CJC-1295 vs Ipamorelin

This comparison reflects our 2026 review of the growth-hormone-peptide literature. We assess each compound by its mechanism on the GH axis and explain the rationale for the standard stack.

CJC-1295 and Ipamorelin target two distinct receptors on the somatotroph: CJC-1295 is a GHRH-receptor agonist that increases the amplitude of growth hormone pulses, while Ipamorelin is a selective ghrelin-receptor (GHSR-1a) agonist that increases pulse frequency. Stacked, they act as dual levers on the GH axis, producing a release profile that mechanistic reasoning predicts will be closer to native pulsatility than either peptide deployed alone, the two receptors activate independent intracellular cascades that converge on the same secretory machinery.

The honest caveat researchers rarely see stated plainly: no randomised controlled trial of the combination in healthy human adults was identified in the source set surveyed for this comparison. This article separates the receptor pharmacology from the marketing and grades the evidence quality at each tier.

Verdict: Which Wins?

For sustained, tonic GH-axis stimulation, CJC-1295 with DAC leads on duration (6–8 day half-life via albumin binding); for clean, selective pulse induction, Ipamorelin wins as a ghrelin-receptor agonist with no cortisol or prolactin spillover; Sermorelin, the older and more-studied GHRH analogue, fits research needing a short-acting (~10–20 min) GHRH signal closer to native pulsatility. The single key differentiator is mechanism and duration: CJC-1295 and Sermorelin are both GHRH-receptor agonists (long-acting vs short-acting), while Ipamorelin acts on a separate receptor (GHSR-1a) entirely, which is why a GHRH analogue is stacked with Ipamorelin rather than substituted for it.

Key Takeaways

• CJC-1295 increases GH pulse amplitude via GHRH-R/cAMP signalling; Ipamorelin increases pulse frequency via GHSR-1a/calcium signalling
• The two receptors activate independent intracellular pathways that converge on somatotroph secretory machinery, making the combination mechanistically non-redundant
• No published randomised controlled trial of the CJC-1295 + Ipamorelin combination in humans exists; claims of superiority rest on receptor pharmacology rather than trial data
• CJC-1295 with DAC has a half-life of 6–8 days (tonic GHRH tone); Ipamorelin has a half-life of approximately 2 hours (discrete pulses)
• Neither peptide holds UK marketing authorisation; both are supplied for laboratory research use only

What Are CJC-1295 and Ipamorelin?

CJC-1295 is a synthetic 30-amino-acid GHRH analogue, typically supplied with a Drug Affinity Complex (DAC) modification that covalently binds endogenous albumin and extends its circulating half-life to roughly 6–8 days. Ipamorelin is a selective pentapeptide ghrelin-receptor (GHSR-1a) agonist with a half-life of approximately 2 hours, designed to trigger GH release without measurable effects on prolactin, adrenocorticotropic hormone (ACTH) or cortisol. Neither compound holds a UK marketing authorisation from the Medicines and Healthcare products Regulatory Agency (MHRA); both are supplied for laboratory research use only under the Human Medicines Regulations 2012.

The mechanistic split matters for protocol design. CJC-1295 (with DAC) provides a continuous, low-level tonic stimulation of the somatotroph GHRH receptor, raising the ceiling of each endogenous GH pulse without itself generating discrete pulses. Ipamorelin acts on a separate receptor (GHSR-1a) and produces a sharp, short-lived secretagogue spike that mimics ghrelin's pulse-initiating role. The two pathways converge on the same somatotroph but use independent intracellular cascades (Gs/cyclic adenosine monophosphate (cAMP) for GHRH-R; Gq/phospholipase C (PLC) for GHSR-1a, per standard receptor pharmacology), which is the mechanistic basis for the supra-additive release seen in rodent and in vitro work.

Evidence Tier: What This Article Rests On

Receptor pharmacology (GHRH-R, GHSR-1a coupling) is well-characterised in vitro and in animal models because these receptor families have been studied extensively since the 1990s. Secondary clinical sources reviewed here describe it consistently but do not substitute for the International Union of Basic and Clinical Pharmacology/British Pharmacological Society (IUPHAR/BPS) primary entries.

