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LENANGIO 5 MG CAP ( STRIP , 10 )

Manufactured by : Dr. Reddy’s Laboratories Ltd

. 820.00 .1410.00 50.85 % OFF You Save : . 717.00
Availability : In stock

DESCRIPTION

Lenalidomide (initially known as CC-5013 and marketed as Revlimid® by Celgene) is a derivative of thalidomide introduced in 2004. It was initially intended as a treatment for multiple myeloma, for which thalidomide is an accepted therapeutic modality, but has also shown efficacy in the hematological disorders known as the myelodysplastic syndromes. [Wikipedia] FDA approved on December 27, 2005.

CATEGORIES

Antineoplastic Agents Immunosuppressive Agents Antineoplastic and Immunomodulating Agents

CHEMICAL FORMULA

C13H13N3O3

COMPOSITION

Lenalidomide 5 MG

INDICATION

Lenalidomide is indicated for the treatment of multiple myeloma in combination with dexamethasone. It is also indicated for the treatment of patients with transfusion-dependent anemia due to low- or intermediate- risk myelodysplastic syndromes (MDS) 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. Lenalidomide does not prolong the QTc interval.

MECHANISM

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

ABSORPTION

Rapidly absorbed following oral administration, with maximum plasma concentrations occurring between 0.625 and 1.5 hours post-dose. Co-administration with food does not alter the extent of absorption (AUC) but does reduce the maximal plasma concentration (Cmax) by 36%. The pharmacokinetic disposition of lenalidomide is linear. Accumulation does not occur following multiple doses.

METABOLISM

Lenalidomide undergoes limited metabolism. Unchanged lenalidomide is the predominant circulating component in humans. Two identified metabolites are hydroxy-lenalidomide and N-acetyl-lenalidomide; each constitutes less than 5% of parent levels in circulation. The cytochrome P450 enzyme system is not involved with the metabolism of lenalidomide.

ROUTE ELIMINATION

Elimination is primarily renal. When a single oral dose of 25 mg is given healthy subjects, 90% and 4% of the dose is eliminated in urine and feces, respectively. Hydroxy-lenalidomide and N-acetyl-lenalidomide represent 4.59% and 1.83% of the excreted dose, respectively.

HALF LIFE

Healthy subjects = 3 hours; Multiple myeloma or MDS patients = 3 - 5 hours.

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.

FOOD INTERACTIONS

Avoid Alcohol