CJC-1295 (no DAC)
A modified growth hormone releasing hormone analog with a shorter half-life than DAC-conjugated CJC-1295, allowing more physiological GH pulsing.
Mod GRF 1-29 — sold as 'CJC-1295 no DAC' — is a tweaked fragment of the hormone that tells your pituitary to release growth hormone. It clears from the blood in minutes, so each shot makes one burst of GH rather than a steady rise, which is why it is injected daily and usually paired with a second peptide like ipamorelin. No human trial has ever been run on this exact molecule; everything known about it is borrowed from related compounds. It is not FDA-approved, an FDA advisory panel voted against allowing it to be compounded, and it is banned in sport.
What is CJC-1295 (no DAC)?
CJC-1295 without DAC (also called Modified GRF 1-29 or Mod GRF) is a modified version of the first 29 amino acids of growth hormone releasing hormone, carrying four substitutions and lacking the albumin-binding linker that gives CJC-1295 DAC its multi-day half-life. It clears from circulation in minutes rather than days, which is the whole point: each injection produces one discrete GH pulse instead of sustained receptor occupancy. The '30-minute half-life' quoted almost universally for this peptide is worth treating with care — no published human pharmacokinetic study of the four-substitution molecule exists, and the closest human measurement, for the single-substitution D-Ala2 analog, found a disappearance half-time of 6.7 minutes against 4.3 minutes for unmodified GHRH(1-29) (PMID 7962295).
What CJC-1295 (no DAC) Is Investigated For
CJC-1295 no-DAC (Modified GRF 1-29) is a GHRH analog investigated for GH pulse optimization, body composition improvement, sleep depth, and recovery — positioned within the GH-secretagogue space specifically as the pulsatile, physiological alternative to the longer-acting DAC-conjugated version. The strongest evidence is actually indirect: the modified GRF 1-29 peptide itself was never independently advanced as a clinical product, so efficacy claims rest on the broader GHRH(1-29) literature (notably the Corpas, Harman and Blackman trial at the National Institute on Aging, in which twice-daily GHRH(1-29) restored GH and IGF-1 levels in older men; PMID 1379256) and on the related analog tesamorelin, which has extensive RCT data for body composition and metabolic effects in HIV lipodystrophy. Direct human trial data specifically for no-DAC Mod GRF 1-29 is sparse. Its clinical positioning is largely mechanistic: rapid clearance preserving discrete GH pulses, typically stacked with a GHRP like ipamorelin for dual-pathway synergy. Even that rests on a number nobody has measured — no human pharmacokinetic study of the four-substitution peptide exists, and the 30-minute half-life quoted everywhere traces to no primary source. It is not FDA-approved, prohibited under WADA S2.2.4 (which names CJC-1295 and GHRH analogues), and the theoretical cancer-promotion and glycemic concerns that attach to any chronic IGF-1 elevation apply here regardless of the 'more physiological' framing.
