In rats treated with telmisartan (0.1, 0.3, and 1 mg/kg), the specific binding of [3H]telmisartan to the surface of living RVSMC saturates rapidly and reaches equilibrium within 1 hour. Telmisartan exhibits slow dissociation from the receptor, with a dissociation half-life (t1/2) of 75 minutes, comparable to candesartan and nearly 5 times slower than angiotensin II (AngII).in vivo, telmisartan dose-dependently attenuates the blood pressure response to exogenous AngII ^[1].

Telmisartan (10 mg/kg/day) effectively inhibits aneurysm pathogenesis following PPE infusion, irrespective of whether treatment commences before or after aneurysm induction or is maintained for a short or prolonged duration. Telmisartan therapy is linked to decreased mRNA levels of CCL5 and matrix metalloproteinases 2 and 9 in aneurysmal aortae, without observable impact on PPARγ-regulated gene expression ^[2].

Telmisartan (1 mg/kg/day) significantly ameliorates neuronal loss and spatial acquisition impairment in 5XFAD mice, without altering NeuN expression in the hippocampus layer. Telmisartan treatment also reduces amyloid burden and microglial accumulation in the brain of 5XFAD mice, induces microglial polarization towards a neuroprotective phenotype, but does not alter the expression levels of NEP and IDE in specific brain areas of 5XFAD mice ^[3].

Telmisartan (0.05, 0.1, 1 mg/kg, pO.) significantly reduces immobility time, antagonizes depression and anxiety, and attenuates serum cortisol, NO, IL-6, and IL-1β in rats ^[4].

Telmisartan (50 μg, i.p.) leads to a 73.2% reduction in tumor growth in mice bearing xenografts derived from OE19 cells. Furthermore, telmisartan significantly alters miRNA expressionin vivo^[5].

In intact RVSMC cells and membrane preparations, telmisartan demonstrates concentration-dependent inhibition of 125I-AngII binding to AT1 receptors, exhibiting an IC50 of 9.2 ± 0.8 nM. Under the same conditions, angiotensin II displaces 125I-AngII with an IC50 value of 2.9 ± 0.5 nM. The specific binding of [3H]telmisartan to SMC membranes is competitively displaced by unlabeled telmisartan with an IC50 of 7.7 ± 1.8 nM and by cold AngII with an IC50 of 32.7 ± 5.7 nM ^[1].

Telmisartan (100 μM) decreases the proliferation of three EAC cell lines (OE19, OE33, and SKGT-4), induces cell cycle arrest in G0/G1 phase, regulates cell cycle-related proteins, promotes AMPK phosphorylation, and modulates cell cycle-related proteins through the AMPK/mTOR pathway in EAC cells. Telmisartan also inhibits the activation of RTKs, downstream effectors, and cell cycle-related proteins ^[5].