Telmisartan
Micardis
Telmisartan (Micardis) is a longevity & bioregulators research compound. Angiotensin II receptor blocker — but uniquely among ARBs it's also a partial PPAR-gamma agonist, the same receptor the glitazone diabetes drugs hit. That second mechanism is why it gets picked over losartan in performance circles: blood pressure control plus a measurable effect on insulin sensitivity and lipids.
Telmisartan quick facts
| Reported research dose | 20–80mg daily |
| Route | Oral |
| Frequency | 1x |
| Half-life | ~24 hours — the longest of the ARBs, so it holds through the morning BP surge. |
| Forms | Oral |
| Evidence level | Large trials for blood pressure; smaller ones for the metabolic effects |
The default BP drug for anyone on AAS or high-dose GH, because the PPAR-gamma activity works with the goal rather than against it. Run a CMP for potassium and creatinine before and after. ⚠️ Contraindicated in pregnancy.
How Telmisartan works
Angiotensin II receptor blocker — but uniquely among ARBs it's also a partial PPAR-gamma agonist, the same receptor the glitazone diabetes drugs hit. That second mechanism is why it gets picked over losartan in performance circles: blood pressure control plus a measurable effect on insulin sensitivity and lipids.
Proposed benefits
Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.
Where to get Telmisartan
Buy Telmisartan at AlgoRx →The evidence for Telmisartan
Graded by what exists behind each claim.
✅ Clinically validated
- Approved, with the ONTARGET trial (25,620 patients) showing it was non-inferior to ramipril for cardiovascular outcomes with better tolerability. The combination arm was worse than either alone — more renal dysfunction — which ended the practice of dual RAS blockade.
- The PPAR-gamma metabolic claim has not been shown to produce hard outcome benefit. Small studies report improved insulin sensitivity and lipid changes; no trial has demonstrated that this translates.
📊 Correlative data
- Widely prescribed. The longest half-life of any ARB at around 24 hours, which gives genuinely full 24-hour coverage and makes it the practical choice for anyone whose blood pressure escapes late in the dosing interval.
- It is used in body composition contexts specifically for the PPAR-gamma effect, which is off-label and not outcome-validated.
🧪 Theoretical / extrapolated
- An angiotensin II receptor blocker that is also a partial PPAR-gamma agonist — the same receptor the thiazolidinedione diabetes drugs target.
- Partial agonism is the interesting part. Full PPAR-gamma agonists like pioglitazone cause weight gain and fluid retention; a partial agonist should in principle capture insulin-sensitizing effects with less of that.
- It is also highly lipophilic and the most tissue-penetrating ARB, which is the proposed basis for effects beyond blood pressure — and remains a proposal.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Telmisartan actually does
The angiotensin half of this drug is the same as every other ARB: it blocks the AT1 receptor rather than the enzyme, so bradykinin is never raised and there is no ACE-inhibitor cough, and plasma renin and angiotensin II both climb because the negative feedback has been removed. If that were all telmisartan did, this page would be a copy of the losartan one. It is not, and there are three structural facts that make it different — only one of which is the famous one.
One: it needs no activation, and no cytochrome touches it. The label is unusually blunt: telmisartan is conjugated to a pharmacologically inactive acyl glucuronide, and “the cytochrome P450 isoenzymes are not involved in the metabolism of telmisartan” U.S. Food and Drug Administration 2012. Losartan depends on CYP2C9 to make its potent metabolite; telmisartan is fully active as swallowed and has no metabolite worth naming.
Two: it barely stays in the blood. Volume of distribution is about 500 liters, which the label reads as “indicating additional tissue binding” U.S. Food and Drug Administration 2012. Total body water in a 70 kg adult is roughly 42 liters, so a Vd of 500 L means the overwhelming majority of the drug in you at any moment is not in plasma — it is partitioned into lipid-rich tissue. That is the physical basis of every claim made for this molecule beyond blood pressure, and it is also why the plasma concentration is a poor proxy for what any tissue receptor is seeing.
