csf1r-in-1

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

Axl Mer-IN-1 is a compound that functions as an inhibitor for Axl Mer receptor tyrosine kinase (Axl Mer RTK) and CSF1R, exhibiting dissociation constants (Kds) of less than 0.1 μM.

CSF1R-IN-13 is a powerful CSF1R inhibitor with potential applications in researching cancer diseases [1]. CSF1R, also known as colony stimulating factor 1 receptor, is a critical growth factor that regulates various cell types, including bone marrow progenitor cells, monocytes, macrophages, and giants [1]. CSF1R-IN-13 shows promise in furthering our understanding of cancer-related disorders (WO2019134661A1, compound 32) [1].

CSF1R-IN-12 is an effective CSF1R inhibitor. CSF1R-IN-12 has research potential in cancer diseases.

CSF1R-IN-14, an isoindolinone derivative compound, is a potent inhibitor of CSF1R. CSF1R-IN-14 has potential for cancer disease research.

CSF1R-IN-17 (compound 9) is a potent and selective antagonist of CSF1R with an IC50 of 0.2 nM, capable of inhibiting osteoclast differentiation [1].

CSF1R-IN-15 (compound 23) serves as an inhibitor of the colony-stimulating factor-1 receptor (CSF1R), a tyrosine kinase located in the macrophage cell membrane. This receptor is activated by colony-stimulating factor-1 (CSF-1) and interleukin-34. Signaling through CSF1R is essential for the differentiation, proliferation, and survival of macrophages [1].

CSF1R-IN-19 is a robust inhibitor of CSF1R that influences the exchange of inflammatory factors between TAMs and glioma cells. It holds potential for cancer research [1].

CSF1R-IN-10 (Compound 48) is a CSF-1R inhibitor with an IC50 of 0.005 μM.

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.

PLX5622 hemifumarate is a highly selective, brain-penetrant, and orally active CSF1R inhibitor with an IC50 of 0.016 μM and Ki of 5.9 nM. It allows for extended and specific microglial elimination preceding and during pathology development and demonstrates desirable PK properties in various animals [1] [2].

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).

JNJ-28312141 is an orally active CSF1R inhibitor and a FLT3 inhibitor. JNJ-28312141 is a new agent with potential therapeutic activity in acute myeloid leukemia and in settings where CSF-1-dependent macrophages and osteoclasts contribute to tumor growth a

AC708 is a small molecule CSF1R inhibitor that effectively inhibits CSF1R phosphorylation mediated by CSF-1 (IC50 = 26 nM) and IL-34 (IC50 = 33 nM). It also inhibited the activity of growth factor-dependent cells cultured in CSF-1 (IC50 = 38 nM) or IL-34

Sulfatinib (KDR-IN-1) (HMPL-012) is a potent and highly selective tyrosine kinase inhibitor against VEGFR1 2 3, FGFR1 and CSF1R with IC 50 s ranging from 1 to 24 nM.

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.

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.

IACS-9439 is a potent, selective, and orally active CSF1R inhibitor with a K(i) of 1 nM, suitable for research on advanced solid tumors [1].

Edicotinib, also known as JNJ-40346527, is a small molecule and orally available inhibitor of colony-stimulating factor-1 receptor (CSF1R; FMS) with potential antineoplastic activity. FMS tyrosine kinase inhibitor JNJ-40346527 blocks the receptor-ligand interaction between FMS and its ligand CSF1, thereby preventing autophosphorylation of FMS. As a result, unphosphorylated FMS cannot activate FMS-mediated signaling pathways, thus potentially inhibiting cell proliferation in FMS-overexpressed tumor cells.

Quizartinib, also know as AC220 and AC010220, is an orally available FLT3 STK1 inhibitor with potential antineoplastic activity. Class III receptor tyrosine kinase inhibitor AC220 selectively inhibits class III receptor tyrosine kinases, including FMS-related tyrosine kinase 3 (FLT3 STK1), colony-stimulating factor 1 receptor (CSF1R FMS), stem cell factor receptor (SCFR KIT), and platelet derived growth factor receptors (PDGFRs), resulting in inhibition of ligand-independent leukemic cell proliferation and apoptosis. Mutations in FLT3, resulting in constitutive activation, are the most frequent genetic alterations in acute myeloid leukemia (AML) and occur in approximately one-third of AML cases.

Cabiralizumab (FPA 008), an anti-CSF1R monoclonal antibody (MAb), promotes T cell infiltration and boosts antitumor immune responses. It also prevents osteoclast activation, thereby inhibiting bone destruction, and is utilized in rheumatoid arthritis (RA) research. Additionally, Cabiralizumab can be paired with Nivolumab in lung cancer studies [1] [2].

Axl Mer CSF1R-IN-2 (Comp 4) serves as an inhibitor for Axl, Mer, and CSF1R [1].