Lenalidomide (CC-5013)

Lenalidomide (CC-5013) is a TNF-α secretion inhibitor with IC50 of 13 nM in PBMCs.

Price Stock Quantity  
In DMSO USD 191 In stock
USD 147 In stock
USD 570 In stock
Bulk Inquiry

Massive Discount Available

Free Overnight Delivery on all orders over $ 500.

Lenalidomide (CC-5013) Chemical Structure

Lenalidomide (CC-5013) Chemical Structure
Molecular Weight: 259.26

Validation & Quality Control

Customer Product Validation(4)

Quality Control & MSDS

Related Compound Libraries

TNF-alpha Inhibitors with Unique Features

  • Most Potent TNF-alpha Inhibitor

    QNZ (EVP4593) TNF-α production, IC50=7 nM.

  • FDA-approved TNF-alpha Inhibitor

    Pomalidomide Approved by FDA for relapsed and refractory multiple myeloma.

  • Newest TNF-alpha Inhibitor

    Necrostatin-1 Specific RIP1 inhibitor and inhibits TNF-α-induced necroptosis with EC50 of 490 nM.

  • Classic TNF-alpha Inhibitor

    Thalidomide A sedative drug, immunomodulatory agent and also is investigated for treating symptoms of many cancers.

Product Information

  • Compare TNF-alpha Inhibitors
    Compare TNF-alpha Products
  • Research Area
  • Combination Therapy
    Combination Therapy

Product Description

Biological Activity

Description Lenalidomide (CC-5013) is a TNF-α secretion inhibitor with IC50 of 13 nM in PBMCs.
Targets TNF-α [1]
IC50 13 nM
In vitro Lenalidomide strongly induces IL-2 and sIL-2R production. Lenalidomide-induced tyrosine phosphorylation of CD28 on T cells is followed by a down-stream activation of NF-κB. [2] Lenalidomide and pomalidomide inhibits autoubiquitination of CRBN in HEK293 T cells expressing thalidomide-binding competent wild-type CRBN, but not thalidomide-binding defective CRBN(YW/AA). Overexpression of CRBN wild-type protein, but not CRBN(YW/AA) mutant protein, in KMS12 myeloma cells, amplifies pomalidomide-mediated reductions in c-myc and IRF4 expression and increases in p21(WAF-1) expression. Long-term selection for Lenalidomide resistance in H929 myeloma cell lines is accompanied by a reduction in CRBN, while in DF15R myeloma cells resistant to both pomalidomide and Lenalidomide, CRBN protein is undetectable. [3] Lenalidomide prevents induction of defects by down-regulating tumor cell inhibitory molecule expression. Lenalidomide prevents induction of tumor-induced T cell lytic synapse dysfunction. Lenalidomide treatment blocks CLL cell-induced T cell actin synapse dysfunction, mimicks antibody blockade, and down-regulates expression of CLL inhibitory ligands and their receptors on T cells. Lenalidomide treatment prevents tumor-induced immune suppression in FL, DLBCL, HL, MM, SCC, and OC and down-regulates immunosuppressive ligand expression on all tumor cells examined. CTL killing function significantly increases following antibody blockade of CLL inhibitory ligands or Lenalidomide treatment compared to control treatments. Treatment of autologous CLL-T cell co-cultures with Lenalidomide reverses impaired CD8+ T cell lytic synapse formation and granzyme B trafficking. [4]
In vivo The induction of angiogenesis by bFGF is significantly inhibited by oral treatment of Lenalidomide in a dose-dependent manner. Lenalidomide significantly decreases the percentage of vascularized area from 5.16% (control group) to 2.58% (50 mg/kg). Lenalidomide significantly reduces the calculated total MVL from 21.07 (control) to 8.11 (50 mg/kg). Lenalidomide significantly inhibites HUVEC migration through the fibronectin-coated membranes towards 0.1 ng/mL of bFGF at 100 μM, 1 ng/mL of VEGF at concentrations of 10 μM and 100 μM. [5]

Protocol(Only for Reference)

Kinase Assay:


Assay for inhibition of TNF synthesis by human PBMCs Human PBMCs from normal donors are obtained by Ficoll−Hypaque density centrifugation. Cells (106 cells/mL) are cultured in RPMI supplemented with 10 AB+ serum, 2 mM l-glutamine, 100 U/mL penicillin, and 100 μg/mL streptomycin. Lenalidomide is dissolved in DMSO at 20 mg/mL; further dilution is done with culture medium. The final DMSO concentration in all assays including the controls is 0.25%. Lenalidomide is added to cells 1 hour prior to the addition of LPS. PBMCs (106 cells/mL) are stimulated with 1 μg/mL of LPS from Salmonella minnesota R595. Cells, in triplicate, are incubated with LPS for 18−20 hours at 37 °C in 5% CO2. Supernatants are then harvested and assayed for cytokine levels. In some experiments, supernatants are kept frozen at −70 °C until use. Cell viability is assayed by Trypan blue exclusion dye method. The concentration of TNFα in the culture supernatants is determined by ELISA. Lenalidomide is assayed in a minimum of three separate experiments. Percent inhibition is determined as 100 × [1 − (cytokine(experimental)/cytokine(control))].

