Flavopiridol protects against inflammation by attenuating leukocyte-endothelial interaction via inhibition of cyclin-dependent kinase-9.
Flavopiridol is a CDKs inhibitor & it is active against various types of tumor. Flavopiridol is reported to have cytotoxic activity against a wide range of cancer cell lines. flavopiridol has demonstrated antitumor activity against several tumor xenograft
Flavopiridol is a semi-synthetic flavonoid derived from Rohitukine. It is a small molecule type drug with molecular weight 401.84. It comes under the drug category of anti neoplastic agents, glycogen phosphorylase inhibitor, growth inhibitors and protein
Flavopiridol is a synthetic flavone closely related to a compound found in a plant native to India, Dysoxylum binectariferum. Currently, the drug is in Phase I and II clinical trials as an antineoplastic agent for breast, gastric, and renal cancers. The d
Flavopiridol is a semisynthetic flavonoid closely related to a compound originally isolated from the stem bark of Dysoxylum binectariferum. Flavopiridol has been shown to be a potent inhibitor of cyclin-dependent kinase (CDK) 1, CDK 2, CDK 4, and CDK 7. I
Flavopiridol, a synthetic flavone closely related to a compound originally isolated from the stem bark of the native Indian plant Dysoxylum binectariferum, has been found to inhibit cyclin-dependent kinases. Flavopiridol has been shown to be a potent inhi
Flavopiridol is a synthetic flavone closely related to a compound originally isolated from the stem bark of the native Indian plant Dysoxylum binectariferum. It is currently undergoing Phase-I clinical trials as a potential antineoplastic agent. Flavopiri
Flavopiridol inhibit potently cyclin dependent kinases (CDKs), a family of kinases which govern progression of cells through the cell cycle. Induction of G2 arrest by flavopiridol appears to be caused by both direct inhibition of CDK1 and interference wit
Its mechanisms of action remain incompletely defined but include targeting of cyclin dependent kinases including the CDK9/cyclin Tcomplex (preventing activation of RNA polymerase II), downregulation of Mcl-1 and other antiapoptotic proteins, induction of
The mechanism of action of flavopiridol involves interfering with the phosphorylation of cyclin-dependent kinases, hampering their activation and blocking cell-cycle progression at growth phase 1 (G1) or G2.
Induce cell cycle arrest at either G1/s or G2/M, concordant with the ability of favopiridol to inhibit both cdk2 and cdk1, respectively.
1). The cyclin-dependent kinase (CDK) inhibitor p27 preferentially inactivates CDK complexes required for progression through the G1/S transition. Loss of p27 is associated with aggressive behavior in a variety of tumors.\r\n2). Directly competes with the AT
Showed about a 100 fold more selectivity for CDKs compared to its activity for tyrosine kinases.
First compound to inhibit Cyclin-Dependent Kinase tested in clinical trials.
Possess tyrosine kinase activity and potent growth inhibitory activity against a series of breast and lung carcinoma cell lines.
it is an potent inhibitor of CDK1, CDK2, and CDK4. Its anti-proliferative activity is unfolded through a variety of mechanisms besides CDK inhibition, for instance, through apoptosis, DNA interaction, and cyclin D1 decreases.
Binds to the ATP-binding pocket of cyclin-dependent kinases (CDKs), and due to its indirect action reducing levels of other cyclins and cdk inhibitors, contributing to its pleiotropic effects. Flavopiridol is a potent apoptotic agent due to its ability to
Flavopiridol strongly inhibits the cyclin dependent kinase activity of multiple CDKs.
Flavopiridol induces cell cycle arrest and apoptosis in a variety of cell lines and is currently in phase II clinical testing. In a phase I infusional trial, postinfusional plasma concentration peaks that are compatible with enterohepatic circulation of F
1). Flavopiridol binds to the ATP-binding domain of CDKs. Because of its broad inhibition of CDKs. Flavopiridol can induce cell cycle arrest and affect other cellular functions, such as transcription and apoptosis.\r\n2). Flavopiridol reduces transcriptional
Flavopiridol is a potent cyclin-dependent kinase inhibitor, and its use is presently under investigation for a variety of solid tumors as well as hematological cancers.