Three: the PPAR-γ arm, stated precisely. Benson 2004 identified telmisartan as structurally unique among the ARBs and showed it functions as a partial agonist of PPAR-γ — the nuclear receptor the thiazolidinedione diabetes drugs occupy. The comparison in that paper is the part worth quoting: none of the other commercially available angiotensin II receptor antagonists activated PPAR-γ when tested at concentrations typically achieved in plasma with conventional oral dosing. So this is not an ARB class effect. It is one molecule.
And here is the number that decides whether any of it happens in a person. Telmisartan is more than 99.5% bound to plasma proteins, primarily albumin and α1-acid glycoprotein U.S. Food and Drug Administration 2012. PPAR-γ is an intracellular nuclear receptor; it can only be occupied by unbound drug that has crossed a membrane. A total plasma concentration and a free concentration differ here by more than two hundred-fold, and the free concentration is the one nobody has published. The 500-liter volume of distribution argues the tissue side of that equation could be much better than the plasma number implies; the 99.5% binding argues it could be far worse. Both arguments are legitimate, neither has been settled by measurement, and any page that presents the PPAR-γ effect as established is skipping the step.
Cell, rodent, human — and where it stops
Step one, in cells. Benson 2004: transactivation assays identify telmisartan as a partial PPAR-γ agonist, with the other marketed ARBs inactive at plasma-achievable concentrations. Cells in a dish, with far less binding protein around them than plasma has.
Step two, human pharmacokinetics, oral, healthy adults — and it is nonlinear, which almost nobody mentions. Absolute bioavailability is about 42% at 40 mg and about 58% at 160 mg, and the label states the pharmacokinetics are nonlinear over 20 to 160 mg, with greater than proportional increases in Cmax and AUC U.S. Food and Drug Administration 2012. Peak concentrations arrive at 0.5 to 1 hour, the terminal half-life is approximately 24 hours — the longest in the class — and food reduces AUC by about 6% at 40 mg and 20% at 160 mg.
Step two and a half, the human variability nobody controls for. Hirvensalo 2020 genotyped the glucuronidation step and found UGT1A3*2 carriers had telmisartan AUC reduced by 64% and 63% in heterozygous and homozygous men and by 57% and 72% in women, and that plasma concentrations were lower in men than in women overall. That is a two- to fourfold exposure spread produced by one gene and by sex, on a drug dosed in three tablet strengths.
Step three, the metabolic endpoint in humans, pooled. Takagi 2014 meta-analyzed 33 randomized trial reports enrolling 2,033 hypertensive patients and found telmisartan associated with a 15.89% greater reduction in HOMA-IR (95% CI −22.01% to −9.78%, P < 0.00001) than other antihypertensive drugs. Real, statistically solid, and measured in surrogate units.
Step four, the hard-outcome trial, which is where the argument stops. Yusuf 2008 — ONTARGET — randomized 25,620 patients with vascular disease or high-risk diabetes to telmisartan 80 mg, ramipril 10 mg, or both. At a median follow-up of 56 months the primary outcome occurred in 1,412 on ramipril (16.5%) and 1,423 on telmisartan (16.7%) — relative risk 1.01, 95% CI 0.94–1.09. Non-inferior. Not superior. And the combination arm obtained no additional benefit over monotherapy but had an increased incidence of renal dysfunction U.S. Food and Drug Administration 2012, which is the result that ended dual renin-angiotensin blockade as routine practice.
The obstacle, stated exactly. ONTARGET is the largest, longest test this molecule will ever get, and its comparator — ramipril — has no PPAR-γ activity at all. If the second mechanism translated into hard outcomes, 25,620 people over 56 months was the setting to detect it, and the answer came back 1.01. So the honest shape of the evidence is: the receptor pharmacology is real and unique in the class, the surrogate improvement in insulin resistance is real and pooled across 33 trials, and nothing connects the two to an outcome. The reason is not that anyone forgot to look. It is that when someone looked, with enormous power, the effect that should have shown up did not.
