Cat. No.: HY-183519

AH057

AH057 is an orally active JAK1 and JAK2 inhibitor. AH057 blocks IL-6-, IFN-α- and IFN-γ-induced JAK/STAT signaling, reduces cancer cell proliferation, invasion and colony formation, and induces apoptosis and G1 cell-cycle arrest. AH057 can be used for cervical cancer research.

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CAS No.: 118499-11-9
Formule: C₁₇H₂₂N₂O
Masse moléculaire:270.37

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Please store the product under the recommended conditions in the Certificate of Analysis.

AH057 Chemical Structure

CAS No.: 118499-11-9

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Activité biologique
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
Références
Calculators
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Classifications
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Activité biologique

Description

IC₅₀ & Target

JAK1

JAK2

STAT3

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In Vitro

AH057 (1 μM; 2 h) selectively inhibits p-JAK2 (Tyr1007/1008) and p-STAT3 (Tyr705) without affecting p-AKT (Ser473) and p-p65 (Ser536) in HeLa cells^[1].
AH057 (0.1-20 μM; 2 h) dose-dependently suppresses JAK2 and STAT3 phosphorylation in HeLa, DU145 and HepG2 cells; HeLa cervical cancer cells display the highest sensitivity^[1].
AH057 (1 μM in HeLa cells, 10 μM in DU145 cells and 20 μM in HepG2 cells; 0.25-3 h) time-dependently inhibits JAK2 and STAT3 activation, and rapidly inhibits JAK2 phosphorylation within 15 min ^[1].
AH057 (1 h pretreatment; followed by IL-6 or IFN-α stimulation at 250 ng/mL for 1 h) blocks IL-6, IFN-α, IFN-γ induced phosphorylation of JAK1, JAK2, TYK2, STAT1 and STAT3 in HeLa, DU145 and HepG2 ^[1].
AH057 (1 h pretreatment; followed by IL-6 or IFN-α stimulation at 250 ng/mL for 4 h) downregulates IL-6-induced SOCS3 , and IFN-α-induced IRF1 and IRF2 mRNA expression in HeLa, DU145 and HepG2 cells^[1].
AH057 (20 μM; 4 h) suppresses total tyrosine phosphorylation and STAT1/STAT3 activation in HEK293T cells overexpressing JAK1/JAK2/TYK2 JH1 kinase domain^[1].
AH057 (0.0005-100 μM; 72 h) inhibits the viability of multiple cancer cell lines, and cervical cancer cell lines HeLa, CaSki and SiHa show IC₅₀ values of 0.62 μM, 11.28 μM and 17.53 μM, respectively^[1].
AH057 (0.2-100 μM; 48 h) impairs invasion capacity of HeLa, CaSki, SiHa cervical cancer cells, with no obvious inhibitory effect on HcerEpic normal cells^[1].
AH057 (125-250 nM; 14 days) dose-dependently reduces colony formation number of cervical cancer cells^[1].
AH057 (200 nM, 10 μM) inhibits wound healing migration of cervical cancer cells (Hela, CaSki) in vitro^[1].
AH057 (0.5-20 μM; 24 h) triggers apoptotic cell death and induces G1/S cell cycle arrest in HeLa and CaSki cells; the proportion of G1 phase cells rises from 69.95% (DMSO) to 81.9% (1 μM AH057) in HeLa cells^[1].
AH057 (500 nM + SGI-1027 (HY-13962) 1 μM; 24 h) combined with SGI-1027 produces synergistic apoptosis and stronger G1 phase arrest in HeLa cells, further downregulates Cyclin D1, Cyclin A2, Cyclin B1, Bcl-XL and Survivin, increases cleaved Caspase-3 and cleaved PARP, the combination therapy shows synergistic downregulation of certain genes (BAX, BCL-XL, BCL-2, MDM2, Cyclin A2, Cyclin D3, and CDK2). ^[1].
AH057 is identified by docking-based virtual screening as a JAK inhibitor candidate, and molecular docking shows that AH057 binds to the JAK2 active site pocket through hydrophobic interaction and hydrogen bonds with key residues including Tyr931 and Leu932^[1].

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

Western Blot Analysis^[1]

Cell Line:

HeLa
Concentration:

10 μM
Incubation Time:

4 h
Result:

Showed the strongest inhibitory activity among nine top-ranking compounds against JAK2 phosphorylation and STAT3 phosphorylation.
Reduced pTyr1007/1008-JAK2 and pTyr705-STAT3 levels while maintaining total JAK2 and STAT3 protein levels.

