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    Flavopiridol (Alvocidib) HCl
    Flavopiridol (Alvocidib) HCl

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1538
    CAS #: 131740-09-5 Purity ≥98%

    Description: Flavopiridol HCl (also known as Alvocidib; NSC 649890; HMR-1275; L-868275; HL-275; MDL-107,826A), the HCl salt of flavopiridol which is a flavanoid, is a broad spectrum and ATP-competitive inhibitor of cyclin-dependent kinases-CDKs with potential antineoplastic activity. It is an ATP-competive inhibitor of CDK that inhibits CDK1, CDK2, CDK4 and CDK6 with IC50s of ~ 40 nM. 

    References: Oncologist. 2002;7 Suppl 3:12-9; J Med Chem. 2000;43(22):4126-34; J Med Chem. 2002;45(18):3905-27.

    Related CAS#:146426-40-6 (free base); 131740-09-5 (HCl) 

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    Molecular Weight (MW)438.3
    CAS No.131740-09-5 (HCl); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 88 mg/mL (200.8 mM)
    Water: <1 mg/mL 
    Ethanol: <1 mg/mL 
    Solubility (In vivo)30% Propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL 
    SynonymsNSC 649890 HCl; HMR-1275; HMR1275; L-868275; L 868275; HL 275; MDL 107,826A; HL-275; NSC 649890 HCl; NSC649890; NSC-649890; HMR 1275; L 86-8275; L868275; HMR 1274; HMR-1274; HMR1274; Flavoperidol; Alvocidib; HMR 1275; HMR-1275; L 86 8275; L86-8275; MDL 107826A; MDL-107826A; NSC 649890.

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    In Vitro

    In vitro activity: Flavopiridol is initially found to inhibit the epidermal growth factor receptor and protein kinase A (IC50 = 21 and 122 μM). Flavopiridol is later shown to inhibit cell proliferation, at more physiologically relevant concentrations (IC50 = 66 nM) when Flavopiridol is tested in the National Cancer Institute Development Therapeutics Program panel of 60 human tumor cell lines. Flavopiridol induces G1 arrest with inhibition of CDK2 and CDK4 in human breast carcinoma cells in a time and concentration dependent manner. Short time treatment of Flavopiridol (~12 hours) induce apoptosis in hematopoietic cell lines including SUDHL4, SUDHL6 (B-cell lines), Jurkat and MOLT4 (T-cell lines ), and HL60 (myeloid). In the clonogenic assay, Flavopiridol functions as a highly potent cytotoxic compound with a mean IC70 with 8 ng/mL in 23 human tumor models. A recent study shows Flavopiridol treatment induces a substantial AKT-Ser473 phosphorylation in human glioblastoma T98G cell line.

    Kinase Assay: CDKs activities are determined in microtiter plates as follows. Forty μg Gst-Rb are mixed with different amounts of Flavopiridol and unlabeled ATP. Reactions are then started by the addition of an ammonium sulfate cut of the S100 fraction obtained from insect cells expressing recombinant human CDKs. The final reaction conditions are 10 mM MgCl2, 50 mM Tris-HCl (pH 7.5), and 1 mM DTT. The final concentration of ATP is adjusted accordingly. Radiolabeled ATP is used as a phosphoryl donor. The reaction is carried out for 2.5 minutes at 30 °C after addition of enzyme and then terminated with the addition of EDTA. The Gst-Rb is then captured with glutathione-Sepharose and the incorporated radioactivity is determined by liquid scintillation counting.

    Cell Assay: Cells grown at a density of 1 × 106 cells/mL are exposed to Flavopiridol for different concentrations and time periods. DNA is extracted. Briefly, cells are washed once with cold phosphate-buffered saline (PBS) and lysed with 3 mL lysis buffer (5 mM Tris-HCL [pH 7.5]; 20 mM EDTA; 0.5% Triton X-100) for 15 minutes at 4 °C. The chromatin of the cell lysates is isolated by centrifugation (20 minutes at 26,000g, 4 °C). The supernatants containing small DNA fragments are extracted sequentially with phenol, phenol:chloroform (1:1), and chloroform. Nucleic acids are precipitated in 0.5 M NaCl, 90% ethanol at -20 °C overnight. RNA is then digested by bovine RNAaseA (60 μg/mL). After sequential reextraction and reprecipitation, DNA is dissolved in 10 mM Tris-HCL (pH 7.5), 1 mM EDTA, 0.5% sodium dodecyl sulfate (SDS) before electrophoresis on 1.6% agarose gel.

    In VivoAt the maximal tolerated dose of 10 mg/kg/day administered p.o. on days 1-4 and 7-11, Flavopiridol effects tumor regression in PRXF1337 and tumor stasis lasting for 4 weeks in PRXF1369. After treatment with 7.5 mg/kg Flavopiridol bolus intravenous (IV) or intraperitoneal on each of 5 consecutive days, 11 out of 12 advanced stage subcutaneous (s.c.) human HL-60 xenografts undergo complete regressions, and animals remain disease-free several months after one course of Flavopiridol treatment. SUDHL-4 s.c. lymphomas treated with flavopiridol at 7.5 mg/kg bolus IV for 5 days undergo either major (two out of eight mice) or complete (four out of eight mice) regression, with two animals remaining disease-free for more than 60 days. The overall growth delay is 73.2%. Daily IV or IP administration of flavopiridol results in peak plasma levels of about 7 µM, followed by a progressive decline to approximately 100 nM in 8 hours.
    Animal modelHuman prostate cancer xenografts, PRXFI337 and PRXFI369, grown s.c. in nude mice Human promyelocytic leukemia HL-60, human B-cell follicular lymphoma SUDHL-4, and acquired immunodeficiency syndrome (AIDS)-r
    Formulation & DosageDissolved in Water; 1% DMSO; ~7.5, 10 mg/kg/day; i.p. or i.v injection and p.o.

    Oncologist. 2002;7 Suppl 3:12-9; Clin Cancer Res. 1997 Feb;3(2):273-9; Blood. 1998 Apr 1;91(7):2482-90.

    These protocols are for reference only. InvivoChem does not independently validate these methods.

     Flavopiridol (Alvocidib) HCl

    Effect of FVP on the expression of PRGs and IRGs in BJ-TERT fibroblasts.  2012 Mar 29;7:11. doi: 10.1186/1747-1028-7-11.

     Flavopiridol (Alvocidib) HCl

    Biphasic effect of FVP in the expression of certain PRG/IRGs.  2012 Mar 29;7:11. doi: 10.1186/1747-1028-7-11.

     Flavopiridol (Alvocidib) HCl

    Certain PRG/IRGs are significantly expressed in the presence of FVP during a mitogenic response.   2012 Mar 29;7:11. doi: 10.1186/1747-1028-7-11.


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