Tesamorelin: The Approved Drug Behind the TH9507 Code

Tesamorelin carries two labels. Catalogues list it as TH9507, the development code assigned by the company that built it. Regulators know the product as Egrifta, approved by the FDA in November 2010 [8].

Both names describe one molecule, and the gap between them hides an unusually complete evidence base.

More than 800 patients entered the phase 3 programme [6]. Paired liver biopsies exist, with transcriptomes run on them [19]. Someone has modelled the population pharmacokinetics [14]. Two controlled trials tested cognition and disagreed [10][23].

Most compounds in a research catalogue have nothing of the kind. Tesamorelin has a decade of controlled trials behind it, and the instructive parts of that record are the places where the effect stops.

Chemical identity

The molecule is human growth hormone-releasing hormone, residues 1 to 44, amidated at the C-terminus. A six-carbon acyl chain sits on the N-terminal tyrosine.

Property	Value
Systematic description	trans-3-hexenoyl-hGRF(1-44)-NH2
Common names	Tesamorelin, TH9507, Egrifta
Molecular formula	C221H366N72O67S
Average mass	5135.9 g/mol
Monoisotopic mass	5134.72 Da
CAS number	218949-48-5
PubChem CID	16137828
InChIKey	QBEPNUQJQWDYKU-BMGKTWPMSA-N
Residues	44
Stereocentres	88
Sulfur atoms	1, from the single methionine
N-terminal modification	trans-3-hexenoyl, E configuration

At 5,136 daltons tesamorelin sits at the top of the peptide range. Solid-phase synthesis of 44 residues is demanding, and that difficulty drives the purity questions covered below.

The sequence

The chain reads YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL, capped as the C-terminal amide. Three features matter in the laboratory.

One methionine sits at position 27, the only sulfur in the molecule. Methionine oxidises to the sulfoxide, adding 16 daltons.

Six arginines and two lysines outweigh two aspartates and two glutamates. Tesamorelin is therefore a basic peptide, and it behaves that way on ion exchange.

The C-terminal amide reproduces the native hormone. A lot ending in a free acid is a different molecule, one dalton heavier.

What the hexenoyl group does

Native GHRH(1-44) begins Tyr-Ala-Asp, and that opening pair is a liability.

Dipeptidyl peptidase IV strips N-terminal dipeptides from substrates carrying alanine in the second position. GHRH presents exactly that motif. Circulating hormone loses its first two residues, and its activity with them.

Acylating the tyrosine amine removes the free N-terminus the enzyme requires. Every residue past position 2 stays identical to the native hormone, so the receptor still sees a familiar ligand.

Baker and colleagues call tesamorelin a stabilised analogue of human GHRH [10]. One word covers the entire structural difference.

The 1992 enzymology that predicted it

Bongers and colleagues worked out the kinetics before this compound existed (PMID 1353684). They incubated synthetic human GRF and a series of analogues with purified placental DPP-IV, then followed the products by HPLC [1].

GRF(1-44)-NH₂ lost its N-terminal dipeptide at roughly 5 µmol/min/mg. The 1-29 and 1-20 fragments went at the same rate, so chain length beyond residue 20 contributed nothing.

Then came the result that mattered. Analogues lacking the alpha-amino group at Tyr1 resisted the enzyme outright, as did analogues carrying a methyl on that nitrogen. Blocking it stopped the reaction rather than slowing it.

Tesamorelin blocks the same nitrogen with an acyl chain. The design followed published enzymology by several years.

Where it sits among GHRH analogues

Two families of GHRH analogue circulate in research use, and they differ in chain length.

The 1-44 sequence is the full native hormone. A 1-29 fragment keeps the receptor-binding region and discards the rest, which is the scaffold behind sermorelin and the CJC-1295 series. Bongers and colleagues found both lengths equally vulnerable to DPP-IV [1].

Each family therefore needed its own stabilising modification. Tesamorelin took the acylation route on the full-length sequence, and other analogues substitute residue 2 or add albumin-binding chemistry instead. Trial evidence gathered here transfers to none of them.

Two names for one molecule

TH9507 runs through the early literature because that is what the sponsor called the compound in development.

Why the code persists

Falutz and colleagues used the code in the 2005 dose-ranging report [2]. Trials from 2007 onward use the generic name [3]. The pooled phase 3 paper hedges and prints both, titling itself a study of “tesamorelin (TH9507)” [6].