Animal Study:


Animal Models Adult male Sprague-Dawley rats bearing HUVECs cells
Formulation 0.5% DMSO
Dosages 50 mg/kg and 250 mg/kg
Administration Administered via i.p.

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)
Body Surface Area (m2)0.0070.0250.
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)


[1] Muller GW, et al. Bioorg Med Chem Lett, 1999, 9(11), 1625-1630.

[2] Zangari M, et al. Expert Opin Investig Drugs. 2005, 14(11), 1411-1418.

view more

Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2015-06-27)

NCT Number Recruitment Conditions Sponsor
Start Date Phases
NCT02232516 Not yet recruiting Adult Nasal Type Extranodal NK/T-cell Lymphoma|Anaplastic Large Cell Lymphoma|Angioimmunoblastic T-cell Lymphoma|Hepatosplenic T-cell Lymphoma|Peri  ...more Adult Nasal Type Extranodal NK/T-cell Lymphoma|Anaplastic Large Cell Lymphoma|Angioimmunoblastic T-cell Lymphoma|Hepatosplenic T-cell Lymphoma|Peripheral T-cell Lymphoma|Stage I Cutaneous T-cell Non-Hodgkin Lymphoma|Stage IA Mycosis Fungoides/Sezary Syndrome|Stage IB Mycosis Fungoides/Sezary Syndrome|Stage II Cutaneous T-cell Non-Hodgkin Lymphoma|Stage IIA Mycosis Fungoides/Sezary Syndrome|Stage IIB Mycosis Fungoides/Sezary Syndrome|Stage III Cutaneous T-cell Non-Hodgkin Lymphoma|Stage IIIA Mycosis Fungoides/Sezary Syndrome|Stage IIIB Mycosis Fungoides/Sezary Syndrome|Stage IV Cutaneous T-cell Non-Hodgkin Lymphoma|Stage IVA Mycosis Fungoides/Sezary Syndrome|Stage IVB Mycosis Fungoides/Sezary Syndrome Northwestern University|Celgene Corporation|National Canc  ...more Northwestern University|Celgene Corporation|National Cancer Institute (NCI) August 2015 Phase 2
NCT02389543 Not yet recruiting Multiple Myeloma Karyopharm Therapeutics, Inc July 2015 Phase 1|Phase 2
NCT02441686 Not yet recruiting Multiple Myeloma Dana-Farber Cancer Institute|Millennium Pharmaceuticals,  ...more Dana-Farber Cancer Institute|Millennium Pharmaceuticals, Inc.|Celgene Corporation June 2015 Phase 2
NCT02472691 Recruiting Leukemia, Myeloid, Acute|Myelodysplastic Syndromes|Leukemia, Myelomonocytic, Chronic Heinrich-Heine University, Duesseldorf|Celgene Corporatio  ...more Heinrich-Heine University, Duesseldorf|Celgene Corporation|Coordination Center for Clinical Trials (KKS) Duesseldorf June 2015 Phase 2
NCT02309515 Recruiting Monoclonal B-Cell Lymphocytosis|Stage 0 Chronic Lymphocytic Leukemia|Stage I Chronic Lymphocytic Leukemia|Stage I Small Lymphocytic Lymphoma Mayo Clinic|National Cancer Institute (NCI) June 2015 Phase 2

view more

Chemical Information

Download Lenalidomide (CC-5013) SDF
Molecular Weight (MW) 259.26


CAS No. 191732-72-6
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms N/A
Solubility (25°C) * In vitro DMSO 52 mg/mL (200.57 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 30% PEG400/0.5% Tween80/5% propylene glycol 5 mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Chemical Name 3-(4-amino-1-oxoisoindolin-2-yl)piperidine-2,6-dione

Customer Product Validation (4)

Click to enlarge
Source Clin Cancer Res 2011 17, 5311-21. Lenalidomide (CC-5013) purchased from Selleck
Method MTT assays
Cell Lines MM.1S cells
Concentrations 1-5 μM
Incubation Time 48 h
Results The combination of low concentrations of MLN2238 and lenalidomide triggered synergistic anti-MM activity, with acombination index (CI) < 1.0.

