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Details

Stereochemistry ACHIRAL
Molecular Formula C33H29N4O2.Na
Molecular Weight 536.5987
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of TELMISARTAN SODIUM

SMILES

[Na+].CCCC1=NC2=C(C=C(C=C2C)C3=NC4=C(C=CC=C4)N3C)N1CC5=CC=C(C=C5)C6=CC=CC=C6C([O-])=O

InChI

InChIKey=RSGAIWOEJXRYRV-UHFFFAOYSA-M
InChI=1S/C33H30N4O2.Na/c1-4-9-30-35-31-21(2)18-24(32-34-27-12-7-8-13-28(27)36(32)3)19-29(31)37(30)20-22-14-16-23(17-15-22)25-10-5-6-11-26(25)33(38)39;/h5-8,10-19H,4,9,20H2,1-3H3,(H,38,39);/q;+1/p-1

HIDE SMILES / InChI

Description

Telmisartan is an orally active nonpeptide angiotensin II antagonist that acts on the AT1 receptor subtype. It was discovered by Boehringer Ingelheim and launched in 1999 as Micardis. It has the highest affinity for the AT1 receptor among commercially available ARBS and has minimal affinity for the AT2 receptor. New studies suggest that telmisartan may also have PPARγ agonistic properties that could potentially confer beneficial metabolic effects, as PPARγ is a nuclear receptor that regulates specific gene transcription, and whose target genes are involved in the regulation of glucose and lipid metabolism, as well as anti-inflammatory responses. This observation is currently being explored in clinical trials. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan works by blocking the vasoconstrictor and aldosterone secretory effects of angiotensin II. Telmisartan interferes with the binding of angiotensin II to the angiotensin II AT1-receptor by binding reversibly and selectively to the receptors in vascular smooth muscle and the adrenal gland. As angiotensin II is a vasoconstrictor, which also stimulates the synthesis and release of aldosterone, blockage of its effects results in decreases in systemic vascular resistance. Telmisartan does not inhibit the angiotensin converting enzyme, other hormone receptors, or ion channels. Studies also suggest that telmisartan is a partial agonist of PPARγ, which is an established target for antidiabetic drugs. This suggests that telmisartan can improve carbohydrate and lipid metabolism, as well as control insulin resistance without causing the side effects that are associated with full PPARγ activators. Used alone or in combination with other classes of antihypertensives for the treatment of hypertension. Telmisartan is used in the treatment of diabetic nephropathy in hypertensive patients with type 2 diabetes mellitus, as well as the treatment of congestive heart failure (only in patients who cannot tolerate ACE inhibitors).

CNS Activity

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
49.5 µM [IC50]
12.2 µM [IC50]
3.0 nM [IC50]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
MICARDIS
Preventing
MICARDIS

Cmax

ValueDoseCo-administeredAnalytePopulation
3200 ng/mL
160 mg single, intravenous
TELMISARTAN plasma
Homo sapiens

AUC

ValueDoseCo-administeredAnalytePopulation
3320 ng × h/mL
160 mg single, intravenous
TELMISARTAN plasma
Homo sapiens

T1/2

ValueDoseCo-administeredAnalytePopulation
17.7 h
160 mg single, intravenous
TELMISARTAN plasma
Homo sapiens

Doses

AEs

Drug as perpetrator​

Drug as victim

Tox targets

PubMed

Sample Use Guides

In Vivo Use Guide
Hypertension - 40 to 80 mg once daily Cardiovascular Risk Reduction - 80 mg once daily
Route of Administration: Oral
In Vitro Use Guide
Telmisartan (0.01-10 nmol/l) concentration dependently attenuated the angiotensin II-mediated (1 nmol/l) enhancement of EFS-evoked sympathetic outflow in the isolated rabbit thoracic aorta.