Reviews from the approval period searched both terms deliberately. Spooner and Olin list each among their search keys [8], which shows the split was causing retrieval problems by 2012.

PubChem records TH9507, TH 9507 and TH-9507 as synonyms of CID 16137828. Search one string without the others and half the record stays hidden.

What it means for sourcing

The practical consequence for a laboratory is narrow and real.

Material labelled TH9507 and material labelled tesamorelin should meet one specification, because they are one compound. Neither name tells you which synthetic route produced the lot in front of you.

Catalogue codes also travel without their literature. Anyone who orders TH9507 and searches that string alone will find the 2005 paper and little else. They will miss 806 patients of phase 3 data.

A releasing factor, not the hormone itself

Recombinant growth hormone delivers the finished hormone into circulation. Tesamorelin acts one step earlier.

It binds the pituitary receptor for the releasing factor and lets the pituitary secrete. González-Sales and colleagues state the sequence plainly: the analogue raises basal and pulsatile growth hormone secretion, and IGF-1 follows [14].

Where the feedback stays intact

Acting upstream leaves the regulatory machinery in place. Somatostatin tone and IGF-1 feedback both act on the pituitary, so both still shape output.

IGF-1 rose 81 percent over 26 weeks in the first phase 3 trial [3], and by 108 ng/mL in the pooled analysis [6]. Baker’s trial in older adults recorded 117 percent at half the dose, with values staying inside the physiological range [10].

A large proportional rise that still lands in range is the signature of a stimulated axis rather than a bypassed one.

What the IGF-1 rise measures

IGF-1 confirms that the pituitary responded. It does not predict the outcome anyone cares about.

Stanley and colleagues found inflammatory markers tracking with visceral fat change even after controlling for IGF-1 [7]. Ellis and colleagues watched IGF-1 climb while the cognitive score refused to follow [23].

Treat IGF-1 as an engagement marker. The fat compartment carries the signal.

Why the distinction shapes trial design

Tesamorelin acts through the pituitary, so it needs a functioning one. Any model system lacking an intact hypothalamic-pituitary axis cannot report on this mechanism.

Feedback also caps the achievable effect. Every trial of tesamorelin reports fat changes in the 10 to 20 percent range, and none reports anything larger.

Pharmacokinetics of a peptide that clears fast

González-Sales and colleagues modelled 38 subjects, patients and healthy volunteers together, on 1 or 2 mg daily for 14 days (PMID 25358450) [14].

Clearance and distribution

A one-compartment model with first- and zero-order absorption and linear elimination described the data.

Plasma clearance came out at 1,060 L/h, varying 33.6 percent between individuals. Volume of distribution was 200 L.

No covariate the authors tested predicted those parameters. Age failed, as did body size, race and HIV status. One thing did change with time: the fraction absorbed by the first-order process ran 13.1 percent higher on day 14 than on day 1.

Why a short pulse is the point

Set the clearance against the volume. Clearance exceeds the distribution volume five times over per hour, so plasma concentration collapses inside an hour of each injection.

That behaviour matches the pharmacology. A releasing factor provokes a secretory episode, and a sustained level would desensitise the receptor tesamorelin depends on.

Daily injection therefore produces a spike, not a plateau. Any assay sampling tesamorelin itself hours after a dose will find nothing, and the informative endpoints sit downstream.

Interactions

Teng and colleagues ran crossover studies against simvastatin and ritonavir to probe CYP3A [11]. Both drugs matter here, ritonavir as antiretroviral therapy and simvastatin for the lipid abnormalities that accompany it.

Simvastatin ratios sat inside the 80 to 125 percent window on every parameter. Ritonavir AUC ratios did too. Its lower bound on C_max reached 74.8 percent, which the authors read as a small absorption change rather than an interaction.

A 44-residue peptide cleared by peptidases has little reason to touch cytochrome activity.

The clinical programme

Six controlled trials of tesamorelin carry the weight, and they scale up rather than repeat.

