Tesamorelin + CJC-1295 + Ipamorelin blend

Growth hormone release is governed by GHRH, which stimulates, and somatostatin, which inhibits. Tesamorelin and CJC-1295 without DAC are both GHRH analogues acting on the same receptor, with tesamorelin being the stabilised, FDA-approved one that has genuine randomised data for reducing visceral adipose tissue. Ipamorelin is a selective GHS-R1a agonist that suppresses somatostatin tone and independently stimulates the somatotroph, which is what turns a GHRH push into a much larger pulse. The awkward part of this formulation is that tesamorelin and CJC-1295 are redundant with each other - two agonists at one receptor, one of which has the evidence and one of which does not - and the six-to-three-to-three ratio structurally prevents you from reaching tesamorelin's evidence-based dose. Egrifta is 2 mg of tesamorelin daily; to draw 2 mg of tesamorelin from this blend you would take 4 mg of total blend, which also delivers 1 mg of CJC-1295 - roughly ten times the saturating GHRH dose - and 1 mg of ipamorelin, three to ten times what anyone uses. The blend is therefore a GH-pulse product with tesamorelin in it, not a way to take tesamorelin.

Targets: GHRH receptor (GHRHR), GHS-R1a (ghrelin receptor), Hypothalamic somatostatin neurons, Pituitary somatotrophs, IGF-1 axis and visceral adipose tissue

• · From a 12 mg vial in 2 mL you have 6,000 mcg/mL of total blend. 1,000 mcg of total blend gives 500 mcg tesamorelin, 250 mcg CJC-1295 and 250 mcg ipamorelin; 2,000 mcg gives 1,000 / 500 / 500. That is 1.7 to 3.3 units on a U-100 syringe, which is an awkwardly small volume - reconstituting in 3 mL instead makes the measurement more forgiving.
• · 250 mcg tesamorelin plus 125 mcg each of CJC-1295 and ipamorelin. Enough to find out whether you get water retention, morning grogginess or hand numbness before committing to a full dose.
• · Closer to physiological pulsatility and what more committed users run. It doubles your daily exposure to all three components simultaneously, which is worth stating plainly - there is no version of this where you increase the ipamorelin pulses without also doubling the GHRH load.

Work out your exact syringe units →

• commonWater retention and morning puffiness— The most reliable dose-related signal on this blend.
• commonFlushing or head rush after injection— The GHRH components. Passes in minutes.
• commonInjection-site redness or a small lump— Tesamorelin is notably more prone to site reactions than ipamorelin.
• commonVivid dreams or lighter sleep— Some report deeper slow-wave sleep, others the opposite.
• uncommonNumbness or tingling in the hands— Early carpal tunnel from fluid retention. Reduce the dose.
• uncommonJoint aching— Classic GH-excess signal on longer or higher-dose runs.
• uncommonRising fasting glucose— GH opposes insulin. Worth a fasting glucose check on any run past twelve weeks.

• Active or recent malignancy.
• Active proliferative diabetic retinopathy.
• Uncontrolled type 2 diabetes or significant insulin resistance.
• Known pituitary adenoma.
• Pregnancy and breastfeeding.
• Drug-tested athletes - prohibited under WADA S2.

• redundanttesamorelin — 6 mg of tesamorelin is already in the vial. Adding standalone tesamorelin on top means two GHRH-receptor agonists plus more of the same one.
• redundantcjc-1295-no-dac — Already in the vial, and already redundant with the tesamorelin sitting next to it.
• redundantipamorelin — 3 mg is already in the vial. If you want more ipamorelin, the blend forces you to take more GHRH with it.
• redundantipamorelin-cjc-1295-blend — This is the same stack with tesamorelin added. Running both is two GHRH analogues and a doubled ipamorelin dose for no additional mechanism.
• redundantmk-677 — MK-677 hits the same GHS-R1a arm ipamorelin already covers, and adds appetite and water retention on top of a blend that already causes fluid retention.
• conflictsomatropin — Exogenous GH suppresses the pituitary axis, leaving three secretagogues with nothing to release.
• cautioninsulin — GH raises insulin requirements. Diabetics on insulin should expect to need adjustment.