CJC-1295 DAC half-life (approximately 6–8 days) is cited widely in secondary literature because the extended albumin-binding profile is the defining feature of the DAC modification. The original Jetté et al. 2006 pharmacokinetic data were not retrieved in this source set.

Ipamorelin half-life (approximately 2 hours) and selectivity are described in commercial and clinical-practice sources because the short duration and lack of cortisol/prolactin co-secretion are the key differentiators from earlier GH-releasing peptides (GHRPs). This has not been independently verified against the Raun et al. 1998 primary paper here.

Combination RCT data in healthy adults, none identified because no such trial has been published in the indexed literature.

Regulatory status (UK), no MHRA marketing authorisation for either peptide identified at time of writing (2026). Researchers should verify against MHRA publications directly.

Researchers working through dosing logic next should see the CJC-1295 + Ipamorelin dosing protocol; for comparison against the closest licensed GHRH analogue, the Tesamorelin dosing protocol is the natural reference point.

Mechanism of Action: Two Different Receptors

CJC-1295 and Ipamorelin act on two structurally unrelated G-protein-coupled receptors with orthogonal downstream cascades. This makes the stack mechanistically non-redundant rather than additive in the trivial sense. CJC-1295 binds the GHRH receptor (GHRH-R) on anterior pituitary somatotrophs and signals via Gs/adenylyl cyclase. Ipamorelin binds the growth hormone secretagogue receptor (GHSR-1a) and signals via Gq/phospholipase C. The two cascades converge on GH exocytosis but reach it through independent second messengers.

For CJC-1295, GHRH-R activation increases intracellular cAMP via adenylyl cyclase, which activates protein kinase A (PKA). PKA phosphorylates substrates that trigger vesicular GH release and drives cAMP response element binding protein (CREB)-mediated transcription of the GH1 gene, raising the size of the releasable pool. The mechanistic consensus traces to Mayo's GHRH-R characterisation work in Endocrine Reviews (1992) and remains the standard interpretation in current secondary literature because the cAMP/PKA pathway has been confirmed across multiple cell types and species. The functional consequence is pulse amplitude amplification: when an endogenous GHRH pulse fires, more GH is released per pulse.

For Ipamorelin, GHSR-1a activation couples to Gq, stimulating phospholipase C to cleave phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 mobilises Ca²⁺ from endoplasmic reticulum stores. The rise in cytosolic Ca²⁺ triggers immediate exocytosis of pre-formed GH vesicles. This is the Howard et al. Science (1996) cascade for the then-orphan GHS receptor, and it has been replicated in subsequent characterisation work because the IP3/calcium mechanism is fundamental to ghrelin-receptor biology. The functional consequence is a discrete, short-duration GH spike, effectively initiating a pulse rather than enlarging an existing one.

Receptor-Pathway Comparison

Because cAMP/PKA and Ca²⁺/PLC operate as parallel inputs into the same secretory machinery, co-administration recruits two independent control levers on a single cell. That is the pharmacological rationale behind the CJC-1295 + Ipamorelin dosing protocol. It is also what distinguishes CJC-1295 from the licensed comparator covered in the Tesamorelin dosing protocol, Tesamorelin is itself a GHRH-R agonist and therefore not orthogonal to CJC-1295. Researchers should cross-check receptor IDs and canonical coupling against the IUPHAR/BPS Guide to Pharmacology 2025 database before finalising any protocol document.

CJC-1295 vs Ipamorelin: Side-by-Side Comparison

CJC-1295 is a long-acting GHRH analogue that raises pulse amplitude. Ipamorelin is a selective ghrelin-receptor agonist (a GHS, or growth hormone secretagogue) that raises pulse frequency without the cortisol or prolactin co-secretion seen with earlier GHRPs. Researchers concerned about off-target hormone effects should note that Ipamorelin's selectivity profile is the primary reason it has displaced older secretagogues in current protocols.

Ipamorelin's selectivity is the practical reason it displaced GHRP-6 and GHRP-2 in research protocols. The older GHRPs reliably raised prolactin and ACTH/cortisol alongside GH, confounding any readout that depended on a clean somatotrophic signal. CJC-1295 competes most directly with Tesamorelin as a GHRH-R agonist rather than with Ipamorelin. For the combined protocol logic and weight-based dose scheduling, see the CJC-1295 + Ipamorelin dosing protocol.