Study	n	Duration	Primary fat finding
Falutz 2005, dose-ranging [2]	61	12 weeks	Trunk fat -9.2% at 2 mg; VAT -15.7%, not significant vs placebo
Falutz 2007 [3]	412	26 weeks	VAT -15.2% vs +5.0% placebo
Falutz 2010 [5]	404	26 + 26 weeks	VAT -10.9% vs -0.6% placebo
Pooled phase 3 [6]	806	26 + 26 weeks	VAT treatment effect -15.4%
Stanley 2014 [13]	50	26 weeks	VAT -34 cm² vs +8 cm² placebo
Stanley 2019 [18]	61	12 months	Hepatic fat fraction -37% relative

The dose-ranging study

The 2005 trial tested placebo against 1 mg and 2 mg in 61 patients over 12 weeks, under the TH9507 name [2]. Trunk fat fell 9.2 percent at the higher dose against a 0.8 percent rise on placebo.

Visceral fat moved 15.7 percent on 2 mg of tesamorelin and missed significance. Sixty-one patients over twelve weeks could not resolve an effect that size. The same endpoint at the same dose reached p below 0.001 once the phase 3 programme enrolled 412 [3]. Sample size defeated the finding, not biology.

Two features of the later trials appeared here first. Subcutaneous fat held steady in every group, and glucose did not move.

The two phase 3 trials

Both ran an identical design: 2 mg daily by subcutaneous injection, randomised 2:1 against matching placebo, 26 weeks, then a 26-week extension that re-randomised the treated arm.

The first enrolled 412 patients (PMID 18057338). Visceral fat fell 15.2 percent against a 5.0 percent gain on placebo. Triglycerides dropped 50 mg/dL while placebo rose 9 [3]. Adverse event rates matched, though more treated patients withdrew because of one.

A second trial enrolled 404 and produced a narrower separation, 10.9 percent against 0.6 percent [5]. Trunk fat, waist circumference and waist-hip ratio all improved, with limb and subcutaneous fat unchanged.

What the pooling added

Falutz and colleagues then pooled both trials: 806 patients, 543 on drug [6].

The pooled treatment effect on visceral fat was -15.4 percent. On subcutaneous fat it was -0.6 percent, at p = 0.08. Body image measures improved on patient and physician rating alike.

Two trials of one design reaching different effect sizes invites a reader to pick whichever suits them. Pooling settles that with the full sample.

Whether modern regimens change the answer

The phase 3 programme finished before integrase inhibitors became standard therapy, and those drugs carry their own association with weight gain.

Russo and colleagues addressed the gap using 38 participants on integrase inhibitor regimens inside the 61-patient liver trial [22]. Visceral fat fell by a median 25 cm² against a 14 cm² gain on placebo, p = 0.001. Hepatic fat fell 4.2 percent against 0.5 percent, p = 0.01. Hyperglycaemia occurred at similar rates in both arms.

Thirty-one participants completed that analysis, so it settles nothing alone. It remains the only dedicated evidence.

Visceral fat falls, subcutaneous fat holds

That pair of findings is the entire clinical argument for tesamorelin.

Visceral adipose tissue dropped 24 cm² against a 2 cm² gain on placebo. Subcutaneous tissue shifted 2 cm² in each direction and separated from placebo not at all [6].

Growth hormone reduces fat everywhere. Tesamorelin left the subcutaneous compartment alone across 806 patients, and the 2005 trial had reported the same preservation in 61 [2]. Nobody has explained the selectivity, and it remains the most interesting unexplained observation in the file.

Fat quality, not only quantity

Lake and colleagues measured fat density on CT rather than area, in patients treated with tesamorelin [20]. Denser fat means smaller adipocytes.

Across 193 responders and 148 placebo participants, visceral density rose 6.2 Hounsfield units against 0.3. Subcutaneous density rose 4.0 against 0.3, both at p below 0.0001.

Controlling for baseline density and area change left the effect standing. So the compartment that did not shrink still changed character.

Muscle

Adrian and colleagues applied segmentation software to the same scans [17].

Across four trunk muscle groups, density rose 1.56 to 4.86 Hounsfield units against placebo, all at p below 0.005. Lean muscle area rose 0.64 to 1.08 cm².

Those are small effects from an exploratory analysis restricted to responders. They point the same way as the fat density work.

Who responded

Roughly 70 percent of participants on tesamorelin met the 8 percent visceral reduction that the statistical plan had defined in advance as response [20].

Mangili and colleagues found three predictors: metabolic syndrome by the NCEP definition, triglycerides above 1.7 mmol/L, and white race [15]. None emerged at three months, only at six. Odds of reaching a visceral area below 140 cm² were 3.9 times higher on drug.

