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Other Names: Micardis, TEL
Molecular Formula: C33 H30 N4 O2
Registry Number: 144701-48-4 (CAS) Chemical Name: (1,1'-Biphenyl)-2-carboxylic acid, 4'-((1,4'-dimethyl-2'-propyl(2,6'-bi-1H-benzimidazol)-1'-yl)methyl)- Chemical Class: Biphenyls and derivatives Phase of Development: Telmisartan is in Phase 2b development as an antifibrotic agent for HIV treatment.

(Compound details obtained from ChemIDplus Advanced,1 Treatment Action Group website,2 DrugBank,3 and ClinicalTrials.gov4)


Mechanism of Action: Antifibrotics. Telmisartan is an FDA-approved drug that is commonly classified as an angiotensin II receptor blocker (ARB). Its approved indications are for 1) treating hypertension and 2) risk reduction of cardiovascular events in certain individuals who are at high risk of developing major cardiovascular events and who are unable to take ACE inhibitors. As such, telmisartan works by selectively blocking angiotensin II – the main effector molecule of the renin-angiotensin system (RAS) – from binding to the AT1 receptor and inhibiting the vasoconstrictor and aldosterone-secreting effects of angiotensin II.2,5,6 Telmisartan is also a partial agonist of peroxisome proliferator-activated receptor-γ (PPAR-γ), a ligand-activated transcription factor involved in adipocyte differentiation and the regulation of lipid and glucose metabolism.3,7,8 Both angiotensin II and PPAR-γ play a role in inflammation and fibrosis, with angiotensin II inducing proinflammatory and profibrotic activities and PPAR-γ activation suppressing these actions.6,8,9

During HIV infection, immune activation induces fibrosis and damage to tissues.10–13 Both lymphoid tissue (LT) fibrosis as well as adipose tissue (AT) fibrosis may facilitate inflammation in the body and contribute to comorbidities. LT fibrosis may lead to increased apoptosis of naive T cells (CD4 and CD8 cells) prior to initiating ART and impaired reconstitution of naive T cells even after the initiation of ART. In addition, LT fibrosis may support the persistence of HIV reservoirs.10–12,14,15 Enhanced TGF-β1 production has been identified as an underlying mechanism of fibrosis; consequently, drugs aimed at inhibiting the TGF-β1 signaling pathway, such as telmisartan, may potentially be beneficial in HIV infection.11,12,15,16

Currently, researchers are evaluating whether telmisartan given in conjunction with ART during acute HIV infection can limit the establishment of HIV reservoirs in the central nervous system (CNS) and limit fibrosis in lymph nodes.17

Half-life (T1/2): Telmisartan has a terminal elimination half-life of 24 hours.5

Metabolism/Elimination: Telmisartan is metabolized in the liver by conjugation and forms an inactive glucuronide that is excreted in the urine. Telmisartan does not undergo CYP-mediated metabolism. The majority (>97%) of an intravenously or orally administered radiolabeled dose of telmisartan is eliminated as unchanged drug in feces, with just small amounts appearing in urine.5,18

Select Clinical Trials

Study Identifiers: ACTG A5317; TRAFIC study; NCT01928927
Sponsor: AIDS Clinical Trials Group
Phase: 2b
Status: This study has been completed.
Study Purpose: The purpose of this open-label study was to evaluate whether telmisartan added to ART could reduce lymph node or adipose tissue fibrosis.
Study Population:
  • Participants were adults with HIV who were virologically suppressed on ART for at least 48 weeks prior to study entry.
  • Participants had no changes in their ART regimen in the 12 weeks prior to study entry and had HIV RNA <50 copies/mL at screening.4,10
Selected Study Results:
Study Identifiers: SEARCH 018; NCT02750059
Sponsor: South East Asia Research Collaboration with Hawaii
Phase: 2
Status: This study is ongoing, but not recruiting participants.
Study Purpose: The primary purpose of this open-label study is to evaluate whether the administration of telmisartan plus ART during acute HIV infection can limit the establishment of HIV reservoirs in the CNS. Investigators will also assess whether telmisartan plus ART can limit the development of lymph node fibrosis.
Study Population:
  • Participants are adults with acute HIV infection who are enrolled in the SEARCH 010/RV 254 study.
  • Participants are able and willing to start ART after HIV diagnosis.17

Note: A separate SEARCH 018 study record (NCT02170246) is also listed on ClinicalTrials.gov. This is a Phase 1 trial that specifically analyzed the effect of telmisartan plus ART on HIV reservoir size. The study has been completed.2,19

Besides being studied for its impact on tissue fibrosis and HIV reservoir establishment in the CNS, telmisartan has previously been evaluated for its effects on other outcomes in individuals with HIV.