Flavopiridol is a potential CDKs inhibitor.In Phase I clinical trials is scheduled to be advanced to Phase II trials against a broad range of tumors
1). Potent growth inhibitor of diverse human tumor cell lines and induces apoptosis in hematopoietic cell lines derived from acute myelogenous leukemia (AML), B- and T-cell lymphomas, and multiple myeloma.\r\n2). Flavopiridol induced apoptosis results in par
Flavopiridol effective CDKs (CDK1, CDK2, and CDK4) inhibitor.
Flavopiridol is ATP-site antagonists that have completed initial phase I and phase II evaluations
1). Interactions between the cyclin-dependent kinase inhibitor flavopiridol (FP) and the histone deacetylase inhibitor sodium butyrate (SB) have been examined in human leukemia cells (U937) in relation to differentiation and apoptosis.\r\n2). Blocked SB-rela
Liver tumour-bearing rabbits treated with cisplatin-eluting GMSs plus flavopiridol, the tumour volume reduction was greater than in the other groups.
1). Flavopiridol arrests cells at the transition of G2/M phases and from G1 to S phase, and also slows the progression of cell cycle through the S phase. Flavopiridol is competitive with ATP when assayed with purified cyclin/CDK complexes, and it inhibits
Molecular mechanisms of rhabdoid tumorigenesis should pave the way to developing molecularly targeted therapies for rhabdoid tumors. The essential role of cyclin D1 for rhabdoid tumorigenesis is targeting the cyclin/CDK axis could be effective in inhibiti
Flavopiridol inhibits CDKs with differentiation-inducing agents such as histone deacetylase inhibitors (HDACIs) in leukemia therapy has several theoretical rationales. For example, HDACIs have been shown to be potent inducers of leukemic cell differentiat
Flavopiridol was originally identified as an inhibitor of the receptor tyrosine kinases, receptor-associated kinases, and cytosolic signal transduction kinases.It selective inhibits CDK4, CDK6(Cyclin D), CDK1(Cyclin B) over CDK2(Cyclin A), CDK2(Cyclin E)
Flavopiridol is a potent inhibitor of Cyclin dependent kinases CDKs via direct binding to the ATP site. it inhibits CDK 1, 2, 4, and 6 in nanomolar concentrations.
Flavopiridol is a potent inhibitor of CDKs via direct binding to the ATP site. Flavopiridol inhibits CDK-1, CDK-2, CDK-4, CDK-6, and CDK-7.flavopiridol also results in the indirect inhibition of cell proliferation by reducing the expression levels of Cycl
Flavopiridol inhibits CDK1, CDK2 and CDK4 . Flavopiridol has the potential to inhibit the proliferation of a broad range of different types of cell lines, human tumours, leukaemias and lymphomas. Flavopiridol analogues thioflavopiridol and oxoflavopiridol
Flavopiridol serves as a model for the potential antitumor agent.Flavopiridol was subsequently shown to block cell cycle progression. MDA-MB-468 breast cancer cells are released from an aphidicolin-induced block at the G1/S boundary in the presence of fla
Flavopiridol is a potent inhibitor of Cyclin dependent kinases CDKs via direct binding to the ATP site.
Flavopiridol semisynthetic derivative of Rohitukine, a chromane alkaloid. flavopiridol, a promising anticancer compound. Currently in Phase III clinical trials, flavopiridol is a potent inhibitor of several cyclin-dependent kinases (CDKs). Flavopiridol in
Specific inhibitor of CDK kinase activity, leading to growth arrest at both, G1/S and G2/M transition phases.
Inhibiting cell cycle progression at G1 or G2 phase by interfering with the phophorylation activity of cyclindependent kinases
Decrease the activity of CDKs and induce cell cycle arrest. Cell cycle regulatory elements such as the CDK inhibitors
Flavopiridol has been found to have strong activity against multiple Cdks.
1). Flavopiridol has been found to have strong activity against multiple Cdks\r\n2). interferes with the cell cycle at two points, it arrests the cell cycle at the G2/M phase and delays the G1 to S phase progression.\r\n3). flavopiridol interferes with binding
Inhibit cyclin-dependent kinases (CDKs), causing cell cycle arrest and growth inhibition.