Rahman and colleagues checked whether dorsocervical fat changed the picture. It did not [21].

The effect ends when the dosing ends

Extension phases exist to answer this, and the answer leaves little room.

How the extension was built

At week 26 the investigators re-randomised patients already on drug. Some continued, some moved to placebo, and the blind held.

Falutz and colleagues report visceral fat reaccumulating in the switched group. They state that the effects do not last beyond the duration of treatment [4]. A second trial found six-month gains lost rapidly after the switch [5].

Patients who stayed on drug held roughly 18 percent through 52 weeks [4], and the pooled figure was -17.5 percent with waist circumference down 3.4 cm [6]. HDL fell slightly across the year, the one lipid measure moving the wrong way.

So tesamorelin suppresses a process rather than correcting one. Any protocol reading a washout as retained effect has misread the design.

One measure that did persist

The picture is not uniform, and one finding cuts against it.

Fourman and colleagues examined patients entering phase 3 with raised transaminases [16]. Among responders, alanine aminotransferase fell 8.9 U/L against a 1.4 U/L rise in non-responders, p = 0.004. Aspartate aminotransferase fell 3.8 against a 0.4 rise.

That improvement held across 52 weeks even in patients switched to placebo, despite partial reaccumulation of visceral fat. Something in the liver lagged behind the fat compartment on the way back up.

Glucose depends on whether the fat responds

Growth hormone raises blood glucose. Tesamorelin raises growth hormone in patients already carrying metabolic risk, so it had to answer for that, so the trials made glucose a primary safety endpoint.

Across 806 patients the finding was no clinically meaningful change at 26 or 52 weeks [6]. Stanley and colleagues found a rise at two weeks in their 50-patient trial, 9 mg/dL against 2 on placebo [13]. It had resolved by six months.

The responder analysis

Stanley and colleagues then split the treated arm by whether visceral fat had fallen 8 percent or more (PMID 22495074) [9].

Responders and non-responders diverged. At 52 weeks fasting glucose moved -1 mg/dL in responders and +8 in non-responders, p below 0.001. HbA1c moved 0.0 percent against 0.2 percent. Triglycerides and adiponectin split the same way.

Reading a glucose signal in this compound

Stimulating the growth hormone axis without shrinking the fat depot is the unfavourable case. Visceral reduction preserves glucose handling, and a trial average conceals two populations drifting in opposite directions.

A 12-month trial in fatty liver disease found no difference in fasting glucose or HbA1c [18]. The integrase inhibitor subgroup showed no excess hyperglycaemia either [22]. Both selected populations that responded.

For anyone designing work here, the rule follows. Measure the fat compartment and the glucose endpoint together, because one without the other cannot be read.

Liver fat and the NAFLD trial

Stanley and colleagues randomised 50 patients to tesamorelin or placebo, measuring liver fat alongside visceral fat [13]. Median liver fat fell 2.0 percent lipid-to-water against a 0.9 percent rise on placebo, a net effect of 2.9 percent at p = 0.003.

A follow-up trial made the liver its primary endpoint (PMID 31611038). Sixty-one patients with hepatic fat fraction of 5 percent or more took 2 mg daily or placebo for 12 months [18].

Hepatic fat fell 4.1 percentage points in absolute terms and 37 percent in relative terms. Thirty-five percent of treated participants finished below the 5 percent threshold against 4 percent on placebo. Paired biopsies showed fibrosis progression prevented across the year.

What the biopsies showed

Fourman and colleagues ran gene set enrichment analysis on those biopsy pairs [19].

Oxidative phosphorylation sets moved up. Sets covering inflammation, tissue repair and cell division moved down. Curated sets tied to favourable and to poor hepatocellular carcinoma prognosis moved in opposite and consistent directions.

Among treated participants, those changes correlated with the fibrosis-related gene score. Mechanism, tissue measurement and histology line up in the same patients here, which happens nowhere else in this record.

The cognition literature does not line up

Two controlled trials tested tesamorelin against cognitive endpoints thirteen years apart, and they disagree.

The 2012 trial

Baker and colleagues randomised 152 adults aged 55 to 87, sixty-six with mild cognitive impairment, to 1 mg daily or placebo for 20 weeks (PMID 22869065) [10]. Note the dose. It is half what the lipodystrophy programme used, given 30 minutes before bedtime.