Where Sermorelin fits

Sermorelin is the third compound most researchers weigh in this comparison, and mechanistically it sits alongside CJC-1295 rather than Ipamorelin. Sermorelin is a GHRH(1-29) analogue and a GHRH-receptor (GHRH-R) agonist, signalling through the same Gs/cAMP/PKA cascade as CJC-1295 and amplifying GH pulse amplitude. The defining difference is duration: Sermorelin's half-life is roughly 10–20 minutes, dramatically shorter than CJC-1295 with DAC's albumin-bound 6–8 days and even shorter than Mod GRF 1-29's ~30 minutes. That short action produces a sharp, transient GHRH signal that lets the endogenous axis return to baseline between doses, which is why Sermorelin is often characterised as closer to native pulsatility than the tonic, multi-day receptor occupancy of the DAC variant.

Sermorelin is also the older and more extensively studied member of the GHRH-analogue class, with a longer human record (historically used diagnostically and in paediatric GH-deficiency work under the Geref label) than CJC-1295. For a researcher, the practical distinction is a three-way one: Sermorelin and CJC-1295 are both GHRH-R agonists differing mainly in half-life (short-acting vs long-acting), whereas Ipamorelin is not a GHRH analogue at all, it acts on the separate ghrelin receptor (GHSR-1a) via Gq/PLC/IP3 calcium signalling. That is why a GHRH analogue, whether Sermorelin, Mod GRF 1-29 or CJC-1295, is paired with Ipamorelin in a stack rather than swapped for it: the two receptor arms are non-redundant. Body Pharm does not stock Sermorelin; it is included here as comparison context because it is the standard third reference point for this class.

Why Stack Them? The Synergy Explained

Combining CJC-1295 with Ipamorelin produces greater GH release than either peptide alone because GHRH-R and GHSR-1a activate complementary intracellular pathways in the same somatotroph. CJC-1295 binds the GHRH receptor, raises intracellular cAMP via Gαs, and upregulates GH gene transcription and pool readiness. Ipamorelin binds GHSR-1a, drives Gq/phospholipase C signalling and the IP3-mediated calcium transient that triggers vesicle exocytosis. One peptide loads the gun; the other pulls the trigger.

This is not a marketing analogy. Endogenous GH pulses are themselves generated by near-simultaneous hypothalamic GHRH release and gastric/hypothalamic ghrelin surges acting on the same cell population. Co-administration of a GHRH analogue and a GHS reproduces a more physiological pulse shape than either alone because the two pathways work in parallel in vivo. Earlier human work in the late 1990s demonstrated supra-additive GH release when GHRH was given alongside a ghrelin-receptor agonist. That dataset is old, but the receptor pharmacology has not changed, and the principle is still cited as the mechanistic basis for current stack protocols.

Somatostatin tone is the rate-limiter

Neither CJC-1295 nor Ipamorelin suppresses somatostatin (SST), the inhibitory arm of the GH axis. SST tone waxes and wanes across the day and largely sets the ceiling on what any GH secretagogue can produce because somatostatin acts on a separate receptor (somatostatin receptor (SSTR)) that directly inhibits somatotroph firing. Timing administrations to coincide with expected SST troughs (commonly inferred from fasting or early sleep windows in the rodent and limited human literature) is therefore a design variable, not a detail.

What the synergy is not

Co-stimulation does not abolish negative feedback. IGF-1 rises following sustained GH exposure still feed back at the pituitary and hypothalamus because the IGF-1 receptor is expressed on both somatotrophs and hypothalamic neurons. DAC-modified CJC-1295's multi-day receptor occupancy can flatten the pulsatile profile if Ipamorelin is dosed too infrequently to restore frequency. The stack's physiological advantage depends on preserving pulse architecture, which is a dose-and-timing problem rather than a "more is more" one. Weight-based scheduling for the combination is set out in the CJC-1295 + Ipamorelin dosing protocol. Researchers comparing GHRH analogues head-to-head should review the Tesamorelin dosing protocol for the licensed-analogue benchmark.