A group of proteins, cyclin-dependent kinases (CDKs), that control the cell cycle, provide new targets for treating cancer. As a result, cyclin-dependent kinase inhibitors (CDKIs) represent a novel class of chemotherapeutic agents. Of these, flavopiridol,
Flavopiridol strongly inhibits the cyclin-dependent kinases (cdk1, cdk2, cdk4, cdk7), with the potential to cause inhibition of cell cycle progression in G(1) and G(2) by multiple mechanisms relatable to cdk inhibition. In certain cell types, Flavopiridol
Flavopiridol is an inhibitor of several CDKs and displays unique anticancer properties. flavopiridol also exhibited other features such as inducing apoptosis in many cancer cell lines, decreasing cyclin D1 concentration, and inhibiting angiogenesis. Relat
1). It inhibits cyclin-dependent kinases and therefore, blocks cell cycle progression in the G1 and G2 phase. It has cytotoxic effect in a number of tumor cells lines and in vivo studies showed significant activity in hematological malignancies and solid
It inhibits the kinase activity of multiple CDKs with CDK1, CDK2, CDK4. It also interferes with the phosphorylation events necessary to activate CDKs and has been shown to downregulate transcription of the cyclin D1 gene.
Flavopridol possess tyrosine kinase activity and potent growth inhibitory activity against a series of breast and lung carcinoma cell lines. It also showed broad spectrum in vivo activity against human tumor xenografts in mice, either alone or in combinat
Flavopiridol has a very interesting mechanism of action in that it is an inhibitor of cyclin dependent kinases (the regulators of the G2 to M transition in the cell cycle).
Has been found to suppress inflammation,inhibit cyclin-dependent kinases, induce apoptosis, and modulate the immune response. The inhibition of TNF-induced inflammation by flavopiridol was associated with inhibition of NF-?B activation. This effect was me
Flavopiridol has been shown to be a potent cyclin-dependent kinase inhibitor. It inhibits CDK1CDK2, and CDK4 by binding to the ATP-binding pocket of the kinase. In addition to inhibition, flavopiridol causes a decrease in cyclin D1, and it was felt that d
1). Inhibit cell proliferation in various human tumour cell lines arresting cells in G1(S) and G2(M) phases. In vitro and in vivo studies have demonstrated that it inhibits several protein kinases, with the greatest activity against CDKs including CDK1, C
1). Potent CDK inhibitory activity. it depletes cyclin D1 and vascular endothelial growth factor mRNA by transcriptional and posttranscriptional mechanisms, respectively.\r\n2). it inhibits positive elongation factor B, leading to transcription halt\r\n3). it
1). Cell-cycle dysregulation is one of the cardinal characteristics of neoplastic cells. For this reason, small molecule inhibitors targeting cyclin-dependent kinases (CDKs), of which flavopiridol is a prototype.\r\n2). Flavopiridol shows several novel mecha
Cyclin-dependent kinases (CDKs) are core components of the cell cycle machinery that govern the transition between phases during cell cycle progression. Genes involved in cell cycle are frequently mutated in human cancer and deregulated CDK activity repre
Flavopiridol was found to inhibit the epidermal growth factor receptor and protein kinase Flavopiridol was later shown to inhibit cell proliferation, flavopiridol inhibits CDK1, CDK2, CDK4, and CDK6 as well as CDK7 by competing with ATP flavopiridol is ex
Flavopiridol is a potent cyclin-dependent kinase inhibitor with preclinical activity against non-small cell lung cancer (NSCLC), inhibiting tumor growth in vitro and in vivo by cytostatic and cytotoxic mechanisms. Flavopiridol causes arrest at both the G1
Flavopiridol is a semisynthetic flavonoid that was originally identified as a CDK inhibitor. Flavopiridol competes with ATP for binding in the active site of many CDKs, and can induce either cell cycle arrest or apoptosis, depending on the cell type, cult
Flavopiridol is a synthetic flavone, derived from the plant alkaloid rohitukine, which was isolated from Dysoxylum binectariferum Hook. f. (Meliaceae). It is currently in phase I and phase II clinical trials against a broad range of tumors, including leuk
Flavopiridol showed most potent activity against human Xenograft. It is effectively used alone or in combination with other anticancer agents to treat a broad rangeof tumors, leukemias, lymphomas and solid tumors.
