Catalog No.S1567 Synonyms: CC-4047
Molecular Weight(MW): 273.24
Pomalidomide inhibits LPS-induced TNF-α release with IC50 of 13 nM in PBMCs.
Cited by 10 Publications
2 Customer Reviews
MM.1S cells were cultured with Len (lenalidomide) or Pom (pomalidomide) for 48 h.
Blood Cancer Journal, 2015, 5: e312. Pomalidomide purchased from Selleck.
OPM2 cells stably expressing either NT or CRBN shRNA were seeded and incubated with pomalidomide at the indicated concentration, followed by MTT assay at day 3 after adding drugs. Each experimental condition was performed in triplicate and repeated at least once.
Blood 2011 118, 4771-4779. Pomalidomide purchased from Selleck.
Purity & Quality Control
Choose Selective TNF-alpha Inhibitors
|Description||Pomalidomide inhibits LPS-induced TNF-α release with IC50 of 13 nM in PBMCs.|
|Features||A derivative of thalidomide and up to 10,000 times more potent than thalidomide.|
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.  Exposure of Raji cells to various concentrations of Pomalidomide (2.5-40 μg/mL) for 48 hours leads to a significant decrease in cell proliferation and DNA synthesis. There is a reduction of ~40% compared to vehicle-treated controls. 
|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. |
Inhibition of TNF-α synthesis:TNF-α inhibitory activity is measured in lipopolysacharide (LPS) stimulated PBMC. Pomalidomide is added to human PBMCs 1 hour prior to the addition of LPS (1 μg/mL) and incubation continued for an additional 18-20 hours. Supernatants are then harvested, and the concentration of TNF-α in the supernatants is determined by ELISA. The concentration of Pomalidomide that inhibits TNF- production by 50% (IC50) is calculated by nonlinear regression analysis. The human whole blood TNF- inhibition assay is run in a similar fashion to the PBMC assay except that heparinized fresh human whole blood is plated directly into microtiter plates.
-  Muller GW, et al. Bioorg Med Chem Lett, 1999, 9(11), 1625-1630.
-  Galustian C, et al. Cancer Immunol Immunother, 2009, 58(7), 1033-1045.
-  Schafer PH, et al. J Pharmacol Exp Ther, 2003, 305(3), 1222-1232.
|In vitro||DMSO||55 mg/mL (201.28 mM)|
|In vivo||1% DMSO+30% polyethylene glycol+1% Tween 80||15 mg/mL|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01495598||Recruiting||Kaposi Sarcoma|Sarcoma, Kaposi||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||December 9, 2011||Phase 1|Phase 2|
|NCT02659930||Recruiting||Kaposi Sarcoma||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||January 4, 2016||Phase 1|
|NCT01688466||Recruiting||Graft vs Host Disease|Graft-Versus-Host Disease||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||August 29, 2012||Phase 2|
|NCT03030261||Not yet recruiting||Multiple Myeloma in Relapse||Washington University School of Medicine|Bristol-Myers Squibb|Celgene||February 28, 2017||Phase 2|
|NCT03015922||Not yet recruiting||Multiple Myeloma||University of Leeds|Myeloma UK|Oncolytics Biotech|Celgene Corporation||February 2017||Phase 1|
|NCT02939183||Recruiting||Relapsed or Refractory Multiple Myeloma||Amgen||January 2017||Phase 1|
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