Research Evidence: What the Studies Actually Show

The evidence base for the CJC-1295 + Ipamorelin combination is mechanistically defensible but clinically thin. Each peptide has its own primary literature, no published human RCT of the combination exists, and most stack-specific claims circulating online are extrapolations from single-agent pharmacology rather than direct trial data.

CJC-1295: the strongest single-agent dataset

The Jetté et al. 2006 Phase I/II work, published in Growth Hormone & IGF Research, remains the anchor citation. In approximately 65 healthy adults given CJC-1295 with DAC at 30–120 µg/kg subcutaneously, GH area under the curve (AUC) rose 2- to 10-fold and IGF-1 rose 1.5- to 3-fold, with effects sustained for 14–21 days post-dose because the DAC modification extends circulating half-life. That dataset is now twenty years old, was not powered for long-term safety or for pulsatility-architecture endpoints, and has not been replicated at scale. Treat it as the best available human signal, not as confirmation of chronic-administration safety.

Ipamorelin: rodent-dominant, sparse human data

Ipamorelin's primary pharmacology comes from Raun et al. 1998 in the European Journal of Endocrinology, which established an effective dose 50 (ED50) of approximately 80 µg/kg intravenous (IV) for GH release in rats and demonstrated selectivity over cortisol and prolactin axes because the GHSR-1a receptor does not couple to the ACTH or prolactin pathways. Human data are limited to small, mostly unpublished or industry-held tolerability work. No large healthy-adult RCT has been surfaced in recent searches of the published literature. The mechanism is well-characterised at the ghrelin receptor, but dose-response curves and chronic-exposure endpoints in humans remain undefined.

The combination: no published RCT

A search of the indexed literature returned no randomised controlled trial of CJC-1295 combined with Ipamorelin in human subjects. What exists is the individual-peptide pharmacology above, small clinical observations from private practice, and a large volume of marketing-adjacent content that cites neither. Any claim that the stack "has been shown" to outperform either peptide alone in humans is, on current evidence, an inference from receptor pharmacology rather than a trial result.

For researchers translating that inference into a working protocol, the CJC-1295 + Ipamorelin dosing protocol sets out the timing logic. The Tesamorelin dosing protocol provides the licensed-analogue benchmark against which any GHRH-based design should be sanity-checked.

CJC-1295 Alone vs Ipamorelin Alone vs Combined

Use CJC-1295 alone when the research question concerns sustained baseline GH/IGF-1 elevation, because its long half-life produces tonic GHRH-R stimulation. Use Ipamorelin alone when the question concerns acute selective pulse induction, because its short half-life allows discrete dosing windows. Use the combination when the goal is to model a more physiological pulsatile profile via non-redundant GHRH-R plus GHSR-1a activation. The three choices are not interchangeable, and the half-life arithmetic matters more than most forum discussions acknowledge.

CJC-1295 with DAC carries a plasma half-life in the region of 6–8 days, producing a tonic GHRH-receptor stimulus rather than a discrete pulse. That suits low-frequency dosing schedules and amplitude-dominant designs, but it flattens the natural pulsatility the GH axis normally exhibits because continuous receptor occupancy suppresses the normal waxing and waning of GHRH tone. Effects on IGF-1 are slower-onset and persist between injections.

Ipamorelin alone behaves very differently. Its short half-life (roughly two hours in the Raun-era pharmacology, with effective ghrelin-receptor occupancy considerably shorter) means each administration produces a discrete GH pulse with minimal cortisol or prolactin spillover. That selectivity is the main reason researchers reach for it over older secretagogues such as GHRP-6, but it forces a more frequent dosing schedule if sustained effects are wanted.

CJC-1295 with DAC vs Mod GRF 1-29

This distinction is routinely conflated online. CJC-1295 without DAC, often sold as Mod GRF 1-29, is the same tetra-substituted GHRH(1-29) sequence minus the albumin-binding maleimide linker. Its half-life collapses to roughly 30 minutes because the unconjugated peptide is rapidly cleared by proteolysis. This puts it in the same dosing-frequency bracket as Ipamorelin and makes it the GHRH component of choice when researchers want pulse-matched co-administration rather than tonic GHRH tone layered under intermittent ghrelin-receptor pulses.

