IHMT-15137
IHMT-15137 is a BMX inhibitor with an IC50 of 26.97 nM. IHMT-15137 covalently binds to BMX Cys496 within the ATP-binding pocket, inhibits BMX phosphorylation at Tyr566, and disrupts the BMX-ERK1/2-Cyclin D1/CDK4/6-E2F1 signaling axis. IHMT-15137 reduces E2F1 protein stability via decreased Ser332/337 phosphorylation, increased ubiquitination, and ubiquitin-proteasome pathway degradation. IHMT-15137 induces cell cycle arrest, apoptosis, DNA damage, and suppresses cell migration and invasion. IHMT-15137 can be used for the research of small cell lung cancer.
For research use only. We do not sell to patients.
- Formula: C21H21F3N6O2
- Molecular Weight:446.43
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
IHMT-15137 (3 μM; 24-168 h) synergizes with cisplatin (5-30 μM) to reduce viability, induce S-phase cell cycle arrest, suppress proliferation, promote apoptosis, increase DNA damage, and disrupt the BMX-ERK1/2-Cyclin D1-E2F1 signaling axis in SCLC patient-derived cells C23084 and LUC22009[1].
IHMT-15137 potentiates the cytotoxic and antiproliferative effects of Cisplatin + Etoposide (HY-13629) chemotherapy in SCLC patient-derived cells C23084 and LUC22009[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SCLC patient-derived cells C23084 and LUC22009
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Concentration:3 μM; 3 μM plus 5 μM Cisplatin
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Incubation Time:48 h
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Result:Induced S-phase cell cycle arrest.
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Cell Line:SCLC patient-derived cells C23084 and LUC22009
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Concentration:3 μM; 3 μM plus 5 μM Cisplatin
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Incubation Time:14 days
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Result:Suppressed cell proliferation compared with DMSO group.
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Cell Line:SCLC patient-derived cells C23084 and LUC22009
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Concentration:10 μM; 10 μM plus 30 μM Cisplatin
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Incubation Time:24 h
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Result:Enhanced apoptosis (cleaved PARP and cleaved caspase-3) and significantly increased DNA damage (γ-H2AX) in the treated groups compared with the monotherapies.
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Cell Line:SCLC patient-derived cells C23084 and LUC22009
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Concentration:3 μM; 3 μM plus 30 μM Cisplatin
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Incubation Time:24 h
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Result:Potentiated the effects of Cisplatin by modulating the ERK1/2-Cyclin D1/CDK4/6 signaling axis and promoting the degradation of E2F1.
IHMT-15137 (100 mg/kg; i.p.) in combination with Cisplatin and Etoposide induces 69.0% tumor growth inhibition, enhances apoptosis, and suppresses proliferation in H446DDPR SCLC xenografts without significant toxicity[1].
IHMT-15137 (100 mg/kg; i.p.) in combination with Cisplatin and Etoposide induces 59.8% tumor growth inhibition, enhances apoptosis, and suppresses proliferation in SCLC patient-derived xenografts without significant toxicity[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NCG mice (female, 6 weeks old, subcutaneous xenograft model implanted with chemoresistant H69AR cells)[1]
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Dosage:100 mg/kg; 100 mg/kg plus 2 mg/kg Cisplatin plus 16 mg/kg Etoposide
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Administration:i.p.
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Result:Achieved 60.1% tumor growth inhibition (TGI).
Reduced final mean tumor weight to 0.96 g compared to vehicle control (2.46 g).
Suppressed chemotherapy-induced increases in tumor tissue levels of p-BMX (Tyr566), p-ERK1/2 (Thr202/Tyr204), Cyclin D1, p-E2F1 (Ser332), and p-E2F1 (Ser337).
Increased tumor apoptosis (TUNEL-positive cells) compared to monotherapies.
Reduced tumor proliferation (Ki-67-positive cells) compared to monotherapies.
Caused no significant body weight loss.
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Animal Model:NCG mice (female, 6 weeks old, subcutaneous xenograft model implanted with chemoresistant H446DDPR cells)[1]
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Dosage:100 mg/kg; 100 mg/kg plus 2 mg/kg Cisplatin plus 16 mg/kg Etoposide
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Administration:i.p.
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Result:Achieved 69.0% tumor growth inhibition (TGI).
Reduced final mean tumor weight to 0.78 g compared to vehicle control (2.52 g).
Suppressed chemotherapy-induced increases in tumor tissue levels of p-BMX (Tyr566), p-ERK1/2 (Thr202/Tyr204), Cyclin D1, p-E2F1 (Ser332), and p-E2F1 (Ser337).
Increased tumor apoptosis (TUNEL-positive cells) compared to monotherapies.
Reduced tumor proliferation (Ki-67-positive cells) compared to monotherapies.
Caused no significant body weight loss.
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Animal Model:NCG mice (female, 6 weeks old, subcutaneous patient-derived xenograft model implanted with PDC C23084 cells)[1]
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Dosage:100 mg/kg; 100 mg/kg plus 2 mg/kg Cisplatin plus 16 mg/kg Etoposide
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Administration:i.p.
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Result:Achieved 59.8% tumor growth inhibition (TGI).
Reduced final mean tumor weight to 0.39 g compared to vehicle control (0.97 g).
Suppressed chemotherapy-induced increases in tumor tissue levels of p-BMX (Tyr566), p-ERK1/2 (Thr202/Tyr204), Cyclin D1, p-E2F1 (Ser332), and p-E2F1 (Ser337).
Increased levels of cleaved PARP and cleaved caspase-3 (apoptosis markers).
Increased tumor apoptosis (TUNEL-positive cells) compared to monotherapies.
Reduced tumor proliferation (Ki-67-positive cells) compared to monotherapies.
Caused no significant body weight loss.
Chemical Information
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Molecular Weight 446.43
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Formula C21H21F3N6O2
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SMILES
FC(F)(F)C1=CC=C(NC(C2=NNC=C2NC(CC3CN(C(C=C)=O)CCC3)=O)=N4)C4=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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