| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg | |||
| Other Sizes |
| Targets |
PDGFRβ 2.3 nM (Kd)
AXL (a TAM family receptor tyrosine kinase). AXL-IN-13 is a potent AXL inhibitor with an IC50 of 1.6 nM and a Kd of 0.26 nM. It binds with high affinity to the ATP-binding pocket of AXL, blocking its kinase activity and downstream signaling. |
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| ln Vitro |
According to ELISA data, AXL-IN-13 (Compound 6li) inhibits Ba/F3-TEL-AXL cell proliferation with an IC50 of 4.7 nM [1]. Inhibition of CSF1R, FLT1/3/4, KLT, PDGFRB, and TIE2 binding affinity has also been demonstrated by AXL-IN-13 [1]. In MDA-MB-231 and 4T1 cells, AXL-IN-13 (0-500 nM, 6 hours) inhibits AXL phosphorylation [1]. In MDA-MB-231 cells, TGF-β1 (10 ng/mL)-induced EMT is blocked by AXL-IN-13 (0-3 μM, 3 days)[1]. MDA-MB-231 cells' migration and invasion caused by TGF-β1 (10 ng/mL) are inhibited by AXL-IN-13 (0-3 μM, 24 hours) [1].
AXL-IN-13 inhibits AXL with an IC50 of 1.6 nM and a Kd of 0.26 nM, representing an 8.75-fold increase in potency over bemcentinib (IC50 = 14 nM). It effectively reverses TGF-beta1-induced epithelial-mesenchymal transition (EMT) and demonstrates significant inhibition of cancer cell migration and invasion in vitro. |
| ln Vivo |
AXL-IN-13 (compound 6li) (50 or 100 mg/kg, oral, 14 days) inhibits 4T1 tumor growth and metastasis[1]. AXL-IN-13 (25 mg/kg, oral) shows a good PK curve, with an AUC of 8410.21 ng/mL/h, a T1/2 value of 4.22 h, and an oral bioavailability (F) of 14.4%[1].
AXL-IN-13 has shown anti-cancer activity in preclinical models. By reversing EMT and inhibiting cell migration and invasion, it may reduce metastasis. It is an orally active compound, suggesting good bioavailability, and in vivo efficacy data are expected from ongoing studies, though detailed efficacy data are not fully published. |
| Enzyme Assay |
Cell-free AXL kinase assays are performed using recombinant human AXL enzyme. The compound is incubated with the enzyme and a peptide substrate in the presence of ATP for 30-60 minutes. Kinase activity is measured using a luminescence-based ADP detection kit. IC50 (1.6 nM) and Kd (0.26 nM) are calculated from dose-response curves and equilibrium binding studies.
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| Cell Assay |
Western Blot Analysis[1]
Cell Types: MDA-MB-231 cells Tested Concentrations: 0, 0.11, 0.33, 1, 3 μM. Incubation Duration: 3 days Experimental Results: Restored the protein levels of E-cadherin and N-cadherin to control levels . Cell Migration Assay [1] Cell Types: MDA-MB-231 cell Tested Concentrations: 0, 0.11, 0.33, 1, 3 μM. Incubation Duration: 24 h Experimental Results: 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. Cancer cell lines (e.g., those undergoing TGF-beta1-induced EMT) are seeded in 96-well plates and treated with AXL-IN-13 at various concentrations. EMT reversal is assessed by measuring expression of mesenchymal markers (e.g., vimentin) and epithelial markers (e.g., E-cadherin) by Western blot or immunofluorescence. Cell migration is measured using transwell assays. Invasion is measured using Matrigel-coated transwells. |
| Animal Protocol |
Animal/Disease Models: Xenograft model derived from highly metastatic 4T1 cells.[1]
Doses: 50 or 100 mg/kg Route of Administration: Oral administration (po) Experimental Results: 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. demonstrated that liver is one of the most common sites of breast cancer metastasis. Animal/Disease Models: Rats[1] Doses: 5 mg/kg (iv), 25 mg/ kg (po) Route of Administration: intravenous (iv) injection (iv), oral administration (po) Experimental Results: pharmacokinetic/PK parameters of AXL-IN-13 (Compound 6li). parameters T1/2 (h) Cmax (ng/mL) AUClast F (%) 5 mg/kg (iv) 3.31 12280.44 11684.24 25 mg/kg (po) 4.22 887.75 8410.21 14.4 For in vivo studies, AXL-IN-13 would be administered orally to mice bearing tumor xenografts. Dosing is typically once or twice daily for 2-4 weeks. Tumor volumes are measured with calipers. At study termination, tumors are excised for analysis of AXL phosphorylation and downstream signaling. Metastasis models could be used to assess inhibition of cancer cell dissemination. |
| ADME/Pharmacokinetics |
AXL-IN-13 is described as an orally bioavailable AXL inhibitor, indicating favorable oral absorption. The compound has a molecular weight of 351.36 (C17H16BrN5). CAS 2376928-82-2. Solubility: DMSO (10-50 mg/mL). For in vivo studies, it is typically formulated in a vehicle such as 0.5% methylcellulose or a DMSO/PEG300/Tween-80/saline mixture. PK parameters not specified.