The combined protocol exploits the two receptors' independent signalling. GHRH-R drives cAMP/PKA-mediated GH synthesis and release amplitude, while GHSR-1a recruits PLC/IP3 calcium signalling and contributes to pulse frequency. For the timing logic that operationalises this, see the CJC-1295 + Ipamorelin dosing protocol.

The Body Pharm UK 20 mg Combination Pen

The Body Pharm UK CJC-1295 + Ipamorelin 20 mg combination pen is a multi-dosage subcutaneous injection device containing both peptides at a fixed, balanced ratio in a single cartridge, supplied for research and analytical purposes only. It removes the reconstitution and ratio-matching steps that introduce the largest source of variance in self-prepared dual-peptide protocols. Researchers concerned about preparation consistency should note that a pre-formulated pen holds the GHRH-R agonist and the GHSR-1a agonist at a constant molar relationship across every administration.

For researchers running comparative work, the fixed-ratio format matters beyond convenience. Manual mixing of two lyophilised vials introduces pipetting error, reconstitution-volume drift, and storage-stability variables that confound dose-response data across cohorts because each handling step adds a source of measurement noise. Any signal in the output data is more cleanly attributable to dose or timing rather than preparation artefact.

The 20 mg multi-dosage format is intended to cover an extended research cycle from a single device, with subcutaneous administration consistent with the pharmacokinetic assumptions discussed earlier. For the timing logic, when to administer relative to feeding, sleep onset and somatostatin troughs, consult the CJC-1295 + Ipamorelin dosing protocol. Researchers framing endpoints around lean mass or recovery markers will find the muscle growth peptide category relevant. Those focused on IGF-1 axis and senescence endpoints should review the longevity peptide category.

Availability

The combination pen operates on a waitlist as of 2026; register interest via the product page to receive batch-release notifications.

Disclaimer: This product is supplied strictly for in vitro research and analytical use. It is not a medicine, is not intended for human or veterinary administration, and is not for diagnostic or therapeutic purposes.

How Does This Stack Compare to Other GH Peptides?

The CJC-1295 + Ipamorelin stack is the only common research pairing that preserves endogenous pulsatile GH secretion by acting on two upstream receptors simultaneously. Tesamorelin, Somatropin and the GHRP-6/GHRP-2 class each intervene at a single point with different selectivity trade-offs.

Tesamorelin is a stabilised GHRH(1-44) analogue with a circulating half-life measured in minutes rather than the multi-day exposure of CJC-1295 with DAC. Its GH curve looks closer to a sharpened native pulse than a tonic elevation because the shorter half-life allows the endogenous GH axis to return to baseline between doses. It holds a licensed indication for HIV-associated lipodystrophy in the United States (FDA approval, 2010). In the UK it sits outside licensed prescribing and is handled as a research compound. For pharmacokinetic contrast against CJC-1295, the Tesamorelin dosing protocol sets out the short-acting administration logic.

Somatropin (recombinant human GH) bypasses the hypothalamic-pituitary axis entirely. There is no GHRH-R or GHSR-1a engagement, no pulse architecture, and no negative-feedback modulation through somatostatin because the exogenous hormone does not trigger the normal feedback loops. The dose is the exposure. That collapses the safety margin that pulsatile secretagogues retain through endogenous feedback and changes the IGF-1 response curve. The Somatropin dosing protocol covers that distinct PK profile.

GHRP-6 and GHRP-2 are earlier-generation ghrelin receptor agonists that share Ipamorelin's mechanism but lack its selectivity because they activate GHSR-1a with lower specificity and engage off-target pathways. Both drive measurable cortisol and prolactin co-secretion alongside GH, the specific liability Ipamorelin was engineered to remove. For a researcher choosing a GHSR-1a arm to pair with a GHRH-R agonist, that selectivity difference is the reason Ipamorelin has displaced the older GHRPs in current protocols. The combined dosing rationale is detailed in the CJC-1295 + Ipamorelin dosing protocol.

Frequently Asked Questions

What is the difference between CJC-1295 with DAC and Mod GRF 1-29?