History & Discovery
CJC-1295 no-DAC, more precisely called Modified GRF 1-29 or Mod GRF 1-29, shares its molecular backbone with the DAC-containing version but lacks the maleimidopropionic acid linker that tethers the peptide to serum albumin in vivo. Both compounds trace back to the same ConjuChem Biotechnologies program in Montreal in the early 2000s — the work that produced CJC-1295 as a long-acting albumin-binding GHRH analog. The four substitutions at positions 2, 8, 15, and 27 (D-Ala2, Gln8, Ala15, Leu27) that distinguish Mod GRF 1-29 from native GHRH(1-29) predate the ConjuChem program, and the usual one-line account of them compresses two separate research threads. Coy and colleagues introduced D-Ala at position 2 in the mid-1980s as a conformational constraint that raised potency — by 40- to 50-fold in the 1-29 species, and already described as a known modification by 1987 (PMID 3100799). The DPP-IV connection came from a different group: Frohman and colleagues identified dipeptidylpeptidase IV as the plasma enzyme cleaving GHRH at the Ala2-Asp3 bond and showed that a D-amino acid at position 1 or 2 blocks that hydrolysis (PMID 2565342). Only the D-Ala2 substitution does that work; Gln8, Ala15 and Leu27 contribute α-helical character, receptor affinity and oxidative stability rather than protease resistance. It is also worth noting that Coy's own pharmacokinetic study concluded the substitutions did not improve metabolic stability in the rat at all (PMID 2896343), while a later human infusion study found the D-Ala2 analog did clear more slowly than the parent (PMID 7962295) — the two findings have never been reconciled, and no study has measured the four-substitution peptide in humans. The 'no-DAC' designation is a research-chemical and compounding-pharmacy naming convention rather than a distinct ConjuChem product. In practical terms, no-DAC CJC-1295 is Mod GRF 1-29 — the same modified peptide that ConjuChem conjugated with the albumin-binding linker to produce the long-acting CJC-1295 DAC. Because the modified GRF 1-29 peptide itself was never independently advanced as a clinical product (ConjuChem's program focused on the DAC-conjugated version), there is no distinct FDA approval history or dedicated clinical trial program for no-DAC CJC-1295. It entered the research-chemical and compounding-pharmacy market in the 2010s as a shorter-acting alternative to CJC-1295 DAC, favored by clinicians who want to preserve natural pulsatility rather than produce sustained receptor occupancy. The 2026 Dominikowski Frontiers in Endocrinology clinical review names CJC-1295 without DAC among the unregulated GH-IGF1-axis PEDs that clinicians increasingly encounter in patients presenting for symptom evaluation — the review consolidates the peer-reviewed pharmacokinetic evidence against typical online self-administration protocols and proposes a clinician-oriented assessment algorithm, formalising the practical reality that no-DAC CJC-1295 has moved past the research-chemical fringe into routine clinical exposure without ever accumulating a dedicated human clinical dataset.
How It Works
Mod GRF 1-29 mimics your body's natural growth hormone releasing hormone, with four tweaks that make it harder for enzymes in the blood to chop up. It tells your pituitary to release growth hormone in a pulse, and that pulse is bigger when a GHRP is injected alongside it.
CJC-1295 no DAC binds the GHRH receptor on pituitary somatotrophs, activating adenylyl cyclase and raising cAMP, which primes the cells for GH release. The molecule carries four substitutions relative to native GHRH(1-29): D-Ala2, Gln8, Ala15 and Leu27. These do different jobs and are often wrongly lumped together. D-Ala2 is the stereochemical change that blocks dipeptidylpeptidase IV from cleaving the Ala2-Asp3 bond, which is the primary route by which plasma inactivates native GHRH (PMID 2565342); the substitution was originally introduced for potency rather than for protease resistance, and raised activity 40- to 50-fold in the 1-29 fragment (PMID 3100799). Gln8, Ala15 and Leu27 contribute α-helical stability, receptor affinity and resistance to methionine oxidation; none of them confers DPP-IV resistance. Note that the sequence is written D-Ala2, not Ala2 — native GHRH already carries L-alanine at position 2, so 'Ala2' would name no substitution at all. When combined with a GHRP, the two act through separate receptors: the GHRH analog primes the somatotrophs and amplifies pulse amplitude, while the GHRP acting at the ghrelin receptor GHS-R1a initiates the pulse. The combined release is greater than either produces alone. The GHRP initiates rather than increases the frequency of pulses — the dosing schedule, not the drug, determines how often a pulse occurs.
Evidence Snapshot
Human Clinical Evidence
Weak, and almost entirely borrowed. No human trial has ever been run on this molecule. The CJC-1295 Phase I/II data usually cited here measured the DAC-conjugated form, whose half-life is 5.8–8.1 days — the opposite pharmacology to the one this page describes — so it is not direct evidence for the no-DAC peptide. The nearest on-backbone human work is a 1992 trial of native, unmodified GHRH(1-29) twice daily in older men (PMID 1379256) and a 1994 infusion study of the single-substitution D-Ala2 analog in ten men (PMID 7962295). Beyond that the page leans on tesamorelin, a stabilized full-length GHRH(1-44) and a different molecule, which does have extensive RCT data for body composition and a controlled trial showing cognitive benefit.
