2. Protein Tyrosine Kinase/RTK TGF-beta/Smad Stem Cell/Wnt
  3. TAM Receptor Discoidin Domain Receptor TGF-β Receptor Hedgehog
  4. Axl-IN-21

Axl-IN-21 is an orally active and selective AXL inhibitor (Kd = 2.7 nM, IC50 = 4.0 nM). Axl-IN-21 displays kinase selectivity and retains strong activity against cancer-related mul-kinases (Mer with Kd = 1.4 nM, DDR1 with IC50 = 22.2 nM, HIPK4 with Kd = 11.0 nM and LOK with Kd =10 nM). Axl-IN-21 overcomes tumor microenvironment-driven resistance by blocking CAF-derived GAS6-induced AXL/STAT3/ABCG1 signaling, restoring chemosensitivity and inhibiting drug efflux in gastric cancer (GC). Axl-IN-21 suppresses TGF-β1-induced epithelial-mesenchymal transition (EMT), migration, and invasion in MDA-MB-231 cells. Axl-IN-21 exhibits no significant cytotoxicity in non-cancerous cells. Axl-IN-21 can be research for triple negative breast cancer and gastric cancer[1] [2] .

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Axl-IN-21

Axl-IN-21 Chemical Structure

CAS No. : 1958081-87-2

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Axl-IN-21 Related Antibodies

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ALK1 ALK2 ALK3 ALK4 ALK5 ALK6 ALK7 TGFβR2 ACVR2A ACVR2B BMP

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Description

Axl-IN-21 is an orally active and selective AXL inhibitor (Kd = 2.7 nM, IC50 = 4.0 nM). Axl-IN-21 displays kinase selectivity and retains strong activity against cancer-related mul-kinases (Mer with Kd = 1.4 nM, DDR1 with IC50 = 22.2 nM, HIPK4 with Kd = 11.0 nM and LOK with Kd =10 nM). Axl-IN-21 overcomes tumor microenvironment-driven resistance by blocking CAF-derived GAS6-induced AXL/STAT3/ABCG1 signaling, restoring chemosensitivity and inhibiting drug efflux in gastric cancer (GC). Axl-IN-21 suppresses TGF-β1-induced epithelial-mesenchymal transition (EMT), migration, and invasion in MDA-MB-231 cells. Axl-IN-21 exhibits no significant cytotoxicity in non-cancerous cells. Axl-IN-21 can be research for triple negative breast cancer and gastric cancer[1] [2] .

IC50 & Target[1]

DDR1

22.2 nM (IC50)

Mer

1.4 nM (Kd)

Axl

4 nM (IC50)

Axl

2.7 nM (Kd)

In Vitro

Axl-IN-21 (compound 9im) (0.1-0.5 μM) dose-dependently inhibits AXL phosphorylation and reverses the epithelial-mesenchymal transition (restoring E cadherin and reducing N cadherin expression) in SNU668 and MKN1 gastric cancer cells, even when co cultured with cancer-associated fibroblasts (CAF), restores chemosensitivity by blocking CAF induced AXL activation and downstream signaling, although co culture with CAFs normally reduces apoptotic markers (cleaved PARP and cleaved caspase 3) following chemotherapy including 5-Fluorouracil (5 FU) (HY-90006) and cisplatin (HY-17394)[1].
Axl-IN-21 (0.5-32 μM) exhibits lower cytotoxicity in non-cancerous cells compared to BGB324 (HY-15150) [1].
Axl-IN-21 (0.1-0.5 μM) inhibits JAK1/STAT3, PI3K/AKT and MEK/ERK signalling pathways and reduces the CAF)-induced enhancement of cell migration in SNU668 cells co-cultured with CAFs, even in the presence of CAF-conditioned media or direct co-culture. [1].
Axl-IN-21 (0.5-2 μM) suppresses CAF-induced AXL activation, downstream signalling, GC cell migration and chemoresistance in inhibiting AXL phosphorylation in SNU668 cocultured with CAFs and/or treated with chemotherapeutic agents[1].
Axl-IN-21 (0.1-0.5 μM) suppresses both the upregulation of ABCG1 expression and the phosphorylation of AXL, JAK1/STAT3, PI3K/AKT, and MEK/ERK in AXL-activated GC SNU668 cells treated with recombinant GAS6[1].
Axl-IN-21 decreased ABCG1 expression and increased cleaved caspase-3 positive cells, indicating enhanced apoptosis when combinate with CAFs and 5-FU[1].
Axl-IN-21 (0.03-3 μM, 6 h) has strong Axl kinase inhibition in MDA-MB-231 breast cancer cells[2].
Axl-IN-21 (0.04-5 μM, 96-144 h) dose-dependently inhibits TGF-β1-induced Axl activation in MDA-MB-231 breast cancer cells[2].
Axl-IN-21 (0.04-5 μM, 24 h) inhibits the migrating process and invasiveness in MDA-MB-231 cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Axl-IN-21 Related Antibodies

Western Blot Analysis[2]

Cell Line: MDA-MB-231
Concentration: 0.03, 0.1, 0.3, 1 and 3 μM
Incubation Time: 6 h
Result: Inhibited phosphorylation of Axl and downstream signaling (pAkt, pAxl).