• · IGF-1 at baseline and at 8 to 12 weeks - aim for the upper half of the age-adjusted range, not above it.
• · Fasting glucose and HbA1c on runs longer than twelve weeks.
• · Morning hand numbness and ring or shoe tightness as early fluid-retention signals.
• · Verify which CJC variant the vial actually contains before the first dose; DAC and no-DAC are not interchangeable schedules.
• · Waist circumference if visceral fat is the goal, since that is the endpoint tesamorelin was actually studied against.

Tesamorelin is FDA-approved as Egrifta for HIV-associated lipodystrophy, but as a single agent - a compounded three-peptide blend containing it is not an approved product. The FDA moved ipamorelin and CJC-1295 out of the compounding-permitted category in 2023, which pushed blends like this from compounding pharmacies to research-chemical vendors. Prohibited in sport under WADA S2.

• Falutz et al., tesamorelin phase 3 trials in HIV-associated visceral adiposity, New England Journal of Medicine and JAIDS (trial)
• Teichman et al. 2006 JCEM, CJC-1295 pharmacokinetics and IGF-1 response in healthy adults (trial)
• Human studies of combined GHRH and GHRP administration showing synergistic GH release (trial)
• Egrifta (tesamorelin) prescribing information (label)
• Vendor labels and certificates of analysis for 12 mg tesamorelin / CJC-1295 / ipamorelin 6-3-3 blend vials (other)

Growth hormone output is set by three inputs, not one, and this vial addresses two of them. GHRH binds GHRHR on pituitary somatotrophs, a class B GPCR coupled to Gs. Activation raises cyclic AMP, activates protein kinase A, and drives both the release of stored GH and transcription of the GH gene via CREB and Pit-1. Tesamorelin and CJC-1295 do the same thing at the same receptor. That is the redundancy at the heart of this product: you have two agonists for one receptor, one of which has phase 3 data and one of which does not. Ghrelin receptor GHS-R1a is a Gq-coupled receptor acting through phospholipase C, IP3 and intracellular calcium release. Ipamorelin acting here does two things. It directly stimulates the somatotroph through a pathway that is independent of and additive to the cAMP arm, and it suppresses hypothalamic somatostatin tone. Somatostatin is the brake, and this is the part that matters most. A GHRH analogue alone pushes against a brake that is still engaged; adding a GHS-R1a agonist releases the brake while pushing. That is why the combination produces GH release substantially greater than either alone, a finding Bowers demonstrated in humans in 1990 and which has been reproduced many times since. The synergy is real and it is one of the better-established pieces of endocrine pharmacology anywhere in this corpus. What that means practically: adding tesamorelin to CJC-1295 adds nothing mechanistically. Both are already saturating the same Gs-coupled receptor at the doses in this vial. Adding ipamorelin to either is what produces the effect people notice. The formulation gives you a redundant GHRH pair and one genuinely complementary component. Downstream, GH acts on hepatic and peripheral GH receptors through JAK2-STAT5b to drive IGF-1 transcription, and IGF-1 mediates most of the anabolic effects while GH itself handles the lipolytic and insulin-antagonist ones. That split explains the clinical picture. The visceral fat reduction tesamorelin was approved for is a direct GH effect on visceral adipocyte lipolysis, which is why it shows up in visceral rather than subcutaneous fat. The fluid retention, carpal tunnel and joint ache are GH-mediated sodium and water retention. The rising fasting glucose is GH antagonising insulin at the level of hepatic glucose output and peripheral uptake. None of these are side effects in the incidental sense - they are the same hormone doing what it does. The formulation's defining flaw is arithmetic. Tesamorelin's evidence-based dose is 2 mg daily. Drawing 2 mg of tesamorelin from a 6-3-3 blend means 4 mg of total product, delivering 1 mg of CJC-1295 - roughly ten times a saturating GHRH dose - and 1 mg of ipamorelin, three to ten times normal. You cannot reach the studied tesamorelin dose without grossly overdosing the other two. This is a GH pulse product that contains tesamorelin, not a way to take tesamorelin.

