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Products are for research use only. Not for human use. We do not sell to patients.
(CC-4047; Actimid; CC4047; CC 4047)
Pomalidomide Chemical Structure
|Product name: Pomalidomide|
|Cat. No.: HY-10984|
Pomalidomide inhibits LPS-induced TNF-α release with IC50 of 13 nM.
IC50 Value: 13 nM
in vitro: Pomalidomide inhibits lipopolysaccharide (LPS) stimulated TNF-alpha release in human PBMC and in human whole blood with IC50 values of 13 nM and 25 nM, respectively. Pomalidomide inhibits the growth of T regulatory cells which is stimulated by IL-2 with an IC50 of ~1 μM. Treatment with Pomalidomide (6.4 nM-10 μM) increases the production of IL-2 in human peripheral blood T cells, and is slightly more potent in the CD4+ subset than in the CD8+ subset. Pomalidomide is significantly more potent than CC-5013 at elevating IL-2, IL-5, and IL-10 levels, but only slightly more potent than CC-5013 at elevating IFN-γ levels. Pomalidomide enhances SEE and Raji cells induced AP-1 transcriptional activity in Jurkat cells in a dose-dependent manner, with a maximal enhancement of 4-fold at 1 μM.
in vivo: Pomalidomide enhances the antitumor effect of rituximab against B-cell lymphomas in severe combined immunodeficient mice. Administration of Pomalidomide in combination with rituximab, gives the mice a median survival period of 74 days compared with 58 days of CC5013/rituximab treatment and 45 days of rituximab nonotherapy. The synergistic effect of Pomalidomide and rituximab can be completely abrogated by depletion of NK cells, supporting the proposal that NK cell expansion is one mechanism by which Pomalidomide may augment rituximab antitumor activity.
|M.Wt||273.24||Storage||Please store the product under the recommended conditions in the Certificate of Analysis.|
|Solvent & Solubility||
DMSO ≥52mg/mL Water <1.2mg/mL Ethanol <1.2mg/mL
|1 mg||5 mg||10 mg|
|1 mM||3.6598 mL||18.2989 mL||36.5979 mL|
|5 mM||0.7320 mL||3.6598 mL||7.3196 mL|
|10 mM||0.3660 mL||1.8299 mL||3.6598 mL|
|Product Name||Sponsor Only||Condition||Start Date||End Date||Phase||Last Change Date|
|Pomalidomide||Celgene Corp||Myelofibrosis||31-AUG-10||31-MAR-17||Phase 3||06-NOV-13|
|Celgene Corp||Multiple myeloma||31-MAR-11||30-JUN-13||Phase 3||07-MAY-13|
|Celgene Corp||Multiple myeloma||31-MAR-11||31-MAY-13||Phase 3||07-NOV-13|
|Celgene Corp||Multiple myeloma||31-DEC-12||31-JAN-17||Phase 3||23-OCT-13|
|Celgene Corp||Multiple myeloma||30-NOV-12||30-NOV-19||Phase 3||18-OCT-13|
. Weing?rtner S, Zerr P, Tomcik M, Palumbo-Zerr K, Distler A, Dees C, Beyer C, Shankar SL, Cedzik D, Schafer PH, Distler O, Schett G, Distler JH.Pomalidomide is effective for prevention and treatment of experimental skin fibrosis.Ann Rheum Dis. 2012 Aug 17.
. Cooney MM, Nock C, Bokar J, Krishnamurthi S, Gibbons J, Rodal MB, Ness A, Remick SC, Dreicer R, Dowlati A.Phase I trial of pomalidomide given for patients with advanced solid tumors.Cancer Chemother Pharmacol. 2012 Aug 9.
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