Animal / Preclinical
Extensive. GHRH analogs are well-studied in animal models for growth, metabolism, and neuroprotection.
Mechanistic Rationale
Strong. GHRH receptor pharmacology is thoroughly understood.
Research Gaps & Open Questions
What the current literature has not yet settled about CJC-1295 (no DAC):
- 01No dedicated human clinical program exists for no-DAC CJC-1295 as a distinct product — clinical data is inferred from GHRH(1-29), modified GRF work, and the CJC-1295 DAC program rather than from direct trials of the no-DAC peptide.
- 02Long-term (>6 month) human safety data for Mod GRF 1-29 at adult wellness doses is absent.
- 03Whether pulsatile (no-DAC) vs. sustained (DAC) GHRH signaling produces meaningfully different long-term safety or efficacy profiles has not been tested head-to-head in humans.
- 04Optimal dosing cadence — whether 2x/day or 3x/day dosing produces clinically meaningful differences in IGF-1 or downstream outcomes — has not been characterized.
- 05Whether monotherapy vs. GHRP-stacked dosing produces clinically meaningful outcome differences has not been validated in controlled human trials; the stacking argument remains pharmacological.
- 06Pituitary desensitization risk with prolonged pulsatile stimulation is theoretical and unquantified.
- 07Compounding-pharmacy sourcing variability affects purity and potency but has not been systematically characterized.
Forms & Administration
Administered via subcutaneous injection, typically 2-3 times daily (before bed and upon waking are common). Usually combined with a GHRP like Ipamorelin at each injection. All injectable peptides should only be administered under the guidance of a qualified healthcare provider. Never self-administer without clinician oversight.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
Commonly discussed protocols for no-DAC CJC-1295 run 100 mcg per dose, administered 1–3 times daily. Many clinicians match the dose to the GHRP it is paired with (typically ipamorelin 100–300 mcg), keeping the two peptides at roughly equimolar ratios. Total daily doses above ~300 mcg of no-DAC rarely produce proportionally greater GH response because the GH pulse amplitude from a single injection is limited by somatotroph capacity rather than by GHRH-receptor availability.
Frequency
Rapid clearance means each injection produces one discrete GH pulse, then clears. The typical stacking rationale with a GHRP mirrors the CJC-1295 DAC + ipamorelin rationale: no-DAC CJC primes somatotrophs via the GHRH receptor while the GHRP triggers release via the ghrelin/GHS-R1a receptor. Combined, the two produce a GH pulse substantially greater than either alone — a synergistic rather than additive effect. Typical 2–3x/day dosing mimics the natural daily GH pulsatility pattern (morning, afternoon, bedtime) and is a key point of difference from DAC-containing CJC-1295, which provides continuous rather than pulsatile signaling.
Timing Considerations
Time of day
Bedtime aligns with the natural nocturnal GH pulse and is the anchor dose in most protocols. Multi-dose regimens typically add an early-morning fasted dose and a pre-workout dose.
Relative to meals
Fasted — at least 30 minutes before food and 2+ hours after a meal. The short-acting no-DAC form is especially sensitive to insulin and amino-acid blunting of the GH response.
Relative to exercise
Independent of training in single-dose protocols; multi-dose protocols commonly include a pre-workout injection on training days.
Cycle Length
Commonly discussed protocols run 8–12 weeks on, followed by a 4+ week break. Because no-DAC CJC-1295 preserves pulsatility and does not produce sustained receptor occupancy, the pituitary-desensitization argument for cycling is weaker here than for MK-677, though it remains a theoretical concern with any chronic GHRH-receptor stimulation. Some clinicians use no-DAC continuously in lower-dose protocols, but no long-duration human trial has validated this approach.