Western Blot Analysis^[1]

Cell Line:

HeLa, DU145, HepG2
Concentration:

HeLa (0.1, 0.5, 1.0, 1.5, 2.0 μM); DU145, HepG2 (1, 5, 10, 15, 20 μM)
Incubation Time:

2 h
Result:

Reduced pTyr1007/1008-JAK2, pTyr705-STAT3 and pSer727-STAT3 levels in a dose-dependent manner.
HeLa cells showed higher AH057 sensitivity than DU145 and HepG2 cells.
Reduced JAK2 and STAT3 phosphorylation in both DU145 and HepG2 cells, confirming inhibition of JAK2/STAT3 signaling across multiple cancer cell lines.

Western Blot Analysis^[1]

Cell Line:

HeLa, DU145, HepG2
Concentration:

1 μM in HeLa cells; 10 μM in DU145 cells; 20 μM in HepG2 cells
Incubation Time:

0.25, 0.5, 1, 2, 3 h
Result:

Time-dependently inhibited JAK2 and STAT3 activation.
Rapidly reduced JAK2 phosphorylation within 15 min, supporting direct inhibition of JAK2 kinase activity.

Western Blot Analysis^[1]

Cell Line:

HeLa, DU145, HepG2
Concentration:

1 μM in HeLa cells; 10 μM in DU145 cells; 20 μM in HepG2 cells
Incubation Time:

1 h pretreatment; IL-6, IFN-α or IFN-γ stimulation at 250 ng/mL for 1 h
Result:

Blocked IL-6-induced JAK1, JAK2 and STAT3 phosphorylation.
Decreased IFN-α-induced JAK1, JAK2, TYK2, STAT1 and STAT3 phosphorylation.
Reduced IFN-γ-induced JAK1, JAK2, STAT1 and STAT3 phosphorylation.

Real Time qPCR^[1]

Cell Line:

HeLa, DU145, HepG2
Concentration:

1 μM in HeLa cells; 10 μM in DU145 cells; 20 μM in HepG2 cells
Incubation Time:

1 h pretreatment; IL-6, IFN-α or IFN-γ stimulation at 250 ng/mL for 4 h
Result:

Suppressed IL-6-induced SOCS3 mRNA transcription and IFN-α-induced IRF1 mRNA transcription in all three cell lines.

Western Blot Analysis^[1]

Cell Line:

HEK293T cells overexpressing JAK1-JH1, JAK2-JH1 or TYK2-JH1
Concentration:

20 μM
Incubation Time:

4 h
Result:

Reduced total tyrosine phosphorylation driven by overexpressed JAK1-JH1, JAK2-JH1 or TYK2-JH1.
Suppressed downstream STAT1 and STAT3 phosphorylation, supporting direct inhibition of JAK kinase domains.

Cell Viability Assay^[1]

Cell Line:

HcerEpic, HeLa, CaSki, SiHa, SK-OVR-3, ES-2, BT549, Huh7, Hep3B, HepG2, DU145, NCI-87, AGS, AsPC-3, U251
Concentration:

0.0005-100 μM
Incubation Time:

72 h
Result:

Inhibited the viability of multiple cancer cell lines.
HeLa cells were the most sensitive tested cancer cells, with an IC₅₀ of 0.62 μM.
CaSki and SiHa cervical cancer cells showed IC₅₀ values of 11.28 μM and 17.53 μM, respectively.
Other cancer cell lines showed IC₅₀ values ranging from 14.06 μM to 48.96 μM.

Cell Invasion Assay^[1]

Cell Line:

HcerEpic, HeLa, CaSki, SiHa
Concentration:

100 μM in HcerEpic cells; 200 nM in HeLa cells; 10 μM in CaSki and SiHa cells
Incubation Time:

48 h
Result:

Impaired invasion ability of HeLa, CaSki and SiHa cervical cancer cells.
Did not significantly reduce invasion of normal HcerEpic cells under the tested condition.

