| Generic Name |
Sitagliptin Phosphate Tablets |
| Strength |
50mg |
| Packing |
28 tablets/box |
| Origin |
China |
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Product name:
Sitagliptin Phosphate Tablets
Character:
Light brown film coating, white or near-white after removal of coating.
Indications:
This product is used in combination with diet control and exercise to improve blood sugar control in patients with type 2 diabetes.
Adverse reactions:
In controlled clinical studies of monotherapy and in combination with metformin or pioglitazone, the overall incidence of adverse reactions, hypoglycemia, and discontinuation due to clinical adverse reactions was similar between the treatment and placebo groups.
Clinical studies of monotherapy or placebo-controlled combination of monotherapy with pioglitazone or glimepiide +/ -metformin: nasopharyngitis (monotherapy) was the adverse event in patients with an incidence of ≥5% higher than that in the placebo-treated group; Upper respiratory tract infection, headache (combined with pioglitazone); Hypoglycemia, nasopharyngitis, headache [combined with glimepiride (+/- metformin)].
Pharmacology and toxicology:
Sitagliptin dipeptidyl peptidase 4 (DPP-4) inhibitors improve blood sugar control in patients with type 2 diabetes by increasing levels of active secret-secreting hormone. Islet hormones, including glucagon-like polypeptide-1 (GLP-1) and glucose-dependent insulin-secreting polypeptide (GIP), are released by the gut throughout the day and are elevated after meals. Islet hormone is part of the endogenous system involved in the physiological regulation of glucose homeostasis. When blood glucose concentrations are normal or elevated, GLP-1 and GIP increase the synthesis and release of insulin by pancreatic beta cells through intracellular signaling pathways involving cyclic adenosine phosphate. In animal models of type 2 diabetes, treatment with GLP-1 or DPP-4 inhibitors improves pancreatic beta cell responsiveness to glucose and promotes insulin biosynthesis and release. As insulin levels rise, tissue uptake of glucose increases. In addition, GLP-1 also inhibits the secretion of glucagon by alpha cells of the pancreas. A decrease in glucagon concentration and an increase in insulin levels can reduce liver glucose production and thus lower blood sugar levels. The effects of GLP-1 and GIP are glucose-dependent, and when the blood glucose concentration is low, GLP-1 does not promote insulin release or inhibit glucagon secretion. When glucose levels are higher than normal concentrations, GLP-1 and GIP enhance their role in promoting insulin release. In addition, GLP-1 does not impair the body's normal glucagon release response to hypoglycemia. The activity of GLP-1 and GIP is limited by the enzyme DPP-4, which rapidly hydrolyzes the islet hormone to produce inactive products. Sitagliptin prevents DPP-4 from hydrolyzing the islet hormone, thereby increasing plasma concentrations of the active forms of GLP-1 and GIP. By increasing active incretin levels, sitagliptin is able to increase insulin release and reduce glucagon levels in a glucose-dependent manner. In people with type 2 diabetes who have hyperglycemia, the above changes in insulin and glucagon levels can lower glycosylated hemoglobin A1c (HbA1c) and lower fasting and postprandial blood sugar levels. The glucose-dependent mechanism of action of sitagliptin differs from that of sulfonylureas, which increase insulin secretion even when glucose levels are low, resulting in hypoglycemia in both type 2 diabetes patients and normal subjects. Sitagliptin is a potent and highly selective inhibitor of the DPP-4 enzyme that does not inhibit DPP-8 or DPP-9, which are closely related to DPP-4, at therapeutic concentrations.
Storage:
Store below 30°C.
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