눈에 묻으면 몇 분간 물로 조심해서 씻으시오. 가능하면 콘택트렌즈를 제거하시오. 계속 씻으시오.
P332+P313
피부 자극이 생기면 의학적인 조치· 조언을 구하시오.
P337+P313
눈에 대한 자극이 지속되면 의학적인 조치· 조언를 구하시오.
NFPA 704
0
2
0
Rosiglitazone maleate C화학적 특성, 용도, 생산
개요
Rosiglitazone maleate, belongs to a novel class of thiazolidine diones
launched for the treatment of non-insulin-dependent diabetes mellitus (NIDDM),
a disease characterized by a pancreatic β-cell defect and insulin resistance in
the liver and peripheral tissues. The racemic base can be obtained by
KnSvenagel condensation between 2, 4-thiazolidinedione and the corresponding
4-substituted benzaldehyde (itself prepared in 2 steps from 2-chloropyridine),
followed by reduction of the benzylidene. Rosiglitazone was shown to be a
potent agonist of peroxisome proliferator activated receptor-gamma (PPARgamma),
a nuclear receptor involved in the differentiation of adipose tissue,
without activating liver PPAR-alpha receptors. This activation of PPAR-gamma
could mediate the down-regulation of leptin gene expression. In animal models,
Rosiglitazone has been shown to normalize glucose metabolism and reduce the
exogenous dose of insulin needed to achieve glycemic control. In patients with
Type II diabetes, daily doses (4 or 8 mg) of Rosiglitazone significantly improved
blood sugar control without affecting cardiac structure or function.
Rosiglitazone maleate is an antihyperglycemic agent in the thiazolidinedione class. It is indicated for the treatment of patients with type 2 diabetes mellitus.
일반 설명
A thiazolidinedione compound that acts as an anti-diabetic agent and serves as a potent and selective agonist of peroxisome proliferator-activated receptor-g (PPARg) (Kd ~40 nM) in fat cells. Shown to reduce fatty acid uptake and ameliorate lipid metabolism and insulin resistance in animal models of type II diabetes. Reported to activate both a1- and a2-containing AMPK complexes. Unlike troglitazone, it does not induce the activity of P4503A4. Significantly improves the differentiation of C3H10T1/2 stem cells into adipocytes. Shown to block estrogen synthesis by interfering with androgen binding to aromatase, but without affecting aromatase mRNA or protein expression.
