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Results for "

alvocidib

" in TargetMol Product Catalog
  • Inhibitors & Agonists
    5
    TargetMol | Inhibitors_Agonists
  • Natural Products
    1
    TargetMol | Natural_Products
Flavopiridol
NSC 649890 HCl, L868275, HMR-1275, Alvocidib
T6837146426-40-6
Flavopiridol (Alvocidib) (Alvocidib) competes with ATP to inhibit CDKs including CDK1, CDK2, CDK4 and CDK6 with IC50 of ~ 40 nM. It is 7.5-fold more selective for CDK1, 2, 4, 6 versus CDK7. Flavopiridol is initially found to inhibit EGFR and PKA. Phase 1 2.
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TargetMol | Inhibitor Hot
Flavopiridol hydrochloride
NSC 649890 HCl, NSC 649890, MDL 107826A, HL 275, FLAVOPIRIDOL HCL, Alvocidib Hydrochloride
T2615131740-09-5
Flavopiridol hydrochloride (MDL 107826A) is a synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis. This agent is also a competitive inhibitor of adenosine triphosphate activity.
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Zotiraciclib citrate
T2026261204918-73-9
Zotiraciclib (also known as TG02 and SB1317) is an innovative small-molecule compound with potent inhibitory effects on CDK, JAK2, and FLT3. By inhibiting cyclin-dependent kinase 9 (CDK9) and depleting Myc, it serves as a treatment for cancers that can penetrate the blood-brain barrier. Zotiraciclib is one of the numerous CDK inhibitors under investigation; other compounds targeting CDK9, utilized for treating acute myeloid leukemia, include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80% of glioblastomas exhibiting this characteristic.
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TP1287
T699652044686-42-0
TP-1287 is an oral phosphate prodrug of the CDK9 inhibitor, alvocidib.
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6-8 weeks
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Zotiraciclib HCl
T708971354567-82-0
Zotiraciclib, also known as TG02 and SB1317, is a novel small molecule potent CDK JAK2 FLT3 inhibitor. Zotiraciclib may be useful for the treatment of cancer that crosses the blood brain barrier and acts by depleting Myc through the inhibition of cyclin-dependent kinase 9 (CDK9). It is one of a number of CDK inhibitors under investigation; others targeting CDK9 for the treatment of acute myeloid leukemia include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80 percent of glioblastomas characterized by this property.
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6-8 weeks
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