Telmisartan pharmacokinetics — how much of it actually gets in
Route: oral, once daily, and the half-life is the reason it is chosen. Terminal elimination half-life is approximately 24 hours U.S. Food and Drug Administration 2012, the longest of the ARBs. Steady state therefore takes roughly four to five days, and a single missed dose still leaves about half of one day’s exposure on board — which is exactly why it holds through the pre-dawn blood-pressure surge where a 2-hour-half-life ARB does not.
What degrades it: a conjugating enzyme, and nothing else. Telmisartan is conjugated to a pharmacologically inactive acyl glucuronide, and cytochrome P450 isoenzymes are not involved U.S. Food and Drug Administration 2012. Then it leaves almost entirely by bile: more than 97% is eliminated unchanged in the feces, with only 0.49% to 0.91% recovered in urine. Two consequences follow and both are practical. First, the entire CYP interaction list — azole antifungals, grapefruit, rifampin, ritonavir — is irrelevant to this drug, which is unusual enough to be worth knowing. Second, the exit is the liver and the bile duct, which is why the label tells prescribers to initiate at low doses and titrate slowly in hepatic insufficiency and biliary obstruction, and why ordinary renal impairment barely matters.
The oral barrier, and the nonlinearity inside it. Absolute bioavailability is ~42% at 40 mg and ~58% at 160 mg, with greater-than-proportional rises in both Cmax and AUC across 20–160 mg U.S. Food and Drug Administration 2012. Read that carefully: doubling the tablet more than doubles the exposure. Most drugs do the opposite. Food takes about 6% of the AUC at 40 mg and about 20% at 160 mg, so a large dose taken with a meal loses more than a small one does. There is no injectable or transdermal telmisartan with published pharmacokinetics, so the gut and the portal circulation are the whole delivery story.
The number that governs the mechanism, and the one that governs the person. Plasma protein binding is greater than 99.5% and the volume of distribution is about 500 liters U.S. Food and Drug Administration 2012 — a molecule that is almost entirely bound in blood and almost entirely out of the blood. And on top of that, Hirvensalo 2020 measured a 57–72% AUC reduction in UGT1A3*2 carriers. Combine the three and the plain statement is that two people on the same 80 mg tablet can differ several-fold in exposure for reasons neither of them can see, and nobody assays telmisartan clinically.
What would have to be true, and how you would know it was not
Four predictions. Two have a lab test attached, one is a dosing experiment anybody can run on themselves, and the fourth is the one that argues the interesting mechanism is not doing much.
1. Potassium and creatinine step up once and settle. A Comprehensive Metabolic Panel (CMP) before starting and again at 1–2 weeks. AT1 blockade removes aldosterone drive (potassium up) and dilates the efferent glomerular arteriole (creatinine up). The label’s own scale for the second: a creatinine rise of at least 0.5 mg/dL occurred in 0.4% on telmisartan against 0.3% on placebo U.S. Food and Drug Administration 2012, so a large move is not the expected course and is worth investigating rather than accepting.
2. If the PPAR-γ arm is doing anything at your dose, fasting insulin moves before the scale does. Fasting insulin and HbA1c at baseline and at 12 weeks, weight logged weekly. The pooled estimate to beat is a 15.89% reduction in HOMA-IR Takagi 2014; at a stable fasting glucose that is carried almost entirely by insulin, so it should be visible in the insulin number alone. Flat fasting insulin at 12 weeks with good blood-pressure control is the clean negative — it says you are getting the ARB and not the PPAR-γ agonist.
3. The dose-separation experiment, which nobody has published and which the label makes possible. Because absorption is nonlinear, 80 mg delivers more than twice the exposure of 40 mg U.S. Food and Drug Administration 2012, while the antihypertensive effect of an ARB is already close to its ceiling at the lower dose. So the prediction is directional and falsifiable: on the step from 40 to 80 mg, fasting insulin should move proportionally more than blood pressure does, if PPAR-γ occupancy is concentration-driven and AT1 occupancy is already saturated. If both move together, or neither does, the metabolic effect is hemodynamic and not nuclear.