The single most damaging error with GH blends is the CJC variant. CJC-1295 with DAC has a verified half-life of 5.8 to 8.1 days and holds GH elevated for six days or more from one dose. CJC-1295 without DAC clears in well under an hour. They are sold under nearly identical names and vendors are careless about the distinction. Dosing a DAC-containing vial nightly gives you a continuously elevated GH and IGF-1 level rather than pulses - which is a completely different endocrine intervention, produces far more fluid retention and glucose disturbance, and abolishes the pulsatility the whole design was meant to preserve. Confirm which variant you have from the certificate of analysis before the first injection. If the vendor cannot tell you, that is your answer about the vendor. The second failure is buying this to get tesamorelin. It does not work. The 6-3-3 ratio structurally caps how much tesamorelin you can take before the other two components become absurd. At the conventional 2 mg nightly total dose you are getting 1 mg of tesamorelin - half the studied dose. To reach 2 mg you would take 4 mg of blend and 1 mg each of CJC-1295 and ipamorelin. If visceral fat is your goal, this product cannot deliver the intervention that produced the trial result. The third is measurement volume. A 12 mg vial in 2 mL means the standard dose is 1.7 to 3.3 units on a U-100 syringe. That is a very small volume to measure repeatably, and dosing error at that scale is large in percentage terms. Reconstitute in 3 mL. The fourth is eating before the shot. Insulin blunts GH release substantially. People take this at bedtime after a late meal, get a fraction of the pulse, conclude it does not work, and increase the dose. Two hours fasted, minimum. The fifth is ignoring the early GH-excess signals. Morning hand numbness, rings that no longer fit, shoes that feel tight and aching joints are not incidental - they are fluid retention from too much GH, and they are the body telling you the dose is above what you need. The correct response is to reduce, not to push through and assume it settles. The sixth is running it indefinitely without checking IGF-1 or glucose. GH is counter-regulatory to insulin and the metabolic cost accumulates quietly. Someone who runs a GH blend for a year with no bloodwork and finds an HbA1c of 6.0 percent has paid a real price for whatever they gained. The seventh is expecting the wrong thing. This is not exogenous GH and it will not produce those effects. It raises GH within a physiological envelope constrained by somatostatin feedback and by your own pituitary reserve. In someone over fifty with a low baseline that can be a meaningful change; in a healthy 25-year-old with a well-functioning axis it often is not. Finally, this is prohibited under WADA S2 at all times, and unlike some things on this site the detection methods for GHRH analogues and GHRPs are established.

1. 500 mcgWeeks 1 to 2 — 500 mcg of total blend nightly - about 250 mcg tesamorelin, 125 mcg CJC-1295 and 125 mcg ipamorelin. From a 12 mg vial in 3 mL this is 1.25 units, which is genuinely hard to measure accurately, and the awkwardness is a real argument for reconstituting in 3 mL rather than 2. The purpose of this step is to find out whether you get water retention, morning grogginess or hand numbness before committing.
2. 1 mgWeeks 3 to 4 — 1,000 mcg of total blend nightly - 500 mcg tesamorelin, 250 mcg CJC-1295, 250 mcg ipamorelin. Dose at bedtime at least two hours after the last meal, because carbohydrate and the resulting insulin blunt the GH pulse substantially. This is where a lot of people should simply stay.
3. 2 mgWeeks 5 to 12 — 2,000 mcg of total blend nightly - 1,000 mcg tesamorelin, 500 mcg CJC-1295, 500 mcg ipamorelin. This is the top of the conventional range and it is where IGF-1 should be checked. Water retention and morning puffiness are the signals to hold rather than progress; hand numbness or ring tightness means come back down a step.
4. 1 mgOptional variant, not an escalation — 1,000 mcg twice daily, on waking fasted and at bedtime. Closer to physiological pulsatility and what more committed users run. Be clear that this doubles daily exposure to all three components at once - there is no version where you add an ipamorelin pulse without also adding a GHRH dose. Only worth considering after twelve weeks of tolerating the nightly protocol with acceptable IGF-1 and glucose.
5. —Week 12 to 16 — Four weeks off. The limit here is not receptor desensitisation - the GHRH arm barely desensitises and ipamorelin does so slowly - but IGF-1 drift, fluid retention and glucose. Recheck IGF-1 and fasting glucose before starting another block.

