Corosolic acid test data

In vitro data

Corosolic acid has cytotoxic activity against several human cancer cell lines. The compound antagonized morphological modification of K-562 leukemic cells. The mechanism of action may be associated with suppression of protein kinase C activity In addition, cytotoxic activity has been documented against human cancer cell lines HL-60 (leukemia carcinoma), MCF-7 (breast carcinoma), and Hep-G2 (hepatic carcinoma).

Animal data

In a 2-stage Berenblum experiment on mouse skin papillomas, the inhibitory effect of corosolic acid was comparable or equivalent to beta-carotene, rosmarinic acid, and alpha-linolenic acid.


Corosolic acid may improve the insulin pathway. The action of insulin is mediated by tyrosine phosphorylation and initiated by the binding of insulin to the insulin receptor. Corosolic acid may act as an insulin sensitizer, enhancing insulin receptor B phosphorylation indirectly by inhibiting certain nonreceptor protein tyrosine phosphatases.Corosolic acid may also enhance GLUT4 glucose transporter processing of glucose uptake into muscle cells. Another study reported that corosolic acid inhibited gluconeogenesis by increasing the production of the gluconeogenic intermediate fructose-2,6-bisphosphate in isolated hepatocytes. Corosolic acid may promote glycolysis.

Animal data

Numerous animal experiments document the effect of corosolic acid on blood glucose. One study in rats found that 1% corosolic acid reduced blood glucose levels at 90 minutes after oral administration.Treatment with corosolic acid lowered plasma insulin levels and reduced the blood glucose levels in KK-Ay mice 2 weeks after a single oral dose of 2 mg/kg. Blood glucose in KK-Ay mice treated with corosolic acid decreased in an insulin tolerance test.Another experiment showed similar inhibitory action against increasing blood glucose levels.Increasing the concentration of corosolic acid may lead to enhanced glucose uptake activity.Corosolic acid induced muscle GLUT4 translocation from low-density microsomal membrane to plasma membrane in genetically-induced type 2 diabetic mice.

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