4. The prediction that cuts against the drug’s reputation: you should not see the glitazone signature, and if you do not, that is evidence the mechanism is small. Full PPAR-γ agonists cause weight gain and fluid retention — that is the receptor being occupied. Telmisartan is a partial agonist Benson 2004, and in the label’s placebo-controlled trials discontinuation for adverse events was 2.8% on telmisartan against 6.1% on placebo U.S. Food and Drug Administration 2012. Weigh daily for eight weeks. No weight gain, no ankle swelling and no insulin movement together mean the most parsimonious reading is that you are taking a very good long-acting ARB, which is what ONTARGET measured and what ONTARGET found Yusuf 2008.
What nobody has tested yet
Nobody has published a free (unbound) telmisartan concentration in a human. This is the single measurement the PPAR-γ claim stands or falls on. The receptor is intracellular; only unbound drug reaches it; the drug is >99.5% protein bound U.S. Food and Drug Administration 2012; and the cell-culture work that established the mechanism was done in a dish with a fraction of plasma’s binding capacity Benson 2004. Equilibrium dialysis on steady-state plasma from a dozen people on 80 mg would produce the number in a week, and it does not exist.
Nobody has measured telmisartan in the tissue where PPAR-γ matters. A 500-liter volume of distribution U.S. Food and Drug Administration 2012 says most of the drug is somewhere other than plasma, and the somewhere that would matter is subcutaneous adipose and skeletal muscle. A fat biopsy and an LC-MS/MS assay in ten people at steady state would say directly whether tissue concentrations reach the range that activates the receptor in vitro. Nobody has done it.
No trial of this drug has ever genotyped UGT1A3. Hirvensalo 2020 showed a 57–72% swing in AUC from one polymorphism, plus a sex difference in the same direction. ONTARGET randomized 25,620 people by milligrams Yusuf 2008. If exposure varies two- to fourfold across a population, a null result on a concentration-dependent secondary mechanism is exactly what you would expect to see even if the mechanism were real in the high-exposure half. Nobody has re-analyzed an ARB trial by genotype.
And nobody has run the head-to-head that would size the partial agonism. Telmisartan against pioglitazone, matched for blood pressure, with a hyperinsulinemic-euglycemic clamp as the endpoint, would say what fraction of a full agonist’s insulin-sensitizing effect this drug actually delivers. The surrogate meta-analysis Takagi 2014 compares telmisartan with other antihypertensives, which answers a different question — is it better than a beta-blocker — and not the one people take it for.
Telmisartan — its own safety story, not its class's
The boxed warning first, because it is absolute. “When pregnancy is detected, discontinue MICARDIS as soon as possible” — drugs acting on the renin-angiotensin system “can cause injury and death to the developing fetus” U.S. Food and Drug Administration 2012. Fetal kidney development requires angiotensin II signaling. This is not a precaution, it is a contraindication with a mechanism.
The interaction almost nobody on this drug is told about is digoxin. The label reports median increases in digoxin peak plasma concentration of 49% and in trough concentration of 20% U.S. Food and Drug Administration 2012. Digoxin has a narrow therapeutic index; a 49% peak rise is a dose change. This is telmisartan’s own interaction — it is not an ARB class effect and it has nothing to do with cytochromes. Lithium is the other one: reversible increases in serum lithium and lithium toxicity are reported with renin-angiotensin blockers U.S. Food and Drug Administration 2012.
Renal function, and the specific way it goes wrong here. NSAIDs plus an ARB can cause deterioration of renal function including possible acute renal failure, particularly in the volume-depleted U.S. Food and Drug Administration 2012, and the ONTARGET combination arm — telmisartan plus ramipril — produced no additional benefit and more renal dysfunction than either drug alone Yusuf 2008. That result is why stacking an ARB on an ACE inhibitor, or on aliskiren, is not a way to get more of a good thing.
What is uniquely its own, in both directions. On the reassuring side: no cytochrome P450 involvement at all U.S. Food and Drug Administration 2012, so the entire azole/grapefruit/rifampin interaction list that applies to losartan does not apply here, and discontinuation for adverse events in the placebo-controlled trials was 2.8% on drug against 6.1% on placebo. On the unresolved side: the reason people outside a clinic take this ARB is the PPAR-γ activity, and a partial PPAR-γ agonist has never been given a long-term safety evaluation as a PPAR-γ drug. The class it borrows its interesting mechanism from carries fluid retention, weight gain and a heart-failure warning; whether a partial agonist at a fraction of the occupancy carries a fraction of that risk, or none of it, has not been studied and will not be by anyone selling either drug.