• GHRH receptor (GHRHR), class B GPCR, Gs-coupled

  Tesamorelin and CJC-1295 both agonise this receptor. Raises cAMP, activates PKA, triggers GH release and GH gene transcription through CREB and Pit-1. Two agonists at one receptor is the redundancy in this vial - at these doses the second one is adding very little.

• GHS-R1a (ghrelin receptor), Gq-coupled

  Ipamorelin. Phospholipase C, IP3 and calcium release drive somatotroph secretion by a pathway independent of the GHRH arm, and suppress hypothalamic somatostatin tone. This is the component that actually adds something, and the release of somatostatin inhibition is why the combination outperforms either mechanism alone.

• Hypothalamic somatostatin neurons

  Reduced somatostatin output takes the brake off the somatotroph. Without this, a GHRH analogue is pushing against active inhibition, which is the whole reason GHRH-alone protocols underdeliver relative to combined ones.

• Corticotroph ACTH and cortisol axis - notable for what does not happen

  Ipamorelin was characterised specifically as the first selective GH secretagogue, with no effect on ACTH or cortisol plasma levels at doses that released GH (Raun et al 1998). This is a genuine and verified advantage over GHRP-2 and GHRP-6, and it is the main reason ipamorelin is the ghrelin-receptor agonist in most blends.

• Hepatic GH receptor and the JAK2-STAT5b pathway

  Downstream of the pulse. Drives IGF-1 and IGFBP-3 transcription. IGF-1 mediates most anabolic effects and is the marker you actually measure, since GH itself is pulsatile and a single GH level is uninterpretable.

• Visceral adipocyte lipolysis

  The direct GH effect that tesamorelin was approved on. In the phase 3 programme, 2 mg daily produced a 15.2 percent reduction in visceral adipose tissue against a 5.0 percent increase on placebo over 26 weeks. This is the one endpoint in this whole record with a real number attached, and this blend cannot reach the dose that produced it.

• Falutz et al, tesamorelin in HIV-associated abdominal fat accumulation (phase 3, published in the New England Journal of Medicine) Phase 3 · n=412 · 26 weeks · 2007

  Percent change in visceral adipose tissue by CT. Tesamorelin 2 mg daily subcutaneously produced a 15.2 percent reduction versus a 5.0 percent increase on placebo (P<0.001). Triglycerides fell 50 mg/dL versus a 9 mg/dL rise on placebo, cholesterol ratios improved, and there were no significant differences in glycaemic measures over 26 weeks. This is the trial the whole tesamorelin story rests on - and note that this blend cannot deliver its 2 mg dose without a tenfold CJC-1295 overdose.

• Falutz et al, pooled analysis of two multicentre double-blind placebo-controlled phase 3 trials of tesamorelin with safety extension Phase 3 pooled analysis · n=806 · 26 weeks · 2010

  Visceral adipose tissue reduction in ART-treated HIV patients with excess abdominal fat, pooled across both pivotal trials with safety extension data. The larger and more robust dataset behind the approval.

• Falutz et al, long-term safety and effects of tesamorelin in HIV patients with abdominal fat accumulation Phase 3 extension · 2008

  Long-term safety and durability of visceral fat reduction beyond the initial 26-week period, including what happens on withdrawal. Relevant because it addresses the question everyone asks about GH secretagogues - whether the effect persists after stopping.

• Stanley et al, effects of tesamorelin on inflammatory markers in HIV patients with excess abdominal fat Phase 3 secondary analysis · n=410 · 2011

  Relationship between visceral adipose reduction and inflammatory markers. Useful for anyone claiming the blend has anti-inflammatory or longevity benefits, because it examines whether the metabolic improvement tracks the fat loss.

• Teichman et al, CJC-1295 pharmacokinetics and GH/IGF-1 response in healthy adults Early-phase randomised placebo-controlled · 2006

  Single subcutaneous doses of CJC-1295 with DAC produced dose-dependent 2- to 10-fold increases in mean plasma GH for 6 days or more and raised IGF-1 for 9 to 11 days, with an estimated half-life of 5.8 to 8.1 days. No serious adverse reactions. This is the source of the DAC half-life figure and the reason a DAC-containing vial dosed nightly is a genuine overdose pattern.

• Bowers et al, GH-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone Human pharmacology study · 1990

  Demonstrated that a GHRP and GHRH given together release substantially more GH than either alone in healthy men. The foundational human evidence for why any GHRH-plus-GHRP stack exists, including this one.