Intent-to-treat analysis favoured the drug on the cognitive composite at p = 0.03. Executive function reached p = 0.005. IGF-1 rose 117 percent and body fat fell 7.4 percent.

Adverse events reached 68 percent against 36 percent on placebo. Fasting insulin rose 35 percent within the normal range in the impaired group, and not in the healthy one.

The 2025 trial

Ellis and colleagues tested 73 people with HIV and abdominal obesity on 2 mg daily for six months [23]. The design was open-label against standard of care, with no placebo arm.

Treated participants trended toward improvement at p = 0.060 while the comparison group did not. Between groups the difference came nowhere near significance, at p = 0.673. Waist circumference fell 2.7 cm more on drug. IGF-1 rose without tracking the cognitive change.

Reading the disagreement

The authors of the later trial flag insufficient power and the missing placebo arm themselves.

Different dose, different population, different design quality. Neither result refutes the other, and the trial carrying a placebo arm is the older one. Anyone citing tesamorelin for cognition is citing a 20-week trial at 1 mg in adults without HIV.

What the record does not establish

The indications that did not survive

Tesamorelin entered development as a general growth hormone axis stimulant, and the sponsor pursued a long list of uses.

Tomlinson catalogued them in 2006, midway through [24]. Phase 3 was running in HIV-associated lipodystrophy. Phase 2 covered sleep maintenance insomnia, chronic obstructive pulmonary disease, hip fracture recovery, immune dysfunction, influenza vaccination response and mild cognitive impairment.

One reached approval. The rest left no controlled evidence that survives, and their absence is informative. A compound tested across eight indications and approved for one has already been measured against most of the claims made for it.

The population problem

Every efficacy trial but one ran in people with HIV on antiretroviral therapy. The fat accumulation under treatment is a consequence of that therapy, so the population is not incidental, and read-across to ordinary central adiposity has no support here.

Makimura and colleagues supply the nearest exception: 39 obese adults with reduced growth hormone secretion and no HIV [12]. IGF-1 rose 102.9 µg/L against 22.8 on placebo, and that rise correlated with phosphocreatine recovery at R = 0.56.

What the paper reports is an association, not a between-group difference on the recovery measure. Entry also required reduced secretion on a stimulation test, so the trial selected an axis with room to move.

Trial populations are narrow in a second way. Participants in the phase 3 analyses were 87 percent male and 83 percent white [20][17]. A response predictor identified inside a sample that homogeneous deserves little weight until someone tests it elsewhere.

Missing comparisons

Stanley and colleagues measured four inflammatory and fibrinolytic markers across 410 patients [7]. All four tracked visceral fat at baseline. Treatment then moved one: tissue plasminogen activator antigen separated from placebo, and PAI-1 antigen did not.

No cardiovascular outcome trial exists. Visceral fat, triglycerides and these markers all stand in for outcomes nobody has measured.

Nobody has run tesamorelin head to head against recombinant growth hormone either. The selectivity argument rests on comparing separate literatures.

Controlled follow-up stops at 52 weeks in phase 3 and 12 months in the liver trial. Spooner and Olin flagged the absence of long-term safety data in 2012 [8], and that gap has not closed. Sustained IGF-1 elevation across years remains unaddressed.

Verifying research material

Tesamorelin has 44 residues and 88 stereocentres, so optical rotation offers no useful identity check. Identity rests on mass and sequence.

Mass and sequence

Average mass is 5135.9 and the monoisotopic mass is 5134.72. Mass spectrometry resolves both at this size.

The informative check is the acyl group. A des-hexenoyl impurity, meaning unmodified GHRH(1-44) amide, sits 96 Da lighter. Such material carries none of the DPP-IV resistance the modification exists to provide [1], so it clears within minutes rather than acting as a weaker analogue.

Geometry is harder. The hexenoyl double bond is E configured, and its Z isomer has an identical mass. Reversed-phase chromatography has to separate them, so a certificate reporting mass alone has not established identity.

Degradation and storage

Two routes of decay dominate, and each shifts the mass in a recognisable direction.

Methionine 27 oxidises to the sulfoxide, adding 16 Da. Being the only sulfur, that single residue accounts for every oxidative impurity in the spectrum.

Deamidation takes the other direction, each asparagine or glutamine adding 1 Da as material ages in solution. Bongers and colleagues saw buffer-induced deamidation at Asn8 during their enzyme work, below 5 percent of total substrate loss [1].