Protocol Notes
No-DAC CJC-1295 (Mod GRF 1-29) is supplied as a lyophilized powder, typically 2 mg or 5 mg per vial, reconstituted in bacteriostatic water. A 5 mg vial in 2 mL yields 2,500 mcg/mL; 100 mcg is approximately 0.04 mL or 4 units on an insulin syringe. Subcutaneous injection into the abdominal fat pad is standard. Because clearance is fast and the intent is to produce discrete pulses aligned with natural GH rhythm, injection timing matters far more than for DAC-containing CJC. Most protocols call for injection on an empty stomach (≥30 min before eating or 2+ hours after a meal) because elevated insulin and circulating amino acids blunt GH response. Common dosing windows are bedtime (aligning with the natural nocturnal GH pulse), early morning, and pre-workout — never immediately post-meal or post-carbohydrate intake. When stacked with ipamorelin, both peptides are typically drawn into the same syringe and injected together at each dosing window.
No-DAC CJC-1295 / Mod GRF 1-29 is not FDA-approved for any indication. The numbers above describe commonly-referenced protocols, not a prescription. Use should be supervised by a qualified clinician with appropriate lab monitoring.
Timeline of Effects
Onset
Sleep-depth improvements are the most reliably reported early benefit, typically within 1–2 weeks of bedtime or multi-daily dosing. Subjective recovery benefits (reduced post-workout soreness, faster training tolerance) follow in a similar window. Body-composition changes — modest fat reduction, lean mass preservation — typically require 4–8+ weeks of consistent use.
Peak Effect
Serum IGF-1 rises progressively over the first 4–6 weeks of multi-daily dosing and plateaus. The IGF-1 elevation magnitude from no-DAC monotherapy is modest compared to MK-677 or high-dose CJC-1295 DAC — reflecting the discrete-pulse profile and short half-life. Subjective benefits most commonly plateau around the 3-month mark. The argument for no-DAC over DAC is qualitative rather than quantitative: preserved pulsatility and a more physiological endocrine profile, not necessarily a larger peak effect.
After Discontinuation
Short half-life and non-suppression of endogenous GHRH mean pulsatile GH returns to baseline within 1–3 days of discontinuation. IGF-1 drifts back to pre-treatment levels over 2–4 weeks. Any accumulated body-composition or sleep benefits wane over weeks to a few months. No HPG-axis suppression, no post-cycle therapy required. The reversibility is clean — distinguishable from the longer tail of DAC-containing CJC, which persists in circulation for 1–2 weeks after the last dose.
Monitoring & Measurement
Bloodwork & Labs
- •IGF-1 (serum) — the practical response marker, drawn at a consistent time relative to the last dose
- •Fasting glucose and HbA1c — GH opposes insulin action
- •Lipid panel
- •Free T4 and TSH — uncorrected hypothyroidism blunts the GH response and will look like non-response
Functional & Performance Tests
- •DEXA scan for lean mass and visceral fat
- •Waist circumference
- •Overnight sleep quality via wearable — the most commonly reported subjective effect, and the one worth measuring rather than recalling
When to Test
Baseline, 6 weeks, and 12 weeks.
Interpretation & Notes
Two things make interpretation harder here than for the DAC form. First, nobody has published what IGF-1 does on sustained multi-daily Mod GRF 1-29 dosing, so there is no expected percentage rise to measure yourself against — treat the baseline-to-12-week change as the signal and ignore the specific numbers quoted in protocol discussions, which are extrapolated from DAC data. Second, because the peptide clears within minutes, IGF-1 rather than GH is the only practical readout; a spot GH level reflects whether you recently injected, not whether the protocol is working. Watch fasting glucose: a rise of more than about 15 mg/dL from baseline warrants a dose reduction, and an HbA1c climbing past 5.7 is the point to stop and reassess. If IGF-1 has not moved at all after 8 weeks, suspect a degraded or underdosed vial before concluding you are a non-responder — reconstitution technique and cold-chain handling are common failure modes in grey-market supply, and this peptide has no verified manufacturing channel. Panels are available direct-to-consumer through LabCorp, Quest, Marek Health and Ulta Lab Tests.
Common Questions
What's the difference between CJC-1295 with and without DAC?