Click to enlarge
Source Obesity 2012 20, 2174-85. Lenalidomide (CC-5013) purchased from Selleck
Method Western Blot
Cell Lines ob/ob mice
Concentrations 50 mg/kg/day
Incubation Time 3 d
Results Although lenalidomide itself did not exert any effect on the expression of these proteins, it significantly attenuated or ablated obesity-induced upregulation of TNF-α, IL-6, Fas, and cleaved caspase-3 without any effect on FasL.

Click to enlarge
Source Harvard Medical School. Lenalidomide (CC-5013) purchased from Selleck
Method AnnexinV/PI staining, Western blotting
Cell Lines MM.1S cells
Concentrations 2 μM
Incubation Time 0-72 h
Results The analysis showed an increase (55.7%) of cells in early and late apoptosis after 72 hours of exposure to combined therapy. Combined AT9283 and lenalidomide increased cleavage of caspase-8 and PARP. Using western blot analysis to delineate the molecular mechanism underlying this combination, we found that combination treatment resulted in downregulation of pSTAT3 and pERK following 4 hours of treatment.

Click to enlarge
Source Harvard Medical School. Lenalidomide (CC-5013) purchased from Selleck
Method Western blotting, Cell proliferation assay
Cell Lines MM.1S cells
Concentrations 2 μM
Incubation Time 4/48 h
Results Combined therapy inhibited 3H-TdR uptake of MM.1S cells cultured in the presence of BMSCs. Interestingly, consistent with this data, We observed that AT9283 plus lenalidomide downregulated the expression of the p-STAT3 and p-ERK in MM.1S cells cultured with BMSCs.

Product Use Citation (22)

Tech Support & FAQs

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.

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

* Indicates a Required Field

Related TNF-alpha Products

  • UMI-77

    UMI-77 is a selective Mcl-1 inhibitor with Ki of 490 nM, showing selectivity over other members of Bcl-2 family.

  • BV-6

    BV-6 is a SMAC mimetic, dual cIAP and XIAP inhibitor.

  • LCL161

    LCL161, a SMAC mimetic, potently binds to and inhibits multiple IAPs (i.e. XIAP, c-IAP). Phase 2.

  • Thalidomide

    Thalidomide was introduced as a sedative drug, immunomodulatory agent and also is investigated for treating symptoms of many cancers. Thalidomide inhibits an E3 ubiquitin ligase, which is a CRBN-DDB1-Cul4A complex.

  • Pomalidomide

    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.

  • Necrostatin-1

    Necrostatin-1 is a specific RIP1 inhibitor and inhibits TNF-α-induced necroptosis with EC50 of 490 nM in 293T cells.

    Features:A powerful tool for characterizing the role of necroptosis with characterized primary target.


    Z-VAD-FMK is a cell-permeable, irreversible pan-caspase inhibitor, blocks all features of apoptosis in THP.1 and Jurkat T-cells.

    Features:A key compound for apoptosis studies.

  • ABT-199 (GDC-0199)

    ABT-199 (GDC-0199) is a Bcl-2-selective inhibitor with Ki of <0.01 nM in cell-free assays, >4800-fold more selective versus Bcl-xL and Bcl-w, and no activity to Mcl-1. Phase 3.

    Features:Re-engineered version of ABT-263 (Navitoclax).

  • ABT-263 (Navitoclax)

    ABT-263 (Navitoclax) is a potent inhibitor of Bcl-xL, Bcl-2 and Bcl-w with Ki of ≤ 0.5 nM, ≤1 nM and ≤1 nM in cell-free assays, but binds more weakly to Mcl-1 and A1. Phase 2.

  • ABT-737

    ABT-737 is a BH3 mimetic inhibitor of Bcl-xL, Bcl-2 and Bcl-w with EC50 of 78.7 nM, 30.3 nM and 197.8 nM in cell-free assays, respectively; no inhibition observed against Mcl-1, Bcl-B or Bfl-1. Phase 2.

Recently Viewed Items

Tags: buy Lenalidomide (CC-5013) | Lenalidomide (CC-5013) ic50 | Lenalidomide (CC-5013) price | Lenalidomide (CC-5013) cost | Lenalidomide (CC-5013) solubility dmso | Lenalidomide (CC-5013) purchase | Lenalidomide (CC-5013) manufacturer | Lenalidomide (CC-5013) research buy | Lenalidomide (CC-5013) order | Lenalidomide (CC-5013) mouse | Lenalidomide (CC-5013) chemical structure | Lenalidomide (CC-5013) mw | Lenalidomide (CC-5013) molecular weight | Lenalidomide (CC-5013) datasheet | Lenalidomide (CC-5013) supplier | Lenalidomide (CC-5013) in vitro | Lenalidomide (CC-5013) cell line | Lenalidomide (CC-5013) concentration | Lenalidomide (CC-5013) nmr
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description
Contact Us