Immunofluorescence[2]

Cell Line: MDA-MB-231
Concentration: 0.04, 0.2, 1 and 5μM
Incubation Time: 96 to 144 h
Result: Dose-dependently restored the protein levels of E cadherin and N-cadherin back to the control levels.
Reversed TGF β1-induced expression level changes of E-cadherin (an epithelial marker) and N-cadherin (a meschenchymal marker) EMT markers in MDA-MB-231 cells.

Cell Migration Assay [2]

Cell Line: MDA-MB-231
Concentration: 0.2, 1.0, 5.0 μM
Incubation Time: 24 h
Result: Moderately inhibited the migrating process in MDA-MB-231 cells, suppressing the TGF β1 (10 ng/mL)-induced wound closure by ∼24.2%, ∼50.6%, and ∼58.4% at concentrations of 0.2, 1.0, and 5.0 μM.

Cell Invasion Assay[2]

Cell Line: MDA-MB-231
Concentration: 0.04, 0.2, 1.0, or 5.0 μM
Incubation Time: 24 h
Result: Inhibited cancer cell invasion by 48.5%, 52.1%, 73.5%, and 78.1% at concentration of 0.04, 0.2, 1.0, and 5.0 μM, respectively.
Parmacokinetics
Species Dose Route AUC0-∞ T1/2 Tmax Cmax CL
Mice[1] 25 mg/kg p.o. 31505 μg/L·h 10.2 h 6 h 1967 μg/L 0.9 L/h/kg
Mice[1] 5 mg/kg i.v. 42325 μg/L·h 25.2 h / 1168 μg/L 0.1 L/h/kg
In Vivo

Axl-IN-21 (compound 9im) (90 mg/kg, p.o., daily for 3 weeks) increases E-cadherin expression in CAF-mixed SNU668 xenograft tumors, indicating that it inhibits CAF-induced AXL activation and downstream signaling pathways[1].
Axl-IN-21 (30, 90 mg/kg, p.o., daily for 21 days) in xenograft model of highly metastatic 4T1 murine breast cancer cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: SNU668 cells (1×106) with or without induced CFAs (1×106, all cells in 100 μL PBS with 50% Matrigel)-BALB/c nude mice (5 weeks old)[1]
Dosage: 90 mg/kg
Administration: p.o., daily for 3 weeks
Result: Increased E-cadherin expression.
Significantly reduced tumor volume and weight when combined with 5-FU whereas either agent alone had only limited effects.
Animal Model: SNU668 cells (1×106) with or without induced CFAs (1×106, all cells in 100 μL PBS with 50% Matrigel)-BALB/c nude mice (5 weeks old)[1]
Dosage: 90 mg/kg
Administration: p.o., daily for 3 weeks
Result: Increases E-cadherin expression.
Significantly reduced tumor volume and weight when combined with 5-FU whereas either agent alone had only limited effects.
Animal Model: 4T1 cells (0.5 × 106) induced-female BALB/c mice[2]
Dosage: 30 or 90 mg/kg
Administration: p.o., daily for 21 days
Result: Did not show an obvious effect on growth of the primary tumor.
Dose-dependently suppressed both size and number of liver metastases (21.3 and 13.0 in the 30 and 90 mg/kg dosing groups, respectively).
Molecular Weight

542.56

Formula

C30H27FN4O5
CAS No.
SMILES

COC1=CC2=C(N=CN=C2OC3=CC=C(C=C3F)NC(C4=C(N(C5=C(C4=O)C=C(C=C5)CC)C)C)=O)C=C1OC
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Axl-IN-21 Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Axl-IN-211958081-87-2TAM ReceptorDiscoidin Domain ReceptorTGF-β ReceptorHedgehogTyro3AxlMerTransforming growth factor beta receptorsAXLDDR1HIPK4LOKAXL/STAT3/ABCG1TGF-β1triple negative breast cancergastric cancerInhibitorinhibitorinhibit

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