Saroglit

Pack	Price	Details
Unit Price	৳ 2100.00	Unit Price: ৳ 70.00 (3 x 10: ৳ 2,100.00)

The recommended dose of Saroglitazar is two tablets of 2 mg once a day.

Pediatric Use: The safety and effectiveness of Saroglitazar in children less than 18 years of age have not been established.

Geriatric Use: Considering the comorbidity and concomitant medications in elderly patients, Saroglitazar should be used with caution in geriatric patients.

In two controlled phase III clinical studies of 12 to 24 weeks treatment duration with Saroglit, the most common adverse events (AEs > 2%) reported were gastritis, asthenia and pyrexia. Most of the AEs were mild to moderate in nature and did not result in discontinuation of the study. Because clinical studies are conducted under widely varying conditions, AE rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice.

Saroglitazar is a potent and predominantly Peroxisome Proliferator Activated Receptor (PPAR)- alpha agonist with moderate PPAR-gamma agonistic activity. PPARs are nuclear lipid-activated transcription factors that regulate the expression of various genes involved in the control of lipid and lipoprotein metabolism, glucose homeostasis and inflammatory processes. Saroglitazar showed both anti-dyslipidemic and anti-diabetic effects mainly mediated via activation of PPAR α and PPARγ respectively.

PPARα activation by saroglitazar increases the hepatic oxidation of fatty acids (FA) and reduces the synthesis and secretion of TG. This in turn increases diversion of FA from peripheral tissues (e.g. skeletal muscle and fat tissue) to the liver, and thereby decreasing both FA synthesis and delivery of TG to peripheral tissues. Saroglitazar also causes increased lipolysis and elimination of TG-rich particles from plasma by activating lipoprotein lipase (LPL) and reducing production of apolipoprotein C-III (an inhibitor of LPL activity). Consistent with the above mechanism, saroglitazar was also found to reduce plasma LDL cholesterol. PPARα activation by saroglitazar also induces an increase in the synthesis of apolipoproteins A-I, A-II and HDL-cholesterol.

Although saroglitazar is predominantly a PPARα agonist, it also causes activation of PPARγ and regulates the transcription of insulin-re-sponsive genes involved in the control of glucose production, transport and utilization. Saroglitazar increases the expression of numerous PPARγ-responsive genes involved in carbohydrate and lipid metabolism, including adiponectin, adipocyte fatty-acid binding protein (aP2), LPL, fatty acid transport protein (FATP) and fatty acid translocase (CD36). By increasing the expression of these genes, saroglitazar decreases the post prandial rise of plasma free fatty acids, improves post-absorptive insulin-mediated suppression of hepatic glucose output, reduces the metabolic burden on liver & muscle and promotes glucose utilization. Robust antidiabetic and insulin sensitizing effects of saroglitazar were observed in preclinical models.

Saroglit treatment should be initiated with caution in patients with abnormal liver or renal function, or history of myopathies. Saroglit should be initiated with caution in patients with type 2 diabetes having cardiac disease with episodic congestive heart failure and such patients should be monitored for signs and symptoms of congestive heart failure. Patients who experience rapid increase in weight should be assessed for fluid accumulation and volume-related events such as excessive edema and congestive heart failure.

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