Night 1: some people notice deeper sleep or vivid dreams immediately, because GH secretion is coupled to slow-wave sleep and a bedtime pulse arrives in the right window. Others report lighter, more disturbed sleep. Both are common and neither predicts whether the compound will work for you. A brief flush or head rush within minutes of injection is the GHRH components and passes quickly. Week 1: sleep quality effects consolidate or do not. Injection-site reactions from the tesamorelin component appear here - it is notably more prone to site redness than ipamorelin. Some early water retention. Weeks 2 to 4: fluid retention becomes the dominant felt effect if the dose is too high. Morning puffiness, tighter rings, occasional hand tingling. Improved recovery between training sessions is commonly reported in this window and is the first plausibly real benefit. Weeks 4 to 8: skin quality, sleep and recovery changes are established by now. IGF-1 has been at its new level for weeks. Body composition changes are beginning but are not yet reliably measurable against normal variation. Weeks 8 to 12: the honest assessment point, and the one that matches the tesamorelin trial timeline. Check IGF-1 and fasting glucose. Waist circumference is the measure that matters if visceral fat is the goal, because that is the endpoint the underlying evidence was generated against - and it is a better measure than the scale, since GH shifts fat and water in opposite directions. Weeks 12 to 26: the trial that produced the 15.2 percent visceral fat reduction ran 26 weeks at a dose this blend cannot reach. Expect a smaller effect over a longer period, or run the standalone compound. After stopping: fluid retention resolves within one to two weeks and people often report looking leaner immediately, which is water rather than fat. IGF-1 returns to baseline over one to two weeks. Whether visceral fat reduction persists is exactly what the tesamorelin extension studies looked at, and it is the right question to ask before treating this as a cycled product.

The most important stacking note is negative and structural: do not add anything else that hits GHS-R1a or GHRHR, because this vial already covers both arms and one of them twice. MK-677 is the most common mistake. It is an orally active GHS-R1a agonist with a roughly 24-hour half-life, so adding it to ipamorelin means the ghrelin receptor is occupied continuously rather than pulsatilely. That defeats the entire design rationale of a short-acting secretagogue, which is to mimic physiological pulses and avoid desensitisation. It also stacks appetite stimulation and fluid retention on top of a blend that already causes fluid retention. If you want the convenience of MK-677, take MK-677 and skip the injections; do not run both. Exogenous GH is a straightforward conflict. Somatropin suppresses the hypothalamic-pituitary axis through IGF-1 negative feedback, leaving three secretagogues stimulating a pituitary that has nothing to release. Choose one approach. Insulin and insulin sensitisers deserve care in both directions. GH raises insulin requirements, so anyone on insulin should expect to need more of it, and should be checking glucose rather than discovering this by symptom. Conversely, metformin is a reasonable and cheap companion for someone running long GH blocks whose HOMA-IR is drifting, and it does not interfere with the GH pulse. Timing beats stacking here. The GH pulse is blunted substantially by insulin, so dose at least two hours after the last meal and keep carbohydrate away from the injection window. This single behavioural point does more for your results than any additional compound. BPC-157 and TB-500, or the Wolverine blend, are commonly run alongside during a recovery block. There is no mechanistic conflict and no data. Raising IGF-1 during a repair phase has a coherent rationale. Thyroid status is worth watching rather than supplementing pre-emptively. GH increases T4 to T3 conversion and can unmask marginal thyroid reserve, so the right response is a blood test, not a pre-emptive dose of levothyroxine. If your actual objective is the visceral fat reduction tesamorelin was approved for, the honest stacking advice is to stop buying blends and run standalone tesamorelin at 2 mg daily, which is the only protocol on this page with phase 3 data behind it.

