AXL-IN-13

Modify Date: 2024-04-09 10:10:32

AXL-IN-13 structure	Common Name	AXL-IN-13
	CAS Number	2376928-82-2	Molecular Weight	632.72
	Density	N/A	Boiling Point	N/A
	Molecular Formula	C₃₄H₄₁FN₆O₅	Melting Point	N/A
	MSDS	N/A	Flash Point	N/A

Use of AXL-IN-13

AXL-IN-13 is a potent and orally active AXL inhibitor (IC50: 1.6 nM, Kd: 0.26 nM). AXL-IN-13 reverses TGF-β1-induced epithelial-mesenchymal transition (EMT), and inhibits cancer cell migration and invasion[1].

Name	AXL-IN-13

Description	AXL-IN-13 is a potent and orally active AXL inhibitor (IC50: 1.6 nM, Kd: 0.26 nM). AXL-IN-13 reverses TGF-β1-induced epithelial-mesenchymal transition (EMT), and inhibits cancer cell migration and invasion[1].
Related Catalog	Research Areas >> Cancer Signaling Pathways >> Protein Tyrosine Kinase/RTK >> PDGFR Signaling Pathways >> Protein Tyrosine Kinase/RTK >> TAM Receptor Signaling Pathways >> Protein Tyrosine Kinase/RTK >> FLT3
Target	PDGFRβ:2.3 nM (Kd)
In Vitro	AXL-IN-13 (化合物 6li) 抑制 Ba/F3-TEL-AXL 细胞增殖，IC50 为 4.7 nM (通过 ELISA 测定)[1]. AXL-IN-13 还显示对 CSF1R、FLT1/3/4、KLT、PDGFRB、TIE2 的结合亲和力[1]。 AXL-IN-13 (0-500 nM，6 小时) 抑制 MDA-MB-231 和 4T1 细胞中 AXL 的磷酸化[1]。 AXL-IN-13 (0-3 μM，3 天) 阻断 MDA-MB-231 细胞中 TGF-β1 (10 ng/mL) 诱导的 EMT[1]。 AXL-IN-13 (0-3 μM，24 小时) 抑制 TGF-β1 (10 ng/mL) 诱导的 MDA-MB-231 细胞迁移和侵袭[1]。 Western Blot Analysis[1] Cell Line: MDA-MB-231 cells Concentration: 0, 0.11, 0.33, 1, 3 μM. Incubation Time: 3 days Result: Restored the protein levels of E-cadherin and N-cadherin to control levels. Cell Migration Assay [1] Cell Line: MDA-MB-231 cell Concentration: 0, 0.11, 0.33, 1, 3 μM. Incubation Time: 24 h Result: Inhibited cell migration at 1 and 3 μM. Inhibited the invasion of MDA-MB-231 cells by 22.6, 34.8, 56.5, and 70.4% at the concentrations of 0.11, 0.33, 1.0, and 3.0 μM, respectively.
In Vivo	AXL-IN-13 (化合物 6li) (50 或 100 mg/kg，口服，14 天) 抑制 4T1 肿瘤生长和转移[1]。 AXL-IN-13 (25 mg/kg, 口服) 显示出较好的 PK 曲线，AUC 为 8410.21 ng/mL/h，T1/2 值为 4.22 h，口服生物利用度 (F) 为 14.4%[1]。 Animal Model: Xenograft model derived from highly metastatic 4T1 cells.[1] Dosage: 50 or 100 mg/kg Administration: Oral administration (p.o.) Result: Suppressed 4T1 tumor growth with a tumor growth inhibition (TGI) of 78.0 and 95.9% at 50 and 100 mg/kg, respectively. Inhibited the phosphorylation of AXL. Showed that liver is one of the most common sites of breast cancer metastasis. Animal Model: Rats[1] Dosage: 5 mg/kg (i.v.), 25 mg/kg (p.o.) Administration: Intravenous injection (i.v.), oral administration (p.o.) Result: Pharmacokinetic parameters of AXL-IN-13 (Compound 6li). parameters T1/2 (h) Cmax (ng/mL) AUClast F (%) 5 mg/kg (i.v.) 3.31 12280.44 11684.24 25 mg/kg (p.o.) 4.22 887.75 8410.21 14.4
References	[1]. Chan S, et al. Discovery of 3-Aminopyrazole Derivatives as New Potent and Orally Bioavailable AXL Inhibitors. J Med Chem. 2022 Nov 24;65(22):15374-15390.

Molecular Formula	C₃₄H₄₁FN₆O₅
Molecular Weight	632.72