2. Protein Tyrosine Kinase/RTK Apoptosis
  3. Anaplastic lymphoma kinase (ALK) Apoptosis
  4. ALK-IN-22

ALK-IN-22 (compound I-24) is a potent ALK inhibitor with IC50 values of 2.3, 3.7 and 2.9 nM for ALK, ALKL1196M and ALKG1202R, respectively. ALK-IN-22 down-regulated the phosphorylation of ALK and its downstream proteins. ALK-IN-22 induces apoptosis. ALK-IN-22 can be used for tumor research.

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ALK-IN-22 Chemical Structure

ALK-IN-22 Chemical Structure

CAS No. : 2468219-09-0

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ALK-IN-22 Related Antibodies

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Description

ALK-IN-22 (compound I-24) is a potent ALK inhibitor with IC50 values of 2.3, 3.7 and 2.9 nM for ALK, ALKL1196M and ALKG1202R, respectively. ALK-IN-22 down-regulated the phosphorylation of ALK and its downstream proteins. ALK-IN-22 induces apoptosis. ALK-IN-22 can be used for tumor research[1].

In Vitro

ALK-IN-22 (compound I-24) (72 hours) has anti-proliferative activities against ALK-positive karpas299, H2228 and H3122 cell lines with IC50 values of 11, 37 and 27 nM, respectively[1].
ALK-IN-22 (compound I-24) (0-100 nM; 24 hours; H2228 cells) has inhibitory effect on ALK and downstream signaling AKT and ERK[1].
ALK-IN-22 (compound I-24) (0-100 nM; 48 hours; H2228 cells) can induce apoptosis and achieve cell cycle arrest in G1 phase[1].

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

ALK-IN-22 Related Antibodies

Western Blot Analysis[1]

Cell Line: H2228 cells
Concentration: 0, 25, 50 and 100 nM
Incubation Time: 24 hours
Result: Downregulated the phosphorylation level of ALK and blocked the expressions of ALK downstream key signaling AKT, ERK along with their activated forms in a dose-dependent fashion.

Apoptosis Analysis[1]

Cell Line: H2228 cells
Concentration: 0, 25, 50 and 100 nM
Incubation Time: 48 hours
Result: The apoptotic rates were 14.23%, 23.94% and 31.70% at concentrations of 25 nM, 50 nM and 100 nM, respectively.

Cell Cycle Analysis[1]

Cell Line: H2228 cells
Concentration: 0, 25, 50 and 100 nM
Incubation Time: 48 hours
Result: The percentage of cells in the G1 phase increased from 49.72% to 58.51% in a dose-dependent fashion.
In Vivo

ALK-IN-22 (compound I-24) (25-50 mg/kg; i.g.; Twice daily, for 14 days) has antitumor efficacy in vivo[1].
ALK-IN-22 (compound I-24) (10 mg/kg; p.o.) shows the Cmax and t1/2 values of 345.7 ng/mL and 4.1 hours, respectively[1].
ALK-IN-22 (compound I-24) (2 mg/kg; i.v.) shows the CL and t1/2 values of 36.2 mL/min/kg and 2.5 hours, respectively[1].

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

Animal Model: Female BALB / c nude mice[1]
Dosage: 25 and 50 mg/kg
Administration: Intragastric; Twice daily, for 14 days.
Result: The tumor growth inhibition (TGI) value of 50 mg/kg reached 93.5%.
Animal Model: SD rats[1]
Dosage: 2 and 10 mg/kg (Pharmacokinetic Analysis)
Administration: Oral administration and intravenous injection
Result: 1.19
Parameter F16 VP-16
Dose (i.v.) mg/kg 10 10
Cmax (ng/mL) 26952 17712
Tmax (min) 5 5
AUCplasma (min*ng/mL) 2878363 409528
T1/2 (min) 151 45
Vd (L/Kg) 0.2341 0.432
CL (L/min/kg) 0.001 0.007
Molecular Weight

477.95

Formula

C24H24ClN7O2
CAS No.
SMILES

O=C(C1=C(C)NC2=C1C=CC(NC3=NC=C(Cl)C(NC4=CC=CC=C4C(NC)=O)=N3)=C2)N(C)C
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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ALK-IN-22 Related Classifications

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Help & FAQs
  • 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:

ALK-IN-222468219-09-0Anaplastic lymphoma kinase (ALK)ApoptosisAnaplastic lymphoma kinaseALK tyrosine kinase receptorCD246Cluster of differentiation 246apoptosisALKphosphorylationantitumorInhibitorinhibitorinhibit

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