Name: Lenalidomide
Brand: BOC Sciences
Price: 298 USD
Availability: MadeToOrder

Purity

≥98% (HPLC)

Solubility

DMSO:25.93mg/mL

Appearance

White solid powder

ShelfLife

>2 years if stored properly

Storage

Store at -20°C

Shipping

Room temperature in continental US; may vary elsewhere.

Synonyms

CC5013; CC-5013; CC 5013; IMiD1; Lenalidomide; US brand name: Revlimid

Melting Point

>250°C (dec.)

Chemical Name

3-(4-Amino-1,3-dihydro-1-oxo-2H-isoindol-2-yl)-2,6-piperidinedione

InChI Key

InChI=1S/C13H13N3O3/c14-9-3-1-2-7-8(9)6-16(13(7)19)10-4-5-11(17)15-12(10)18/h1-3,10H,4-6,14H2,(H,15,17,18)

InChI

GOTYRUGSSMKFNF-UHFFFAOYSA-N

SMILES

NC1=C2CN(C(C2=CC=C1)=O)C3CCC(NC3=O)=O

Biological Activity

Thalidomide analog. Immune modulatory drug and cereblon binding compound. Induces ubiquitination and degradation of casein kinase (CK) 1α by the E3 ubiquitin ligase CRL4CRBN. Also TNF-α inhibitor and angiogenesis inhibitor. Promotes degradation of transcription factor SALL4.

Mechanism

E3 Ligase: Lenalidomide engages the cereblon (CRBN) E3 ubiquitin ligase complex, a key substrate receptor within the CRL4 ligase system, promoting the formation of a ternary complex that directs neosubstrate recognition and ubiquitination.

Target Protein: The compound selectively targets transcription factors IKZF1 and IKZF3, zinc finger proteins that regulate gene expression, facilitating their recruitment to CRBN for ubiquitin-mediated processing.

Degradation Mechanism: Degradation occurs through the ubiquitin–proteasome system. Lenalidomide-induced proximity of CRBN to the target proteins drives polyubiquitination, after which the 26S proteasome recognizes and degrades the tagged substrates, enabling controlled and selective protein turnover in cells.

Applications

• Molecular Glue for E3 Ligase Recruitment: Lenalidomide acts as a molecular glue by recruiting CRBN, a component of the E3 ubiquitin ligase complex, to target neosubstrates for ubiquitination and subsequent proteasomal degradation. This property is pivotal in studying protein homeostasis and the modulation of protein degradation pathways in cellular models.

• Targeted Degradation of Ikaros and Aiolos: By facilitating the recruitment of specific transcription factors such as Ikaros and Aiolos to the ubiquitin-proteasome system, Lenalidomide enables targeted degradation. Researchers can leverage this mechanism to dissect transcriptional regulation and its impact on cellular differentiation and immune response.

• Modulation of Protein-Protein Interactions: Lenalidomide's ability to alter protein-protein interactions within the E3 ligase complex serves as a powerful tool for investigating the dynamic nature of protein networks. This application is crucial for understanding the structural and functional relationships governing cellular signaling pathways.

• Inducing Synthetic Lethality in Cancer Models: The use of Lenalidomide to induce synthetic lethality through targeted protein degradation offers a strategic approach for cancer research. By selectively degrading oncogenic proteins, researchers can explore novel therapeutic vulnerabilities and resistance mechanisms in tumor cells.

1.Oral Ixazomib, Lenalidomide, and Dexamethasone for Multiple Myeloma.

Moreau P, Masszi T, Grzasko N, Bahlis NJ, Hansson M, Pour L, Sandhu I, Ganly P, Baker BW, Jackson SR, Stoppa AM, Simpson DR, Gimsing P, Palumbo A, Garderet L, Cavo M, Kumar S, Touzeau C, Buadi FK, Laubach JP, Berg DT, Lin J, Di Bacco A, Hui AM, van de Vel N Engl J Med. 2016 Apr 28;374(17):1621-34. doi: 10.1056/NEJMoa1516282.

BACKGROUND: Ixazomib is an oral proteasome inhibitor that is currently being studied for the treatment of multiple myeloma.

2.A study of high-dose lenalidomide induction and low-dose lenalidomide maintenance therapy for patients with hypomethylating agent refractory myelodysplastic syndrome.

Cherian MA1, Tibes R2, Gao F3, Fletcher T1, Fiala M1, Uy GL1, Westervelt P1, Jacoby MA1, Cashen AF1, Stockerl-Goldstein K1, DiPersio JF1, Vij R1. Leuk Lymphoma. 2016 Apr 27:1-6. [Epub ahead of print]

Myelodysplastic syndromes (MDS) are clonal hematopoietic disorders characterized by bone marrow failure which frequently progress to acute myeloid leukemia. Patients who fail to respond to, or progress on first-line DNA hypomethylating agents (HMA) have a poor prognosis. Conventionally dosed lenalidomide has activity in 5q-MDS. In other subtypes, it may reduce RBC transfusion requirements but does not result in cytogenetic responses. We previously reported that high-dose lenalidomide induction (50 mg/day) results in complete remissions in a high fraction of patients. We, therefore, conducted a Phase 2 trial of the same regimen in MDS refractory to HMA. Marrow complete remissions were seen in 33% of patients and hematological improvement in 8% of patients. Significant infections complicated more than 50% of cases. Future trials to explore alternative dosing schedules of high-dose lenalidomide to increase efficacy while decreasing toxicity are warranted.

HPLC

HNMR

Hi, how does Lenalidomide exert anti-cancer effects?

Lenalidomide triggers the activation of pro-apoptotic caspase-8, enhances tumor cell sensitivity to FAS-induced apoptosis, and downregulates NF-κB, an anti-apoptotic protein.7 Independent of its immunomodulatory effects, lenalidomide mediates anti-angiogenic effects by inhibiting angiogenic growth factors released by tumor cells, such as vascular endothelial growth factor (VEGF), basic fibroblastic-growth factor (BFGF), and hepatocyte-growth factor.

15/12/2017

Dear Sirs, how does Lenalidomide augment the apoptosis of myeloma cells?

Hello, Lenalidomide downregulates the production of IL-6 directly and also by inhibiting multiple myeloma (MM) cells and bone marrow stromal cells (BMSC) interaction, which augments the apoptosis of myeloma cells.

15/4/2018

Would you like to tell me the toxicity of Lenalidomide?

The toxicity of Lenalidomide doses up to 15, 22.5, and 45 mg/kg via IV, IP, and PO routes of administration. Limited by solubility in our PBS dosing vehicle, these maximum achievable Lenalidomide doses are well tolerated with the exception of one mouse death (of four total dosed) at the 15 mg/kg IV dose. Notably, no other toxicities are observed in the study at IV doses of 15 mg/kg (n=3) or 10 mg/kg (n=45) or at any other dose level through IV, IP, and PO routes.

31/5/2018

block cell adhesion molecules

In vitro, lenalidomide blocks cell adhesion molecules such as ICAM-1, LFA-1, β2 and β3 integrins, as well as gap-junction function, thereby preventing metastasis of malignant cells. I'm glad to have such a good product.

26/11/2016

inhibit growth of mature B-cell lymphomas

We used this in cell culture studies and got good results. Lenalidomide specifically inhibits growth of mature B-cell lymphomas, including multiple myeloma, and induces IL-2 release from T cells.

28/11/2016

stimulate T cell proliferation

I think it's not bad! Lenalidomide is potent in stimulating T cell proliferation and IFN-γ and IL-2 production.

21/2/2021

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Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C₁V₁ = C₂V₂