Sources read for this page
- U.S. Food and Drug Administration. MICARDIS (telmisartan) tablets, for oral use - full prescribing information (NDA 020850).. FDA approved labeling, revision 2012
- Benson SC. Identification of telmisartan as a unique angiotensin II receptor antagonist with selective PPARgamma-modulating activity.. Hypertension 2004 · PMID 15007034
- Yusuf S. Telmisartan, ramipril, or both in patients at high risk for vascular events.. N Engl J Med 2008 · PMID 18378520
- Takagi H. A meta-analysis of randomized trials of telmisartan versus active controls for insulin resistance in hypertensive patients.. J Am Soc Hypertens 2014 · PMID 25151319
- Hirvensalo P. UGT1A3 and Sex Are Major Determinants of Telmisartan Pharmacokinetics-A Comprehensive Pharmacogenomic Study.. Clin Pharmacol Ther 2020 · PMID 32498119
- Vanderheyden PM. Distinction between surmountable and insurmountable selective AT1 receptor antagonists by use of CHO-K1 cells expressing human angiotensin II AT1 receptors.. Br J Pharmacol 1999 · PMID 10193788
Telmisartan — safety, from the human record
Not a prediction. This one has been studied in people. What follows is drawn from the human record — trials, labels and pharmacovigilance — rather than from what the mechanism implies. Where the way it is used here differs from what was studied, the card says so. How evidence is graded here →
What the mechanism predicts
Derived from the molecule, not a trial.
- One axis, two places to block it. ACE inhibitors (lisinopril) stop angiotensin I becoming angiotensin II; ARBs (losartan, telmisartan) leave the conversion alone and block the receptor. The predicted consequences follow from the axis rather than from either drug: less vasoconstriction, less aldosterone, less sodium retention — and therefore first-dose hypotension, and reduced glomerular filtration pressure that shows up as a creatinine rise.
- The cough belongs to the ACE inhibitors only, and it is mechanism rather than allergy: ACE also degrades bradykinin, so blocking it lets bradykinin accumulate. That is why switching to an ARB resolves it, and why the cough is not a reason to avoid the whole axis.
- Telmisartan carries a second mechanism the others do not — partial PPAR-gamma agonism, the receptor the glitazones hit. That is the reason it gets chosen in performance circles, and it is also the reason its effects on lipids, insulin sensitivity and fluid balance are not simply 'losartan with better numbers'.
What has actually been reported
- A creatinine rise of up to about 30% after starting is expected hemodynamics, not injury, and is the single most common reason these get stopped unnecessarily. A larger or continuing rise is a different matter and needs review.
- Hyperkalemia is the dose-limiting effect for most people, and it compounds with potassium supplements, potassium-sparing diuretics, NSAIDs and reduced kidney function.
- Dry cough on ACE inhibitors is common and can begin weeks in. Angioedema is rare and is an emergency — it involves the airway, it can appear after months of uneventful use, and it does not reliably recur on rechallenge, which is why people talk themselves back onto it.
- Losartan is uricosuric — it lowers urate. That is a genuine advantage for anyone whose diuretic or diet pushes uric acid up, and it is a real difference between ARBs rather than marketing.
How to reduce the risk
Same mechanism as the prediction.
- Start low and take the first dose at night. Most first-dose hypotension is a one-off, and being horizontal for it is free.
- Book the two-week bloods when you start, not when you remember. Potassium and creatinine are the two things that go wrong, and neither produces a symptom until it is well advanced.
- Know the sick-day rule: hold these during significant vomiting, diarrhea or dehydration, and restart when you are eating and drinking normally.
- If the cough starts, ask about switching to an ARB rather than abandoning the axis — same benefit, no bradykinin.
What it does to your bloodwork
A fact about the assay.
- Electrolytes and creatinine 1–2 weeks after starting or after any dose change — that is where hyperkalemia and a filtration drop both show up, and both are silent.
