LGM Pharma

Lenalidomide

CAS No: 191732-72-6

Lenalidomide

LGM Pharma is a Lenalidomide 191732-72-6 active pharmaceutical ingredient supplier, based in the USA.

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Product Details:

CAS No: 191732-72-6
Synonyms:
  • CC-5013
  • CDC 501
  • IMiD3
ATC code: L04AX04
Molecular Weight: 259.2606 g/mol
PubChem: 216326
Chemical Formula: C21H28O2
DrugBank: DB00480 (APRD01303)
Assay/Purity: Typically NLT 98%
IUPAC Name: 3-(4-amino-1-oxo-2,3-dihydro-1H-isoindol-2-yl)piperidine-2,6-dione
SMILES: NC1=CC=CC2=C1CN(C1CCC(=O)NC1=O)C2=O
InChl: GOTYRUGSSMKFNF-UHFFFAOYSA-N

Additional Details: [+]

Indication:

For the treatment of patients with transfusion-dependent anemia due to low- or intermediate- risk myelodysplastic syndromes associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities.

Pharmacodynamics:

Lenalidomide, a thalidomide analogue, is an immunomodulatory agent possessing immunomodulatory and antiangiogenic properties. Lenalidomide inhibits the secretion of pro-inflammatory cytokines and increases the secretion of anti-inflammatory cytokines from peripheral blood mononuclear cells. Lenalidomide inhibits cell proliferation with varying effectiveness (IC50s) in some but not all cell lines. Lenalidomide is effective in inhibiting growth of Namalwa cells (a human B cell lymphoma cell line with a deletion of one chromosome 5) but is much less effective in inhibiting growth of KG-1 cells (human myeloblastic cell line, also with a deletion of one chromosome 5) and other cell lines without chromosome 5 deletions.

Mode of Action:

The mechanism of action of lenalidomide remains to be fully characterized, however it has been demonstrated that lenalidomide inhibits the expression of cyclooxygenase-2 (COX-2), but not COX-1, in vitro. In vivo it induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity

Metabolism:

The metabolic profile of lenalidomide in humans has not been studied. In healthy volunteers, approximately two-thirds of lenalidomide is eliminated unchanged through urinary excretion. The process exceeds the glomerular filtration rate and therefore is partially or entirely active.

Toxicity:

The most frequently reported adverse events were related to blood and lymphatic system disorders, skin and subcutaneous tissue disorders, gastrointestinal disorders, and general disorders and administrative site conditions.

General Reference:

  1. List A, Kurtin S, Roe DJ, Buresh A, Mahadevan D, Fuchs D, Rimsza L, Heaton R, Knight R, Zeldis JB: Efficacy of lenalidomide in myelodysplastic syndromes. N Engl J Med. 2005 Feb 10;352(6):549-57. Pubmed
  2. Chang DH, Liu N, Klimek V, Hassoun H, Mazumder A, Nimer SD, Jagannath S, Dhodapkar MV: Enhancement of ligand-dependent activation of human natural killer T cells by lenalidomide: therapeutic implications. Blood. 2006 Jul 15;108(2):618-21. Epub 2006 Mar 28. Pubmed
  3. Anderson KC: Lenalidomide and thalidomide: mechanisms of actionãsimilarities and differences. Semin Hematol. 2005 Oct;42(4 Suppl 4):S3-8. Pubmed


Lenalidomide News:

  • Lenalidomide created quite a stir on Wall Street on July 11, 2013 when shares of Celgene’s Revlimid, the brand name of Lenalidomide, soared after positive Phase 3 study data was revealed for this blood cancer drug.
  • The patent for Celgene’s Revlimid expires on October 4, 2019.
  • Lenalidomide is also in a novel class of medications called immunomodulatory drugs.

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