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| Toxicity/Toxicokinetics |
No specific toxicity data are reported for AXL-IN-13. As an AXL inhibitor, potential on-target toxicities may include effects on immune function, as AXL plays a role in immune regulation. Comprehensive toxicological assessments have not been published. The compound is for research use only and is not FDA-approved.
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| References | |
| Additional Infomation |
Other information: AXL-IN-13 (CAS 2376928-82-2) is a research compound and not FDA-approved. It is a potent and orally bioavailable AXL inhibitor with an IC50 of 1.6 nM and a Kd of 0.26 nM. It reverses TGF-beta1-induced EMT and inhibits cancer cell migration and invasion. For research use only. Synonyms: Axl-IN-13.
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| Molecular Formula |
C34H41FN6O5
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|---|---|
| Molecular Weight |
632.724951505661
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| Exact Mass |
632.312
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| CAS # |
2376928-82-2
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| PubChem CID |
139533572
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| Appearance |
Off-white to light yellow solid powder
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| LogP |
5.6
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
12
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| Heavy Atom Count |
46
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| Complexity |
942
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| Defined Atom Stereocenter Count |
0
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| SMILES |
N1(C)C=C(C(NC2CCCCC2)=O)C(NC2=CC=C(OC3C4C(N=CC=3)=CC(OCCCN3CCOCC3)=C(OC)C=4)C(F)=C2)=N1
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| InChi Key |
QBRQTJMZEYORSP-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C34H41FN6O5/c1-40-22-26(34(42)38-23-7-4-3-5-8-23)33(39-40)37-24-9-10-30(27(35)19-24)46-29-11-12-36-28-21-32(31(43-2)20-25(28)29)45-16-6-13-41-14-17-44-18-15-41/h9-12,19-23H,3-8,13-18H2,1-2H3,(H,37,39)(H,38,42)
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| Chemical Name |
N-cyclohexyl-3-[3-fluoro-4-[6-methoxy-7-(3-morpholin-4-ylpropoxy)quinolin-4-yl]oxyanilino]-1-methylpyrazole-4-carboxamide
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: ~100 mg/mL (~158.1 mM; with ultrasonication)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 2.5 mg/mL (3.95 mM) in 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), Clear solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of DMSO stock solution (25.0 mg/mL) to 400 μL of PEG300 and mix well; then add 50 μL of Tween-80 and mix well; finally add 450 μL of physiological saline and adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: 2.5 mg/mL (3.95 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), Clear solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of DMSO stock solution (25.0 mg/mL) to 900 μL of 20% SBE-β-CD saline and mix well. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Solubility in Formulation 3: 2.5 mg/mL (3.95 mM) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), Clear solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of DMSO stock solution (25.0 mg/mL) to 900 μL of corn oil and mix well. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.5805 mL | 7.9023 mL | 15.8045 mL | |
| 5 mM | 0.3161 mL | 1.5805 mL | 3.1609 mL | |
| 10 mM | 0.1580 mL | 0.7902 mL | 1.5805 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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