The DAC (Drug Affinity Complex) is a maleimidopropionic acid linker that covalently binds the peptide to serum albumin in circulation, extending the measured half-life to 5.8–8.1 days (PMID 16352683). Without it the peptide clears in minutes, so each injection gives one discrete GH pulse rather than sustained elevation — which is why no-DAC is dosed daily or several times daily and DAC is dosed weekly. Many clinicians prefer no-DAC on the argument that pulsatile signalling is closer to normal physiology. One caveat on the numbers: the '30 minutes' usually quoted for the no-DAC form is not traceable to a published human study, and the nearest measured value is considerably shorter (see 'How long does Mod GRF 1-29 actually last?' below).
How long does Mod GRF 1-29 actually last in the body?
Shorter than the number everyone quotes, as far as anyone has actually measured. There is no published human pharmacokinetic study of the four-substitution Mod GRF 1-29 molecule itself. The closest human data come from a 1994 infusion study in ten men that tested the single-substitution D-Ala2-GHRH(1-29)-NH2: its disappearance half-time was 6.7 ± 0.5 minutes versus 4.3 ± 1.4 minutes for unmodified GHRH(1-29)-NH2, with metabolic clearance roughly halved (PMID 7962295). A 1988 rat study of several D-amino-acid-substituted analogs found half-lives of 4.7–7.4 minutes, none significantly different from the 6.2-minute parent compound, and concluded that the conformational changes which boosted potency 'did not alter the susceptibility of the peptide to proteolytic degradation' (PMID 2896343). So the honest statement is single-digit minutes for the measured analogs and unknown for this exact peptide. The '30 minutes' figure appears to be an extrapolation that got repeated into the status of fact. Nothing practical changes — the clearance is fast either way, and the discrete-pulse rationale for daily dosing holds — but the page should not report an unmeasured number as though it were data.
Should Mod GRF be used alone or with a GHRP?
It is most commonly combined with a GHRP like Ipamorelin for synergistic GH release. The GHRH analog amplifies the pulse initiated by the GHRP.
Who CJC-1295 (no DAC) Is NOT For
- •Active or recent-history cancer — GH and IGF-1 elevation may accelerate proliferation of existing malignancies.
- •Pregnancy — no human pregnancy safety data; reproductive-toxicology characterization is absent.
- •Breastfeeding — no data on transfer into breast milk or effects on nursing infants.
- •Diabetes or uncontrolled insulin resistance — GH opposes insulin action; glycemic monitoring is prudent with any GH secretagogue.
- •Pediatric use outside a diagnosed GH deficiency — development-related endocrine effects from unmonitored secretagogue use are a concern.
- •Active acromegaly or pituitary adenoma — further stimulation of GH-producing cells is contraindicated.
- •Uncontrolled hypertension or moderate-to-severe sleep apnea — GH elevation can worsen fluid retention and airway effects.
- •Known hypersensitivity to GHRH analogs or to excipients in compounded preparations.
Drug & Supplement Interactions
Documented clinical drug interactions for no-DAC CJC-1295 are sparse because no formal human post-marketing dataset exists. Class-derived concerns mirror those of other GHRH analogs. Glucocorticoids (prednisone, dexamethasone) blunt somatotroph responsiveness and attenuate the GH-releasing effect at the pituitary level. Somatostatin analogs (octreotide, lanreotide) directly oppose GHRH signaling and pharmacologically antagonize Mod GRF 1-29. Thyroid hormone status matters — uncorrected hypothyroidism reduces GH response. Glucose-regulating medications: insulin, sulfonylureas, and GLP-1 agonists may require dose adjustment as GH/IGF-1 rise over weeks of use. The glycemic effect of no-DAC is milder than MK-677's because of the pulsatile rather than sustained GH profile, but is not zero. Oral estrogens reduce hepatic IGF-1 generation and can blunt apparent lab responses — relevant for monitoring. As with any peptide therapy, concurrent medications should be disclosed to the prescribing clinician.
Safety Profile
Common Side Effects
Cautions
- • Not FDA-approved
- • Monitor IGF-1 levels
- • Use under clinician guidance
What We Don't Know
Long-term effects of sustained use for anti-aging purposes are not established through clinical trials.
