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 19 Publications
3 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.
A) Quantitative determination of monopolar spindles in MM.1S cells treated with the vehicle (control), PD, F or PDF for 24h. Representative micrographs showing cells immunostained with anti-tubulin antibody (shown in green) to visualize microtubules and DAPI (blue) to evidence nuclei using confocal microcopy. Bar = 15 μm in lower magnification micrograph; bar = 5 μm in higher magnification insert). Data are presented as the mean ± SD of two independent experiments. Statistical significance was evaluated with Student’s t-test.
Haematologica, 2017, 102(12):2113-2124. 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||54 mg/mL (197.62 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03732703||Not yet recruiting||Relapsed Refractory Multiple Myeloma||Multiple Myeloma Research Foundation|AbbVie|Celgene Corporation|Eli Lilly and Company|Genentech Inc.|Janssen LP|Takeda|Multiple Myeloma Research Consortium||December 10 2018||Phase 1|Phase 2|
|NCT03715478||Not yet recruiting||Relapsed and/or Refractory Multiple Myeloma||Myeloma Canada Research Network|GlaxoSmithKline||December 1 2018||Phase 1|Phase 2|
|NCT03227432||Withdrawn||Multiple Myeloma||Dana-Farber Cancer Institute|Bristol-Myers Squibb||December 2018||Phase 2|
|NCT03651128||Not yet recruiting||Multiple Myeloma||Celgene||November 30 2018||Phase 3|
|NCT03713294||Not yet recruiting||Refractory Plasma Cell Myeloma||Mayo Clinic|National Cancer Institute (NCI)||November 8 2018||Phase 2|
|NCT03520985||Recruiting||Refractory Multiple Myeloma||Swiss Group for Clinical Cancer Research||October 1 2018||Phase 2|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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Frequently Asked Questions
Is S1567 in the 1% DMSO+30% polyethylene glycol+1% Tween 80 suitable for oral administration?
S1567 in 1% DMSO+30% polyethylene glycol+1% Tween 80 is a suspension. This formulation is for oral gavege.
I would like to know if the pomalidomide is racemic or optically active?
Our S1567 Pomalidomide is racemic.