability of 79.22%.

Antifibrotic agent 1 is an orally active medication designed to treat idiopathic pulmonary fibrosis (IPF). It effectively mitigates IPF-related processes, including TGF-β-induced epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transition (FMT), as well as profibrotic M2 polarization. Antifibrotic agent 1 selectively inhibits CSF-1R, PDGFR-α, and Src family kinases (SFKs), while sparing VEGFR, FGFR, and Abl to minimize off-target toxicity. In a bleomycin (BLM)-induced pulmonary fibrosis mouse model, it demonstrates strong antifibrotic activity.

OSI-930, an orally active inhibitor of c-Kit and the vascular endothelial growth factor receptor-2 (VEGFR-2), targets cancer cell proliferation and blood vessel growth (angiogenesis) in tumors.

Nampt-IN-1 (LSN3154567) (LSN3154567) is a potent and selective NAMPT inhibitor. Nampt-IN-1 inhibits purified NAMPT with an IC50 of 3.1 nM.

cFMS Receptor Inhibitor II is a CSF1R kinase (FMS Receptor; colony stimulating factor 1 receptor; Macrophage colony-stimulating factor receptor) inhibitor with an IC50 of 2.8 nM, demonstrating significant selectivity over other kinases. This compound also exhibits notable CSF1R inhibition with an IC50 of 1.4 μM in cellular assays.

CSF1R-IN-6 is a potent inhibitor of CSF1R, which is expressed in macrophages and relies on the CSF-1 CSF-1R signaling pathway for macrophage survival and differentiation (Compound 5).

CSF1R-IN-4 is a potent CSF-1R inhibitor that can modulate the exchange of inflammatory factors between TAM and glioma cells, presenting potential for cancer research [EGFR-IN-40].

CSF1R-IN-5 is a potent CSF1R inhibitor that can influence the exchange of inflammatory factors between TAM and glioma cells, and has potential applications in cancer disease research.

CSF1R-IN-20 (compound 7a), a CSF-1R inhibitor, exhibits an IC 50 of 467 nM and effectively inhibits CSF-1R auto-phosphorylation [1].

CSF1R-IN-21 (compound 7e), a CSF-1R inhibitor, exhibits potent inhibition with an IC 50 of 31 nM and effectively blocks CSF-1R auto-phosphorylation. It is utilized in researching neurodegenerative diseases [1].

CSF1R-IN-22 (Compound C19), a potent orally administered CSF-1R selective inhibitor (IC50 <6 nM), significantly enhances CXCL9 secretion from M2 macrophages and promotes CD8+ T cell infiltration. Moreover, it amplifies the anti-tumor immune responses in conjunction with anti-PD-1 and triggers apoptosis in tumor cells. Additionally, CSF1R-IN-22 effectively reprograms M2-like TAMs (tumor-associated macrophages) to an M1 phenotype, modulates the tumor microenvironment (TME) by fostering the recruitment of CD8+ T cells, and diminishes the presence of immunosuppressive Tregs and MDSCs [1].