Legal Status
United States
No-DAC CJC-1295 / Mod GRF 1-29 is not FDA-approved for any medical indication, is not on the 503A Bulks List, and as of FDA's 14 May 2026 nominations list appears in no 503A category. FDA's published compounding lists name 'CJC-1295' without distinguishing the DAC and no-DAC forms, and there has never been a separate FDA entry for Mod GRF 1-29. CJC-1295 was in 503A Category 2 (bulk drug substances that may present significant safety risks) and moved to FDA's 'nominated but withdrawn' table after its nominators withdrew their nominations; removal from Category 2 reflects that withdrawal, not a finding of safety, and is not authorization to compound. The more decisive event is one the no-DAC form does not escape by being unnamed. On 4 December 2024 FDA's Pharmacy Compounding Advisory Committee voted on five CJC-1295 bulk drug substances and rejected all of them for the 503A Bulks List — and it voted on the non-DAC forms separately from the DAC ones. CJC-1295 (free base) was rejected 0 for and 13 against and CJC-1295 acetate 1 to 12, alongside the three DAC forms at 0–13 each. So the peptide this page describes was specifically considered and specifically turned down, with a committee member noting the lack of evidence for effectiveness. It is widely sold in the research-chemical market labeled 'not for human consumption,' which is not an authorized channel for human use.
International
The European Medicines Agency and UK MHRA have not authorized Mod GRF 1-29 as a medicine. Australia's TGA classifies GHRH analogs and GH secretagogues as Schedule 4 prescription-only substances. Canada treats it as an unapproved investigational agent.
Sports & Competition
No-DAC CJC-1295 / Mod GRF 1-29 is prohibited under WADA's S2.2.4 (growth hormone releasing factors), which covers 'growth hormone-releasing hormone (GHRH) and its analogues' and names CJC-1295 among the examples — prohibited at all times, in and out of competition. The entry is identical in the 2026 list and in the 2027 list that takes effect on 1 January 2027, so nothing changes for athletes at the turn of the year. A WADA-compliant nano-LC-Orbitrap method for GHRH and its analogues in human urine has been published with detection limits of 0.5 ng/mL or better (PMID 41138283). Athletes subject to WADA code must avoid it.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
No-DAC CJC-1295 is just 'shorter-acting CJC-1295' — it's the same drug with faster clearance.
Reality
They are different molecules with different pharmacology. DAC-containing CJC-1295 has a maleimidopropionic acid linker that covalently binds serum albumin, giving a multi-day half-life and a flat, sustained exposure profile. No-DAC (Mod GRF 1-29) lacks this linker and clears in about 30 minutes, producing discrete GH pulses rather than sustained receptor occupancy. Dosing cadence, stacking rationale, and physiological effect shape differ materially.
Myth
No-DAC CJC-1295 is safer than DAC because it clears faster.
Reality
Faster clearance does reduce some specific concerns (chronic receptor occupancy, accumulation), and the pulsatile profile is arguably more physiological. But both versions elevate IGF-1 via the same downstream pathway, and the theoretical long-term concerns about IGF-1-mediated cancer promotion attach to both. 'Faster clearance' is not 'lower total exposure over a treatment period' — multi-daily dosing of no-DAC produces comparable cumulative IGF-1 elevation over weeks.
Myth
Mod GRF 1-29 is FDA-approved because it's 'just a fragment of natural GHRH.'
Reality
It is not FDA-approved for any indication. It is a modified peptide (four amino acid substitutions from native GHRH 1-29) that is not identical to endogenous GHRH, and it has never been through an FDA approval pathway. 'Fragment of a natural hormone' does not confer regulatory approval.
Myth
No-DAC CJC-1295 plus ipamorelin is 'safer than HGH.'
Reality
The stack preserves physiological pulsatility better than flat exogenous rhGH, which does attenuate some specific side effects like edema and carpal tunnel symptoms. But the downstream mediator — IGF-1 — is the same pathway, and the theoretical concerns about cancer promotion, glucose tolerance, and metabolic impact attach to the stack too. 'Safer in degree' is not 'fundamentally safe.'
Myth
Mod GRF 1-29 is undetectable in drug testing.
