Lenalidomide (CC-5013)

Catalog No.S1029

For research use only.

Lenalidomide (CC-5013) is a TNF-α secretion inhibitor with IC50 of 13 nM in PBMCs. Lenalidomide (CC-5013) is a ligand of ubiquitin E3 ligase cereblon (CRBN), and it causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKZF3, by the CRBN-CRL4 ubiquitin ligase. Lenalidomide promotes cleaved caspase-3 expression and inhibit VEGF expression and induces apoptosis.

Lenalidomide (CC-5013) Chemical Structure

CAS No. 191732-72-6

Selleck's Lenalidomide (CC-5013) has been cited by 129 publications

Purity & Quality Control

Choose Selective E3 ligase Ligand Inhibitors

Biological Activity

Description Lenalidomide (CC-5013) is a TNF-α secretion inhibitor with IC50 of 13 nM in PBMCs. Lenalidomide (CC-5013) is a ligand of ubiquitin E3 ligase cereblon (CRBN), and it causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKZF3, by the CRBN-CRL4 ubiquitin ligase. Lenalidomide promotes cleaved caspase-3 expression and inhibit VEGF expression and induces apoptosis.
Targets
CRBN [3]
()
VEGF [1]
()
TNF-α [1]
(PBMCs)
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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
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TE-12 MoTzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn\ZTWM2OD17ND6zNFU2KM7:TR?= NYjkemV6RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNQDR6Lze+V2FPT0WUPD;hQi=>
MDA-MB-361 M1S5T2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUHJR|UxRTl4LkC1NVYh|ryP NYTlPFExRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNQDR6Lze+V2FPT0WUPD;hQi=>
DF15 MnrtSpVv[3Srb36gZZN{[Xl? M1XC[|QhcHK| M2jTWWlv\HWldHnvckBw\iCFUly0M2NTSk5idXLpdZVqfGmwIHzp[4F{\S2vZXTpZZRm\CCjaX;sc5Mh\GWpcnHkZZRqd25iaX6gbJVu[W5iRF[xOUBk\WyuczDlfJBz\XO|aX7nJJBNV0NvZWDMMZRi\2enZDDhbY9td3NiYX\0[ZIhPCCqcoOgZpkhdHWvaX7ld4NmdmOnIHLhd4VlKGKndHGt[4Ft[WO2b4Pp[IF{\SCnbor5cYUh\nKjZ33lcpRifGmxbjDjc41xdGWvZX70ZZRqd25iYYPzZZktKEWFNUCgQUAxNjB3MzFOwG0v M17tR|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ6M{W4OVA4Lz5{OEO1PFUxPzxxYU6=
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T-cells NF7US3hHfW6ldHnvckBie3OjeR?= M1\YSlIhfG9iMzDkZZl{ M3XWSmlvcGmkaYTpc44hd2ZiSVytNkBxem:mdXP0bY9vKGmwIHj1cYFvKFRiY3XscJMhdWWjc4Xy[YQh[W[2ZYKgNkB1dyB|IHThfZMh[nliRVzJV2EtKEWFNUCgQUAxNjF3IN88UU4> M2rlOVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ|MU[4NFE6Lz5{M{G2PFAyQTxxYU6=
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CD34+ progenitor cells M2\EW2Z2dmO2aX;uJIF{e2G7 MnHRNVQh\GG7cx?= M4HkdmRm[3KnYYPlJIlvKGW{eYTodo9q\CCmaX\m[ZJmdnSrYYTpc44hd2ZiQ1SzOEsheHKxZ3XubZRweiClZXzsd{Bnem:vIH35[Yxw\Hm|cHzhd5Rq[yC|eX7kdo9u\SCmZXyoOZEqKHCjdHnlcpQh[XO|ZYPz[YQh[XNiQ1SzOkBmgHC{ZYPzbY9vKGGodHXyJFE1KGSjeYO= M3vXPVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzF5NUe2PVI1Lz5zN{W3OlkzPDxxYU6=
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CD34+ progenitor cells MVvGeY5kfGmxbjDhd5NigQ>? NYLwSWQ1OTRiZHH5dy=> NWLtT4R{TGWlcnXhd4UhcW5iZYL5eIhzd2mmIHTp[oZmemWwdHnheIlwdiCxZjDDSFM1MyCycn;n[Y5qfG:{IHPlcIx{KG[{b32gcZlmdG:meYPwcIF{fGmlIIP5coRzd22nIHTlcEg2eSlicHH0bYVvfCCjc4Pld5Nm\CCjczDncJlkd3Cqb4LpckBCKGW6cILld5Nqd25iYX\0[ZIhOTRiZHH5dy=> NUTHV3d5RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUe1O|Y6OjRpPkG3OVc3QTJ2PD;hQi=>
CD34+ progenitor cells MojaS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MYSxOEBl[Xm| NEDLVXhKdmirYnn0bY9vKG:oIHPlcIwheHKxbHnm[ZJifGmxbjDv[kBETDN2KzDwdo9o\W6rdH;yJINmdGy|IH\yc40hdXmnbH;kfZNxdGG|dHnjJJN6dmS{b33lJIRmdCh3cTmgdIF1cWWwdDDh[pRmeiBzNDDkZZl{ NYXEO2F7RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUe1O|Y6OjRpPkG3OVc3QTJ2PD;hQi=>
CD34+ progenitor cells MmnmS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MV:xOEBl[Xm| MVHHdo94fGhiaX7obYJqfGmxbjDv[kBETDN2KzDwdo9o\W6rdH;yJINmdGy|IH\yc40hdm:wLXTlcEg2eSlibYnlcI9lgXOybHHzeIlkKHO7bnTyc41mKHCjdHnlcpQh[W[2ZYKgNVQh\GG7cx?= MWm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8yPzV5NkmyOEc,OTd3N{[5NlQ9N2F-
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Assay
Methods Test Index PMID
Western blot phospho-IKKβ / IKKβ ; MDM2 / p-MDM2 / p-p53 / p53 22698399 22525275
Growth inhibition assay Cell viability 22698399
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 (from reference)