Store lyophilised tesamorelin cold and dry. Reconstitute immediately before use. Peptides this long also aggregate, and aggregates cost potency without changing the mass a routine assay reports.

What a certificate should report

Purity by reversed-phase HPLC with the gradient stated, mass by electrospray or MALDI against the 5135.9 average, and sequence confirmation.

Peptide content deserves as much attention as chromatographic purity. Lyophilised material carries counterions and water, so a lot at 95 percent purity may be 80 percent peptide by weight.

Kimera publishes third-party certificates of analysis for every lot in its COA database. Laboratories source TH9507 as a GHRH receptor agonist, often against CJC-1295 without DAC as the 1-29 analogue. Others run it alongside ipamorelin or IGF-1 LR3, where a different point in the axis is under study. Related work appears in the peptides category.

Common questions about tesamorelin

Identity and mechanism

Is TH9507 a different compound? No. TH9507 is the development code for the same molecule, and PubChem lists it as a synonym of CID 16137828. The 2005 dose-ranging trial used the code [2], and everything from 2007 onward used the generic name [3].

How does it differ from injecting growth hormone? Tesamorelin acts on the pituitary receptor for the releasing factor, so the pituitary secretes and its feedback still applies [14]. The visceral-selective fat effect is the observable consequence [6].

Why does subcutaneous fat stay put? Nobody has explained the selectivity. The observation holds across 806 pooled patients, at p = 0.08 for subcutaneous change against a -15.4 percent visceral effect [6].

How long does it last in plasma? Not long. Clearance of 1,060 L/h against a 200 L distribution volume means concentrations fall away inside the hour [14].

Evidence and limits

Does the effect persist after stopping? Visceral fat reaccumulated in patients switched to placebo, and the investigators state the effect does not outlast treatment [4][5]. Liver enzyme improvements in responders held longer [16].

Does it raise blood glucose? Not measurably in the pooled phase 3 data [6]. The responder analysis complicates that: patients whose visceral fat did not fall drifted 8 mg/dL higher by 52 weeks [9].

What is the strongest single result? The 12-month fatty liver trial. Hepatic fat fell 37 percent in relative terms, and paired biopsies showed fibrosis progression prevented [18].

Does it improve cognition? The two controlled trials disagree, and the 2025 trial found no between-group difference at p = 0.673 [23].

Does it still work on modern antiretroviral regimens? One dedicated analysis covered 38 participants on integrase inhibitors and found visceral and hepatic fat both falling [22]. That is the only evidence on the question.

Summary of the evidence

Identity: trans-3-hexenoyl-hGRF(1-44)-NH₂, C₂₂₁H₃₆₆N₇₂O₆₇S, 5135.9 g/mol, CAS 218949-48-5. Catalogue code TH9507, approved product Egrifta from November 2010 [8].

Design: the N-terminal acyl group blocks DPP-IV, which cleaves native GRF(1-44) amide at the Ala2-Asp3 bond and cannot touch analogues modified at the Tyr1 amine [1].

Pharmacokinetics: clearance 1,060 L/h, volume of distribution 200 L, no predictive covariates, minimal effect on CYP3A substrates [14][11].

Efficacy: visceral fat treatment effect -15.4 percent across 806 pooled phase 3 patients, subcutaneous fat unchanged, IGF-1 up 108 ng/mL [6]. Fat and muscle density both rose among responders [20][17]. Response rate near 70 percent, predicted by metabolic syndrome and baseline triglycerides [15], unaffected by dorsocervical fat [21].

Durability: none for the fat. Visceral tissue returns on withdrawal [4][5]. Transaminase improvements outlasted it [16].

Liver: hepatic fat down 37 percent in relative terms over 12 months, fibrosis progression prevented, with matching transcriptomic shifts in paired biopsies [18][19].

Limits: HIV populations throughout, no cardiovascular outcomes, no head-to-head against growth hormone, follow-up capped at 12 months [8][12][7]. Cognition data conflict [10][23]. Integrase inhibitor evidence rests on 38 participants [22]. Seven other indications produced nothing [24].

Status: supplied for laboratory research use only.

References

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Tesamorelin is sold for laboratory research use only. Not for human consumption, nor medical, veterinary, or household uses.

Literature retrieved from PubMed.