Against the ipamorelin plus CJC-1295 blend: this is that stack with tesamorelin added, and tesamorelin is a GHRH analogue exactly like the CJC-1295 already in the vial. You are paying more for a second agonist at a receptor that is already being driven. The marketing frames tesamorelin as an upgrade because it is FDA-approved, but approval attaches to a 2 mg standalone dose you cannot reach here. If you want a GH pulse product, the two-peptide stack is cheaper and pharmacologically equivalent. Against standalone tesamorelin: not close if visceral fat is the goal. Standalone tesamorelin at 2 mg daily is the intervention with 412-patient and 806-patient phase 3 data, a 15.2 percent visceral adipose reduction, and an FDA approval. The blend delivers a quarter to a half of that dose. Choosing the blend over standalone tesamorelin for visceral fat is choosing convenience over the only real evidence in the category. Against MK-677: MK-677 is oral, cheap, raises IGF-1 reliably and needs no needles. It also occupies GHS-R1a continuously rather than pulsatilely, causes marked appetite stimulation, and produces more fluid retention and glucose disturbance. If you want simplicity, MK-677 is the pragmatic choice; if you want to preserve pulsatility, the injectable route is the reason to bother. Against exogenous GH: somatropin is more effective, far more expensive, legally controlled in most jurisdictions, and suppresses your own axis. Secretagogues work within a ceiling set by your pituitary reserve and somatostatin feedback, which is simultaneously their safety advantage and the limit on what they can do. Against a GLP-1 for fat loss: if the objective is losing fat generally rather than visceral fat specifically, semaglutide or tirzepatide have phase 3 data of an entirely different magnitude, and no GH blend competes. The specific case for tesamorelin is visceral adipose tissue in a population that had a defined problem with it - a narrower claim than how these blends are usually sold.

$140–$400/month. A 12 mg vial at the conventional 1 to 2 mg nightly total dose lasts six to twelve days, so a month is roughly two and a half to five vials. That makes this by far the most expensive blend in the class to run properly. Grey-market 12 mg vial pricing has generally sat in the fifty to ninety dollar range. Add bacteriostatic water, syringes, and the IGF-1 and metabolic bloodwork that this compound genuinely requires rather than merely benefits from. Worth comparing against standalone tesamorelin at 2 mg daily before committing. Observed market ranges, not verified against current pricing this session.

• ?The 6-3-3 ratio has no published rationale. It appears to be a vendor formulation choice, and it structurally prevents reaching tesamorelin's evidence-based dose.
• ?No trial of these three peptides together exists, in any population, at any dose.
• ?Nobody has shown that adding tesamorelin to CJC-1295 achieves anything a higher CJC-1295 dose would not, since both act at the same receptor and both are likely near saturation at these amounts.
• ?The tesamorelin evidence base is entirely in HIV-associated lipodystrophy. Whether a 15.2 percent visceral fat reduction transfers to a metabolically healthy person without that condition has not been established.
• ?Half-life figures for CJC-1295 without DAC and for ipamorelin were not verified in this session. Only the DAC version's 5.8 to 8.1 day half-life is verified, from Teichman et al 2006.
• ?No verified receptor binding affinity figures were resolved for tesamorelin at GHRHR or ipamorelin at GHS-R1a, so those fields are left empty.
• ?Tesamorelin's bioavailability and terminal half-life were not reported in the population PK abstract I could access; only apparent clearance and apparent volume of distribution are given, and both are apparent values that already incorporate unknown bioavailability.
• ?Molecular weights for all three components are omitted deliberately - none was verified in this session.
• ?The IGF-1 target of the upper half of the age-adjusted range is standard clinical practice for GH replacement, not a validated target for secretagogue use in healthy people.
• ?Whether long-term GH secretagogue use in people with normal pituitary function carries meaningful cancer risk is unresolved. The theoretical concern via IGF-1 is real and unquantified at these doses.
• ?The twelve-week-on, four-week-off convention is inherited from bodybuilding practice and has no clinical basis - the underlying trials dosed continuously for 26 weeks and longer.
• ?Participant numbers and durations for the Teichman CJC-1295 study and the Bowers synergy study were not resolved, so those fields are null despite the trials themselves being verified.
• ?Cost ranges are general market observation and were not verified against current vendor pricing this session.
• ?Component sequences and modifications are established chemistry but were not independently resolved this session, hence verified false.