These completed studies include:
  • NCT01578772, a Phase 2 study that assessed whether telmisartan could improve blood vessel function in older adults with HIV who were on suppressive ART and who were at risk for cardiovascular disease.20
  • MATH (NCT01088295), a Phase 2 study that evaluated whether telmisartan could reduce adipose tissue volume in adults with HIV who were on suppressive ART.21
  • TAILoR (EudraCT: 2012-000935-18), a Phase 2 trial that evaluated the use of telmisartan for the reduction of insulin resistance in adults on ART.22

Adverse Events

ACTG A5317; TRAFIC study (NCT01928927):

In this study, 29 participants received ART plus telmisartan and 15 participants received ART alone. Of those participants who received ART plus telmisartan, three developed Grade 3 or 4 adverse events (AEs); none of these events, however, were found to be related to study treatment. No cases of hypotension were reported with telmisartan.23

Additional AEs known to be associated with telmisartan are described in the FDA-approved Full Prescribing Information for Micardis.5

Drug Interactions

Telmisartan does not undergo CYP-mediated metabolism. Except for the potential of telmisartan inhibiting drugs that are metabolized by CYP2C9, interactions are unlikely to occur between telmisartan and drugs that either inhibit CYP enzymes or are metabolized by CYP enzymes.5

Additional known interactions between telmisartan and coadministered drugs are described in the FDA-approved Full Prescribing Information for Micardis.5