Cell Proliferation Assay^[1]

Cell Line:

HcerEpic, HeLa, CaSki, SiHa
Concentration:

50, 100 μM in HcerEpic cells; 125, 250 nM in HeLa cells; 1, 5 μM in CaSki and SiHa cells
Incubation Time:

14 days
Result:

Dose-dependently reduced colony formation in HeLa, CaSki and SiHa cervical cancer cells.
Did not significantly reduce colony formation of normal HcerEpic cells at 50 μM or 100 μM.

Cell Viability Assay^[1]

Cell Line:

HeLa
Concentration:

500 nM; 1 μM SGI-1027 (HY-13962)
Incubation Time:

48 h
Result:

Synergistically reduced HeLa cell viability.
The combined effect of AH057 and SGI-1027 was time-dependent, and combination treatment induced stronger cell death than either single compound.

Apoptosis Analysis^[1]

Cell Line:

HeLa
Concentration:

500 nM; 1 μM SGI-1027 (HY-13962)
Incubation Time:

4 h
Result:

Increased both early and late apoptotic cell populations.
Combination treatment induced a higher percentage of apoptotic cell death than either AH057 or SGI-1027 alone.

Western Blot Analysis^[1]

Cell Line:

HeLa
Concentration:

500 nM; 1 μM SGI-1027 (HY-13962)
Incubation Time:

24 h
Result:

Enhanced cleaved PARP and cleaved caspase-3 levels.
Reduced the anti-apoptotic proteins Bcl-XL and Survivin, with stronger effects under combination treatment than either single compound.
Decreased Cyclin D1, Cyclin A2 and Cyclin B1 protein levels.
Combination treatment further potentiated the decrease in these cell-cycle regulators compared with AH057 alone.

Cell Cycle Analysis^[1]

Cell Line:

HeLa
Concentration:

500 nM; 1 μM SGI-1027 (HY-13962)
Incubation Time:

24 h
Result:

Induced G1/S cell-cycle arrest. SGI-1027 alone increased S-phase accumulation, whereas combination treatment induced a higher G1-phase population than either single compound.

In Vivo

AH057 (50 mg/kg/day; p.o.; once daily; for 30 days ) suppresses tumor growth, induces tumor-cell apoptosis and reduces tumor-cell proliferation in HeLa xenograft BALB/c nude mouse model^[1].
AH057 (50 mg/kg/day; p.o. ; for 24 days) combined with SGI-1027 (HY-13962; 50 mg/kg/day; p.o.) suppresses tumor growth in HeLa xenograft BALB/c nude mouse model, and the cardiac and renal toxicity of the compounds is inappreciable^[1].

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

Animal Model:

Female 3-4 week-old BALB/c nude mice were subcutaneously injected with HeLa cells (1.5 × 10⁶ cells/mouse) in the xenograft model ^[1]
Dosage:

50 mg/kg/day
Administration:

Oral gavage (p.o.); once daily; for 30 days
Result:

Significantly reduced HeLa xenograft tumor volume.
Was well tolerated with no mortality and no significant body weight loss during the trial.
Increased TUNEL-positive apoptotic cells in tumor tissues.
Reduced Ki67-positive tumor cells, indicating decreased tumor-cell proliferation.

Animal Model:

Female 3–4 week-old BALB/c nude mice were subcutaneously inoculated with 1.5 × 10⁶ HeLa cells per mouse to establish xenograft combination models and combined with 50 mg/kg/day SGI-1027^[1]
Dosage:

50 mg/kg/day
Administration:

Oral gavage (p.o.); once daily; for 24 days
Result:

Suppressed HeLa xenograft tumor growth under oral administration.
Combination treatment showed stronger tumor-growth inhibition than vehicle treatment.
Cardiac and renal toxicity was inappreciable according to the accompanying toxicity data.

Chemical Information

CAS No. 118499-11-9
Masse moléculaire 270.37
Formule C₁₇H₂₂N₂O
SMILES

OCC(CC)/N=C1C2=C(CCC/1)C3=C(C=CC(C)=C3)N2
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureté et documentation

Instruction de manipulation (2659 KB)

Références

[1]. She S et al. Combined inhibition of JAK1/2 and DNMT1 by newly identified small-molecule compounds synergistically suppresses the survival and proliferation of cervical cancer cells. Cell Death Dis. 2020 Sep 7;11(9):724. [Content Brief]

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AH057

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Activité biologique

Chemical Information

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Références

Calculators

Help & FAQs

AH057 Related Classifications

HY-183519 Related Classifications