- Repeat renal function during anything that causes volume depletion: a stomach bug, a hot race, a fasting protocol. The 'sick day rule' exists because dehydration plus RAAS blockade plus an NSAID is the classic acute kidney injury.
- Losartan lowers uric acid, so a urate result on it is not a clean baseline.
What it overlaps with
- NSAIDs blunt the antihypertensive effect and add to the renal risk. Potassium-sparing diuretics and potassium supplements add to the hyperkalemia risk. Neither is an interaction claim — both are the same mechanism arriving from two directions.
Don't run this if
- Pregnancy or trying to conceive. Both classes are fetotoxic in the second and third trimesters. This is not a caution, it is a contraindication.
- Bilateral renal artery stenosis, or a single functioning kidney with stenosis — the drop in filtration pressure is the whole problem there.
- A prior episode of angioedema on an ACE inhibitor.
- Do not combine an ACE inhibitor with an ARB. The combination increased harm without benefit in trials and there is no version of the longevity argument that survives that finding.
The honest unknown
- Whether any of the geroprotective signal survives in normotensive people. Every outcome trial behind these drugs enrolled people with hypertension, heart failure, diabetic kidney disease or established cardiovascular disease. Taking a blood-pressure drug for longevity with a normal blood pressure is an extrapolation, and the honest position is that it is untested rather than disproven.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Telmisartan — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Telmisartan moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Potassium and creatinine are the two that matter, and a CMP has both. ACE inhibitors and ARBs raise potassium by reducing aldosterone, and they cause a small expected rise in creatinine when started — a rise under about 30% is hemodynamic and is not kidney damage.
What to do: Baseline, then again 1–2 weeks after starting or after any dose increase. That second draw is the one people skip and it is the one that matters. - Cystatin C with eGFR — ◆ worth watching
A better read of kidney filtration than creatinine if you carry a lot of muscle — creatinine-based eGFR reads falsely low on a muscular person and turns a normal kidney into a scary number.
What to do: Worth one measurement if creatinine-based eGFR looks borderline and you train hard. - Uric Acid — ↓ expected to fall
Losartan specifically is uricosuric — it lowers uric acid, which is a genuine and under-used advantage if gout is in the picture. This is NOT a class effect; the other ARBs do not do it.
What to do: Relevant only if you have gout or a high baseline urate.
Beta-blockers are a different mechanism to the two above and carry their own specific caution: never stop one abruptly. Rebound tachycardia and hypertension are well documented. They also blunt the adrenaline response, which masks the early warning signs of hypoglycemia and flattens the training heart-rate response.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Telmisartan in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Telmisartan
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Chronic low-grade inflammation is the process most of these target |
| ApoB (Apolipoprotein B) | Counts the particles that actually cause plaque, unlike LDL-C |
| HbA1c (Hemoglobin A1c) | Glycation, which is the other half of the ageing story |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney — the two organs that clear everything you take |
| Complete Blood Count (CBC) with Differential | The cheapest broad screen there is |
The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.
Check results you already have → · All 103 markers A–Z
Telmisartan — frequently asked questions
What is Telmisartan?
Telmisartan (Micardis) is a longevity & bioregulators research compound. Angiotensin II receptor blocker — but uniquely among ARBs it's also a partial PPAR-gamma agonist, the same receptor the glitazone diabetes drugs hit. That second mechanism is why it gets picked over losartan in performance circles: blood pressure control plus a measurable effect on insulin sensitivity and lipids.
Is the full Telmisartan protocol on this page?
The reported research dose is on this page, along with how Telmisartan works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Telmisartan?
Telmisartan has an approximate half-life of ~24 hours — the longest of the ARBs, so it holds through the morning BP surge., which is part of what determines how often it's dosed.
What's the evidence behind Telmisartan?
Current evidence level: Large trials for blood pressure; smaller ones for the metabolic effects. Telmisartan is offered for research purposes only and is not an approved medicine.
Telmisartan inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Telmisartan is used for
Telmisartan appears under 2 goals in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Telmisartan is the arm with mortality data of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.