Irbesartan (SR-47436) is an Angiotensin 2 Receptor Blocker. The mechanism of action of irbesartan is as an Angiotensin 2 Receptor Antagonist.

Administering 7 mg/kg of Irbesartan daily to rats with congestive heart failure induced by lily alkaloid significantly inhibited skeletal muscle cell apoptosis and intramuscular atrophy. This effect is associated with a decrease in TNFα levels and is attributed to AT1 receptor blockade. Oral administration of 1 mg/kg Irbesartan in conscious rats with normal blood pressure reduced angiotensin II-induced hypertension, exhibiting effects similar to losartan treatment. However, its efficacy in normotensive monkeys was significantly higher than that of 10 mg/kg losartan.

At a concentration of 10 μM, Irbesartan inhibits the increase in mRNA and protein levels of integrins αv, β1, β3, and β5, osteopontin, and α-actinin in rat cardiac fibroblasts induced by angiotensin II, resulting in reduced cell adhesion to the extracellular matrix (ECM) proteins. Additionally, Irbesartan significantly induces the expression of the adipogenic marker gene, fatty acid-binding protein 2 (aP2), in 3T3-L1 cells in a concentration-dependent manner, with an EC50 of 3.5 μM and inducing effects being 3.3 times stronger at 10 μM. Also, 10 μM Irbesartan substantially induces peroxisome proliferator-activated receptor-γ transcriptional activity by 3.4 times, independent of its AT1 receptor antagonist action. Pre-treatment with 10 μM Irbesartan in rat vascular smooth muscle cells reduces angiotensin II-induced apoptosis by inhibiting angiotensin II internalization, demonstrating concentration dependency. Irbesartan competes with angiotensin II for binding to the AT1 receptor subtype with an IC50 of 1.3 nM and exhibits 10 times higher efficacy than Losartan in antagonizing AII-induced spasms in rabbit aortic rings, with IC50 values of 4 nM compared to Losartan's 14 nM and 25 nM, respectively.