• Metabolic effects of a growth hormone-releasing factor in patients with HIV Falutz J, Allas S, Blot K, Potvin D, Kotler D, Somero M, Berger D, Brown S, Richmond G, Fessel J, Turner R, Grinspoon S, New England Journal of Medicine, 2007 · PMID 18057338

  The pivotal tesamorelin trial. 412 patients, 26 weeks, 2 mg daily, visceral adipose tissue down 15.2 percent versus a 5.0 percent rise on placebo. Every claim made for the tesamorelin component of this blend traces back here, and reading it makes clear how far the blend's achievable dose sits below the studied one.

• Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in HIV-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data Falutz J, Mamputu JC, Potvin D, Moyle G, Soulban G, Loughrey H, Marsolais C, Turner R, Grinspoon S, Journal of Clinical Endocrinology and Metabolism, 2010 · PMID 20554713

  806 patients pooled across both pivotal trials with safety extension. The most robust efficacy and safety dataset for any peptide in this blend by a wide margin.

• Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation Falutz J, Allas S, Mamputu JC, Potvin D, Kotler D, Somero M, Berger D, Brown S, Richmond G, Fessel J, Turner R, Grinspoon S, AIDS, 2008 · PMID 18690162

  The extension data. Read this for what happens when you stop, which is the question that matters most for anyone treating a GH secretagogue as a cycled compound.

• Population pharmacokinetics of tesamorelin in HIV-infected patients and healthy subjects Gonzalez-Sales M, Barriere O, Tremblay PO, Nekka F, Mamputu JC, Boudreault S, Tanguay M, Clinical Pharmacokinetics, 2015 · PMID 25358450

  The source of every hard PK number in this record: apparent clearance 1,060 L/h, apparent volume of distribution 200 L, one-compartment model with mixed absorption, 38 subjects dosed 1 or 2 mg daily for 14 days, no effect of age, body size, race or health status. Also the finding that absorbed fraction rises 13.1 percent by day 14.

• Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA, Journal of Clinical Endocrinology and Metabolism, 2006 · PMID 16352683

  The CJC-1295 human data, and specifically the DAC version: half-life 5.8 to 8.1 days, GH raised 2- to 10-fold for 6 days or more, IGF-1 raised for 9 to 11 days. Anyone about to dose a CJC-containing blend nightly should read this first and then confirm which variant is in their vial.

• Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO, Journal of Clinical Endocrinology and Metabolism, 1990 · PMID 2108187

  The original human demonstration that a GHRP and GHRH together release far more GH than either alone. This is the single piece of real evidence underpinning the design of every GH blend on the market, including this one.

• Ipamorelin, the first selective growth hormone secretagogue Raun K, Hansen BS, Johansen NL, Thogersen H, Madsen K, Ankersen M, Andersen PH, European Journal of Endocrinology, 1998 · PMID 9849822

  The characterisation paper for ipamorelin, establishing GH release via a GHRP-like receptor with no effect on ACTH or cortisol. This selectivity is the reason ipamorelin rather than GHRP-2 or GHRP-6 is in this vial, and it is why cortisol and prolactin should not move on a genuine product.

• Impact of tesamorelin, a growth hormone-releasing factor analog, on CYP3A activity assessed with simvastatin and ritonavir Teng S, Potvin D, Mamputu JC, Vincent G, Zoltowska M, Morin J, Hatimi S, Michaud SE, High K, Ducharme MP, Clinical Pharmacology in Drug Development, 2013 · PMID 27121785

  The formal drug-interaction study. Relevant to anyone on a statin or a protease inhibitor who wants to know whether tesamorelin interferes with hepatic metabolism of their other medication.

• Reduction in visceral adiposity is associated with an improved metabolic profile in HIV-infected patients receiving tesamorelin Stanley TL, Falutz J, Marsolais C, Morin J, Soulban G, Mamputu JC, Assaad H, Turner R, Grinspoon SK, Clinical Infectious Diseases, 2012 · PMID 22495074

  Establishes that the metabolic benefit tracks the visceral fat reduction specifically, which matters if your reason for running this blend is metabolic rather than cosmetic.

• Effects of tesamorelin on inflammatory markers in HIV patients with excess abdominal fat: relationship with visceral adipose reduction Stanley TL, Falutz J, Mamputu JC, Soulban G, Potvin D, Grinspoon SK, AIDS, 2011 · PMID 21516030

  410 patients. The inflammatory marker analysis, useful for calibrating the longevity and inflammation claims that get attached to GH blends.