Telmisartan was patented in 1991 and came into medical use in 1999.[7] It is available as ageneric medication.[8] In 2022, it was the 228th most commonly prescribed medication in the United States, with more than 1million prescriptions.[9][10] It is available in combination with hydrochlorothiazide astelmisartan/hydrochlorothiazide;[11] with cilnidipine as telmisartan/cilnidipine;[12] and with amlodipine astelmisartan/amlodipine.[6][13]
Side effects includetachycardia andbradycardia (fast or slow heartbeat),hypotension (low blood pressure) andedema (swelling of arms, legs, lips, tongue, or throat, the latter leading to breathing problems).Allergic reactions may also occur.[6]
Due to its mechanism of action, telmisartan increases bloodpotassium levels. Combination with potassium preparations orpotassium-sparing diuretics could causehyperkalaemia (excessive potassium levels). Combination withNSAIDs, especially in patients with impaired kidney function, has a risk of causing (usually reversible)kidney failure.[15]
Telmisartan is an angiotensin II receptor blocker that shows high affinity for theangiotensin II receptor type 1 (AT1), with a binding affinity 3000 times greater for AT1 thanAT2.[citation needed]
In addition to blocking therenin–angiotensin system, telmisartan acts as a partial agonist ofperoxisome proliferator-activated receptor gamma (PPAR-γ), a central regulator ofinsulin andglucose metabolism. It is believed that telmisartan's dual mode of action may provide protective benefits against the vascular and renal damage caused bydiabetes andcardiovascular disease (CVD).[16][14]: 171 As a partial agonist, it activates the receptor by 25–30%. Clinical trials have shown that telmisartan increases insulin sensitivity, reduces cardiac fibrosis and hypertrophy, and improves endothilial function; all these effects can be attributed to its activity on PPAR-γ.[17] The kidney-protecting activity of telmisartan is attributed to both angiotensin II antagonism and improved endothelial function from PPAR-γ.[17]
Telmisartan does not cause rapid cancer growth like the PPAR-δ agonist GW 501516, but whether it causes a change in cancer rates is disputed. Short-term use is not associated with an increased incidence of cancer over other ARB drugs, according to a large 2016 analysis of UK patients.[29] A 2022 meta-analysis finds that a longer duration of taking ARBs (including telmisartan) is associated with an increase in cancer rates. Patients who have taken an ARB for more than 3 years appears 11% more likely to develop cancer.[30] A 2023 large-scale study on Lebanese patients finds that taking ARBs reduces the incidence of cancer, with greater effects on those who have taken the drug for a long time. A 2021 Korean study and a 2012 Japanese study finds similar results.[31]
^Yin SN, Liu M, Jing DQ, Mu YM, Lu JM, Pan CY (2014). "Telmisartan increases lipoprotein lipase expression via peroxisome proliferator-activated receptor-alpha in HepG2 cells".Endocrine Research.39 (2):66–72.doi:10.3109/07435800.2013.828741.PMID24067162.
^Stangier J, Su CA, Roth W (2000). "Pharmacokinetics of orally and intravenously administered telmisartan in healthy young and elderly volunteers and in hypertensive patients".The Journal of International Medical Research.28 (4):149–167.doi:10.1177/147323000002800401.PMID11014323.S2CID33299699.
Yusuf S, Teo KK, Pogue J, Dyal L, Copland I, Schumacher H, et al. (April 2008). "Telmisartan, ramipril, or both in patients at high risk for vascular events".The New England Journal of Medicine.358 (15). Massachusetts Medical Society:1547–1559.doi:10.1056/nejmoa0801317.hdl:2437/81925.PMID18378520.
Yusuf S, Teo K, Anderson C, Pogue J, Dyal L, Copland I, et al. (September 2008). "Effects of the angiotensin-receptor blocker telmisartan on cardiovascular events in high-risk patients intolerant to angiotensin-converting enzyme inhibitors: a randomised controlled trial".Lancet.372 (9644):1174–1183.doi:10.1016/S0140-6736(08)61242-8.PMID18757085.S2CID5203511.
