Exendin-4 acetate

Exendin-4 (100 μg/kg; i.p.; once daily; 12-13 weeks) acetate reduces fasting blood glucose in diabetic db/db mice and decreases A1C by 47%, with similar beneficial effects observed in non-diabetic mice^[1]. Exendin-4 (administered via intraperitoneal injection at doses ranging from 0.1 μg to 100 μg per rat, twice daily for 5-6 weeks) acetate reduces A1C by 41.3% and improves insulin sensitivity by 76% in obese diabetic ZDF rats; dose-dependent benefits are observed even at a dose of 0.1 μg per rat administered twice daily for 6 weeks^[1]. Exendin-4 (100 μg/kg; subcutaneous injection; single administration) acetate produces a maximum 37% reduction in plasma glucose levels in fasted diabetic rhesus monkeys, with an ED₅₀ of 0.25 μg/kg^[1]. Exendin-4 (0.4 nmol/kg; intravenous injection; single administration) acetate exhibits potent glucose-dependent insulinotropic activity in fasted Wistar rats, with an ED₅₀ of 0.014 nmol/kg^[1]. Exendin-4 (i.p.; once daily; for 10 consecutive days at a dose of 1 nmol/kg) acetate attenuates the progression of diabetes in pancreatectomized rats, reduces their blood glucose levels by 40% compared with untreated rats, and increases β-cell mass by 40% via β-cell differentiation and proliferation^[1]. Exendin-4 (3 μg/kg/day; subcutaneous injection; once daily; postnatal days 2-6) acetate increases pancreatic insulin content and β-cell mass in newborn prediabetic GK rats on postnatal day 7, and reduces fasting blood glucose levels at 2 months of age^[1]. Exendin-4 (3 μg/kg; i.p.; once daily; postnatal days 2-6) acetate increases the β-cell mass of neonatal Wistar rats treated with Streptozotocin (HY-13753) to 71% of the healthy level on day 7^[1]. Exendin-4 (intraperitoneal injection, once daily, on postnatal days 1-6, at a dose of 1 nmol/kg) acetate prevents impaired glucose tolerance in neonatal rats with intrauterine growth restriction (IUGR), maintains their normal fasting blood glucose levels and β-cell mass until 8 months after birth, and restores β-cell proliferation capacity and PDX-1 expression to normal levels^[1]. Exendin-4 (100 μg/kg, subcutaneous injection, twice daily for 15 consecutive days) acetate reduces blood glucose levels in diabetic db/db mice by promoting β-cell proliferation, and increases their β-cell mass by 30%-60%^[1]. Exendin-4 (1 nmol/kg; i.p.; once daily; for 2 weeks) acetate reduces fasting blood glucose levels, improves oral glucose tolerance, and increases β-cell mass by 1.4‑fold in diabetic db/db mice^[1]. Exendin-4 (100 pmol/kg‑1 nmol/kg; i.p.; once daily; for 2 consecutive weeks) acetate reduces blood glucose levels in both healthy and diabetic mice, increases insulin secretion, lowers A1C levels by 20%-45%, and promotes β‑cell neogenesis and PDX‑1 expression in normoglycemic mice^[1]. Exendin-4 (24 nmol/kg; i.p.; once daily; initiated 2 days before Streptozotocin injection and continued until 3 days after injection) acetate reduces the β‑cell apoptosis rate by 76% in C57Bl/6 mice, decreases blood glucose levels, and maintains high plasma insulin levels for up to 55 days after Streptozotocin injection^[1]. Exendin-4 (0.1‑100 μg; i.p.; twice daily; for 6 weeks) acetate dose‑dependently reduces food intake (ED₅₀ 0.14 μg) and body weight (ED₅₀ 0.42 μg) in obese diabetic Zucker rats, and sustained benefits for glycemic control and fat deposition are observed over a 56‑day treatment period^[1]. Exendin-4 (10 μg; administered via tail vein; single dose; administered immediately after reperfusion) acetate reduces cerebral infarction volume by approximately 47% in male C57BL/6 mice with ischemic stroke at 24 h, improves neurological function, inhibits oxidative stress and inflammatory responses, reduces cell death, and increases intracellular cyclic AMP and phosphorylated CREB levels^[2]. Exendin-4 (0.1 μM; subcutaneous injection; daily administration; throughout the entire study period) acetate restores glycemic control, ameliorates pancreatic and brain pathology, enhances motor function, and increases survival rate by 18% in mouse models of Huntington's disease, while inducing moderate blood glucose reduction and motor function improvement in wild‑type mice^[3].