Animal Research:

[5]

  • Animal Models: Adult male Sprague-Dawley rats bearing HUVECs cells
  • Dosages: 50 mg/kg and 250 mg/kg
  • Administration: Administered via i.p.
  • (Only for Reference)

Solubility (25°C)

In vitro

DMSO 52 mg/mL
(200.57 mM)
Water Insoluble
Ethanol Insoluble

In vivo

Add solvents to the product individually and in order
(Data is from Selleck tests instead of citations):
5% DMSO+40%PEG 300+5%Tween80+ddH2O
For best results, use promptly after mixing.

10mg/mL

* 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 Information

Molecular Weight 259.26
Formula

C13H13N3O3

CAS No. 191732-72-6
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles C1CC(=O)NC(=O)C1N2CC3=C(C2=O)C=CC=C3N

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

mg/kg g μL

Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

Calculation results:

Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT05091372 Not yet recruiting Drug: Belantamab mafodotin|Drug: Lenalidomide Myeloma Multiple M.D. Anderson Cancer Center April 30 2022 Phase 2
NCT04903197 Recruiting Drug: VAY736|Drug: lenalidomide Non-Hodgkin Lymphoma Diffuse Large B Cell Lymphoma Novartis Pharmaceuticals|Novartis January 31 2022 Phase 1
NCT04974216 Not yet recruiting Drug: Tafasitamab|Drug: Lenalidomide|Drug: Rituximab DLBCL The Lymphoma Academic Research Organisation December 15 2021 Phase 2
NCT04539236 Recruiting Drug: Lenalidomide|Drug: Luspatercept Myelodysplastic Syndromes Mikkael Sekeres MD|Celgene|Bristol-Myers Squibb|University of Miami November 9 2021 Phase 1|Phase 2
NCT04669171 Recruiting Biological: EO2463|Drug: lenalidomide|Biological: rituximab Follicular Lymphoma|Marginal Zone Lymphoma Enterome July 5 2021 Phase 1|Phase 2

(data from https://clinicaltrials.gov, updated on 2022-01-17)

Tech Support

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.

Handling Instructions

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Frequently Asked Questions

Question 1:
What is the formulation for mouse injection(i.p.)?

Answer:
This paper has the information you need: http://link.springer.com/article/10.1208/s12248-012-9401-2. Add lenalidomide to the appropriate volume of sterile phosphate-buffered saline (PBS) containing 1% hydrochloric acid (HCl). the pH of this preparation was adjusted to 7.0–7.6 using sodium hydroxide and sterile filtered using a 0.22 μm Steriflip filter.

Question 2:
what is the procedure to resuspend this compound?

Answer:
You can resuspend this compund by DMSO, the solubility is about 52 mg/mL (200.57 mM). For in vivo study, you can prepare the working solution with the vehicle of: 30% PEG400/0.5% Tween80/5% propylene glycol for oral administration.

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