Thalidomide

  • #LGM Pharma is a Thalidomide CAS# 50-35-1 API supplier distributor based in the USA. Inquire about DMF, cGMP, price, availability, delivery, purity, and more.
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  • #LGM Pharma offers this active ingredient but not the finished dosage forms.

Product Details:

  • CAS No: 50-35-1
  • AHFC code:
  • Synonyms: alpha-phthalimidoglutarimide N-Phthalimidoglutamic acid imide N-Phthaloylglutamimide N-Phthalylglutamic acid imide Thalidomine USP26
  • ATC Code: L04AX02
  • Chemical Formula: C7H8N4O2
  • Molecular Weight: 258.2295
  • Assay/Purity: Typically NLT 98%
  • DrugBank: DB01041 (APRD01251)
  • SMILES: O=C1N(C2CCC(=O)NC2=O)C(=O)C2=CC=CC=C12
  • InChl: UEJJHQNACJXSKW-UHFFFAOYSA-N
  • PubChem: 5426
  • IUPAC: 2-(2,6-dioxopiperidin-3-yl)-2,3-dihydro-1H-isoindole-1,3-dione

Additional Details

Indication:
For the acute treatment of the cutaneous manifestations of moderate to severe erythema nodosum leprosum (ENL). Also for use as maintenance therapy for prevention and suppression of the cutaneous manifestations of ENL recurrence.
Pharmacodynamics:
Thalidomide is an immunomodulatory agent with a spectrum of activity that is not fully characterized. Thalidomide is racemic ã it contains both left and right handed isomers in equal amounts: one enantiomer is effective against morning sickness, and the other is teratogenic. The enantiomers are converted to each other in vivo. That is, if a human is given D-thalidomide or L-thalidomide, both isomers can be found in the serum. Hence, administering only one enantiomer will not prevent the teratogenic effect in humans.
Mode of Action:
In patients with erythema nodosum leprosum (ENL) the mechanism of action is not fully understood. Available data from in vitro studies and preliminary clinical trials suggest that the immunologic effects of this compound can vary substantially under different conditions, but may be related to suppression of excessive tumor necrosis factor-alpha (TNF-a) production and down-modulation of selected cell surface adhesion molecules involved in leukocyte migration. For example, administration of thalidomide has been reported to decrease circulating levels of TNF-a in patients with ENL, however, it has also been shown to increase plasma TNF-a levels in HIV-seropositive patients. As a cancer treatment, the drug may act as a VEGF inhibitor.
Metabolism:
Thalidomide itself does not appear to be hepatically metabolized to any large extent, but appears to undergo non-enzymatic hydrolysis in plasma to multiple metabolites. Thalidomide may be metabolized hepatically by enzymes of the cytochrome P450 enzyme system. The end product of metabolism, phthalic acid, is excreted as a glycine conjugate.
Toxicity:
The R-configuration and the S-configuration are more toxic individually than the racemic mixture. The LD50 could not be established in mice for racemic thalidomide, whereas LD50 values for the R and S configurations are reported to be 0.4 to 0.7 g/kg and 0.5 to 1.5 g/kg, respectively.
General Reference:
Products currently covered by valid US Patents are offered for R&D use in accordance with 35 USC 271(e)+A13(1). Any patent infringement and resulting liability is solely at buyer risk.

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