Reality
Validated methods exist. A WADA-compliant nano-LC-Orbitrap assay screens and confirms GHRH and its synthetic analogues — sermorelin/CJC-1293, tesamorelin and CJC-1295 — in human urine at detection limits of 0.5 ng/mL or better (PMID 41138283), and the substance is named outright on the Prohibited List at S2.2.4, so it does not fall through a definitional gap. Two honest qualifications. Clearance is fast, so the detection window is short and testing has to be well timed. And no published anti-doping case distinguishes the no-DAC form from CJC-1295 generally — sanctions involving CJC-1295 are on record, but the documented ones turned on possession and purchase rather than a positive test, so nobody should assume a no-DAC-specific analyte has been identified in competition.
Published Research
18 studiesThe emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration
Dominikowski and colleagues, Frontiers in Endocrinology 2026. Narrative clinical review that explicitly names CJC-1295 without DAC alongside CJC-1295 DAC, sermorelin, tesamorelin, GHRPs, AOD9604, and IGF-1 analogues as unregulated GH-IGF1-axis PEDs commonly encountered in self-administration protocols. Stratifies each into evidence tiers from regulatory-grade RCT data to complete absence of human studies, catalogues clinically reported adverse effects (prolactin and cortisol elevations, dysglycaemia, fluid-retention syndromes, musculoskeletal symptoms), and proposes a clinician-oriented assessment algorithm for exposure-history taking and symptom triage without legitimising off-label regimens.
Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance
A new era of doping? Use of peptide and peptide-analog drugs in recreational and professional sport and bodybuilding
Analysis of growth hormone releasing hormone and its analogs in urine using nano liquid chromatography coupled with quadrupole/orbitrap mass spectrometry.
Netnography of Female Use of the Synthetic Growth Hormone CJC-1295: Pulses and Potions.
Effects of growth hormone-releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults: results of a controlled trial.
Class context, not direct evidence. Participants self-administered tesamorelin, not Mod GRF 1-29 — different molecules, and no trial of this kind has ever been run on the no-DAC peptide. Cited because it is the best-quality evidence that GHRH-receptor agonism can move a cognitive endpoint at all.
Effects of tesamorelin, a growth hormone-releasing factor analog, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension.
Class context. This is the trial whose own abstract spells out the distinction the page relies on, describing the agent as tesamorelin, GHRH(1-44) — a full-length analog, not a GRF 1-29 analog like this peptide.
Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects.
Tesamorelin, a human growth hormone releasing factor analogue.
Class context. A review of tesamorelin, included because it is the only GHRH analog with a completed approval-grade dataset and therefore the nearest benchmark for what a properly developed GHRH analog looks like. It does not study modified GRF 1-29.
Metabolic effects of a growth hormone-releasing factor in patients with HIV.
Class context. The agent studied is tesamorelin; modified GRF 1-29 is not administered or measured in this trial.
Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse.
Prolonged stimulation of growth hormone and insulin-like growth factor I secretion by CJC-1295 in healthy adults
Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats
Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men
Differential effects of N-terminal modifications on the biological potencies of growth hormone releasing factor analogues with varying chain lengths.
Pharmacokinetic evaluation of superactive analogues of growth hormone-releasing factor (1-29)-amide.
Dipeptidylpeptidase IV and trypsin-like enzymatic degradation of human growth hormone-releasing hormone in plasma.
Frohman and colleagues, J Clin Invest 1989 — the paper that actually explains why Mod GRF 1-29 has a D-amino acid at position 2. It identified dipeptidylpeptidase IV as the plasma enzyme that cleaves GHRH at the Ala2-Asp3 bond and showed that a D-amino acid at position 1 or 2 prevents that hydrolysis. The DPP-IV resistance of this peptide is attributable to D-Ala2 alone; the other three substitutions do different work.
Growth hormone (GH)-releasing hormone-(1-29) twice daily reverses the decreased GH and insulin-like growth factor-I levels in old men
Quick Facts
- Class
- GHRH Analog
- Tier
- B
- Evidence
- Moderate
- Safety
- Moderate Data
- Updated
- Nov 2026
- Citations
- 18PubMed
Also known as
Tags
Peptide Families
Related Goals
Evidence Score
Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.