  1. United States National Library of Medicine. ChemIDplus Advanced: Telmisartan. https://chem.nlm.nih.gov/chemidplus/rn/144701-48-4. Accessed September 13, 2019
  2. Treatment Action Group website. Research toward a cure trials. http://www.treatmentactiongroup.org/cure/trials. Accessed September 13, 2019
  3. DrugBank. Telmisartan. https://www.drugbank.ca/drugs/DB00966. Accessed September 13, 2019
  4. AIDS Clinical Trials Group. Effects of telmisartan on fibrotic and inflammatory contributors to end-organ disease in HIV-infected patients well controlled on antiretroviral therapy. In: ClinicalTrials.gov. Bethesda (MD): National Library of Medicine (US). Registered August 22, 2013. NLM Identifier: NCT01928927. https://clinicaltrials.gov/ct2/show/NCT01928927. Accessed September 13, 2019
  5. Boehringer Ingelheim Pharmaceuticals, Inc. Micardis: full prescribing information, October 25, 2018. DailyMed. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=cfb9309f-e0df-4a55-9542-0e869fce05fb. Accessed September 13, 2019
  6. Benigni A, Cassis P, Remuzzi G. Angiotensin II revisited: new roles in inflammation, immunology and aging. EMBO Mol Med. 2010;2(7):247-257. doi:10.1002/emmm.201000080
  7. El Akoum S. PPAR gamma at the crossroads of health and disease: a masterchef in metabolic homeostasis. Endocrinology & Metabolic Syndrome. 2014;03(01). doi:10.4172/2161-1017.1000126
  8. Tyagi S, Gupta P, Saini AS, Kaushal C, Sharma S. The peroxisome proliferator-activated receptor: a family of nuclear receptors role in various diseases. J Adv Pharm Technol Res. 2011;2(4):236-240. doi:10.4103/2231-4040.90879
  9. Wei J, Bhattacharyya S, Jain M, Varga J. Regulation of matrix remodeling by peroxisome proliferator-activated receptor-γ: a novel link between metabolism and fibrogenesis. Open Rheumatol J. 2012;6:103-115. doi:10.2174/1874312901206010103
  10. Utay NS, Kitch D, Fichtenbaum C, et al. Telmisartan does not improve lymph node or fat fibrosis in treated HIV infection. Poster presented at: Conference on Retroviruses and Opportunistic Infections (CROI); February 13-16, 2017; Seattle, WA. Poster 251. http://www.croiconference.org/sites/default/files/posters-2017/251_Utay.pdf. Accessed September 13, 2019
  11. Zeng M, Smith AJ, Wietgrefe SW, et al. Cumulative mechanisms of lymphoid tissue fibrosis and T cell depletion in HIV-1 and SIV infections. J Clin Invest. 2011;121(3):998–1008. doi:10.1172/JCI45157
  12. Zeng M, Southern PJ, Reilly CS, et al. Lymphoid tissue damage in HIV-1 infection depletes naïve T cells and limits T cell reconstitution after antiretroviral therapy. PLoS Pathog. 2012;8(1). doi:10.1371/journal.ppat.1002437
  13. Douek DC. Immune activation, HIV persistence, and the cure. Top Antivir Med. 2013;21(4):128-132.
  14. AIDS Clinical Trials Group website. HIV treatment associated with reduced scar tissue in fat, lymph nodes of people living with HIV. https://actgnetwork.org/node/815452. Accessed September 13, 2019
  15. Valcour Lab website. SEARCH 018: adjunctive therapy with telmisartan instituted with ART during acute HIV infection to reduce the establishment of CNS reservoirs of HIV and lymph node fibrosis. http://valcourlab.ucsf.edu/search-018-old.html. Accessed September 13, 2019
  16. Theron AJ, Anderson R, Rossouw TM, Steel HC. The role of transforming growth factor beta-1 in the progression of HIV/AIDS and development of non-AIDS-defining fibrotic disorders. Front Immunol. 2017;8. doi:10.3389/fimmu.2017.01461
  17. South East Asia Research Collaboration with Hawaii. Adjunctive therapy with telmisartan instituted with ART during acute HIV infection to reduce the establishment of CNS reservoirs of HIV and lymph node fibrosis. In: ClinicalTrials.gov. Bethesda (MD): National Library of Medicine (US). Registered May 30, 2015. NLM Identifier: NCT02750059. https://clinicaltrials.gov/ct2/show/NCT02750059. Accessed September 13, 2019
  18. National Library of Medicine and National Institute of Diabetes and Digestive and Kidney Diseases. LiverTox: Telmisartan. https://livertox.nih.gov/Telmisartan.htm. Accessed September 13, 2019
  19. Yale University. Adjunctive therapy with telmisartan instituted with ART during acute HIV infection to reduce the establishment of central nervous system reservoirs of HIV and lymph node fibrosis [Southeast Asia Research Collaboration with Hawaii (SEARCH) 018]. In: ClinicalTrials.gov. Bethesda (MD): National Library of Medicine (US). Registered May 22, 2014. NLM Identifier: NCT02170246. https://clinicaltrials.gov/ct2/show/NCT02170246. Accessed September 13, 2019
  20. University of California, Los Angeles. Telmisartan and Flow-Mediated Dilatation in Older HIV-Infected Patients at Risk for Cardiovascular Disease. In: ClinicalTrials.gov. Bethesda (MD): National Library of Medicine (US). Registered February 1, 2012. NLM Identifier: NCT01578772. https://clinicaltrials.gov/ct2/show/NCT01578772. Accessed September 13, 2019
  21. University of California, Los Angeles. Metabolic abnormalities, telmisartan and HIV infection. In: ClinicalTrials.gov. Bethesda (MD): National Library of Medicine (US). Registered March 16, 2010. NLM Identifier: NCT01088295. https://clinicaltrials.gov/ct2/show/NCT01088295. Accessed September 13, 2019
  22. EU Clinical Trials Register. EudraCT Number: 2012-000935-18; TAILoR – (telmisartan and insulin resistance in HIV): a dose-ranging Phase II randomised open-labelled trial of telmisartan as a strategy for the reduction of insulin resistance in HIV-positive individuals on combination antiretroviral therapy (cART). https://www.clinicaltrialsregister.eu/ctr-search/trial/2012-000935-18/GB. Accessed September 13, 2019
  23. Utay NS, Kitch DW, Yeh E, et al. Telmisartan Therapy Does Not Improve Lymph Node or Adipose Tissue Fibrosis More Than Continued Antiretroviral Therapy Alone. J Infect Dis. 2018;217(11):1770-1781. doi:10.1093/infdis/jiy064

Last Reviewed: September 13, 2019