Flavopiridol pan-CDK inhibitor studied in clinical trials. Flavopiridol has been shown to inhibit several tumor cell lines in vitro with its antiproliferative effects being tribute to potent inhibition of CDK1, CDK2, CDK4, and CDK6. Flavopiridol was cytos
The drug is a potent inhibitor of several cdks, including CDK1 (CDC2), CDK2, CDK4, and CDK7, because it has been shown to directly inhibit the kinase activity of CDKs from exponentially growing cells.A portion of flavopiridol interferes with binding of AT
Flavopiridol,a semisynthetic flavonoid derived from an indigenous plant from India,is a broad inhibitor of cyclindependent kinases (cdk) and is being tested in clinical trials Treatment of cancer cells with flavopiridol results in a decrease in cyclins D1
Flavopiridol arrest both in G1 and G2 phases of the cell cycle. It inhibits CDK1, CDK2 and CDK4.This inhibition is irreversible and competitively blocked by ATP by binding to the ATP packets and flavopiridol decreases in the level of cyclin D1 and altera
Cyclin-dependent kinases (cdks) are key regulators of orderly progression through the cell cycle and of RNA transcription. Inhibition of their activity in vitro can cause cell cycle arrest at the G1-S or G2-M boundaries.
Flavopiridol is an antitumor agent in clinical trials work by blocking cell cycle progression promotes differentiation and induces apoptosis in various types of cancerous cells. Cell cycle abnormalities are the root of cancer and its progression is regula
Flavopiridol is a CDKs inhibitor with ATP antagonist activity.
found to inhibit cyclin-dependent kinases, suppress inflammation, modulate the immune response and induce apoptosis, particularly in tumour cells of haematopoietic origin. In human leukaemia cells, flavopiridol-mediated cell death is through the induction
Flavopiridol is a semisynthetic flavonoid derived from rohitukine, an indigenous plant from India. Initial studies with this flavonoid revealed clear evidence of G1/S or G2/M arrest, due to loss in cdk1 and cdk2. In addition to directly inhibiting cdks, f
Flavopiridol is a novel semisynthetic flavone analogue of rohitukine, a leading anticancer compound from an Indian tree. Flavopiridol inhibits most cyclin-dependent kinases and displays unique anticancer properties.
Flavopiridol inhibits CDKs in multiple myeloma is a(Flavopiridol) Rohitukine alkaloid that binds tightly to the CDK at ATP binding site and broadly inhibits multiple CDKs, including CDKs 1, 2, 4/6, and 7. Flavopiridol induces perturbations in various prot
Synthetic flavone derived from rohitukine, Flavopiridol representing the first cyclin-dependent kinase inhibitor. The mechanism of action involves interfering with the phosphorylation of cyclin-dependent kinases and arrest cell-cycle progression at growth
Ability of flavopiridol to decrease the activity of CDKs and induce cell cycle arrest. Cell cycle regulatory elements such as the CDK inhibitors p15 and p16 are altered in ALL between diagnosis and relapse, indicating that this loss of checkpoint control
The mechanism of action of flavopiridol involves interference with the phosphorylation of cyclin-dependent kinases, hampering their activation, thus blocking cell cycle progression at G1 or G2. In phase I clinical trials with flavopiridol secretory diarrh
Although its exact mechanism of action remains unknown, it is the first anticancer agent to enter clinical trials as a potent inhibitor of the cyclin-dependent kinases (CDKs). Detect no evidence of apoptosis in the peripheral lymphocytes of patients treat
Flavopiridol be a potent inhibitor of cyclin-dependent kinase CDK 1, CDK 2, CDK 4 and CDK 7. It inhibits CDKs by competing with adenosine triphosphate at the nucleotide-binding site on CDKs as indicated by kinetics studies The tyrosine phosphorylation of