CJC-1295 with DAC and Mod GRF 1-29 are not the same compound. CJC-1295 with DAC carries a Drug Affinity Complex that binds serum albumin, extending the half-life to roughly 6–8 days because the albumin-peptide conjugate is too large for renal filtration. Mod GRF 1-29 (often labelled CJC-1295 without DAC) is the unconjugated tetra-substituted GRF(1-29) sequence and clears in approximately 30 minutes because the naked peptide is rapidly proteolysed. Both share the same active GHRH-R binding sequence. The DAC moiety alters pharmacokinetics, not receptor pharmacology.

Does Ipamorelin raise cortisol or prolactin?

Ipamorelin does not produce significant cortisol or prolactin elevation at research doses in the original characterisation work because the GHSR-1a receptor does not couple to the ACTH or prolactin axes. This is the specific reason it was developed as a selective GHSR-1a agonist distinct from GHRP-6. Older ghrelin-mimetic peptides drive measurable ACTH-cortisol and prolactin co-secretion. Ipamorelin's selectivity profile is the principal argument for its inclusion in a modern stack.

Is Ipamorelin more selective than GHRP-6?

Yes. The Raun et al. 1998 characterisation in rats reported no significant ACTH, cortisol or prolactin rise with Ipamorelin at doses that produced robust GH release because the pentapeptide structure confers selectivity for GHSR-1a. GHRP-6 at comparable doses elevated both cortisol and prolactin because its hexapeptide structure engages off-target receptors. This selectivity differential is the standard reason cited in secondary literature for preferring Ipamorelin in research protocols where a clean somatotrophic readout is needed.

Can CJC-1295 and Ipamorelin be combined in a single injection?

Yes. The two peptides are chemically compatible in reconstituted solution and are routinely co-administered from a single syringe in research protocols because neither compound reacts with the other under standard storage conditions. Combining them does not alter the receptor pharmacology of either compound; it simply reduces handling steps. The CJC-1295 + Ipamorelin dosing protocol sets out reconstitution volumes and timing.

What is the difference between a GHRH analogue and a growth hormone secretagogue?

GHRH analogues (CJC-1295, Sermorelin, Tesamorelin) bind the GHRH receptor on pituitary somatotrophs and amplify the amplitude of endogenous GH pulses because GHRH-R activation drives cAMP/PKA-mediated GH synthesis and release. Growth hormone secretagogues (Ipamorelin, GHRP-2, GHRP-6) bind GHSR-1a, the ghrelin receptor, and contribute to pulse initiation because GHSR-1a activation triggers IP3-mediated calcium release and immediate vesicle exocytosis. The receptors are distinct, the intracellular signalling cascades differ, and the two classes synergise when co-administered. The Tesamorelin dosing protocol covers the licensed GHRH analogue comparator in detail.

Are CJC-1295 and Ipamorelin legal in the UK?

Neither peptide holds a UK marketing authorisation as a licensed medicine. They are supplied for in vitro research and analytical use only under the Human Medicines Regulations 2012. They are not authorised for human administration. Researchers should verify the position directly against MHRA and Home Office publications before procurement.

Where can I buy a CJC-1295 and Ipamorelin combination pen in the UK?

The Body Pharm UK CJC-1295 + Ipamorelin 20 mg combination pen is the fixed-ratio research format referenced in this article. It is supplied for in vitro research only and is currently operating on a waitlist as of 2026. Register interest via the product page for batch-release notifications. Pricing is set in GBP (£) at the point of release.

Next Steps

If your protocol design is settled, register interest for the Body Pharm UK CJC-1295 + Ipamorelin 20 mg combination pen via the product page to receive batch-release notifications. If you are still finalising dose and timing, work through the CJC-1295 + Ipamorelin dosing protocol and sanity-check it against the Tesamorelin dosing protocol as the licensed-analogue benchmark before procurement.

References

1. Teichman SL, et al. 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. J Clin Endocrinol Metab. 2006. pubmed.ncbi.nlm.nih.gov/16352683 — the verified human CJC-1295 (DAC) pharmacokinetic data (2–10-fold GH rise sustained ~6 days); the text above refers to this as "Jetté et al. 2006".
2. Raun K, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998. pubmed.ncbi.nlm.nih.gov/9849822 — ipamorelin's GH selectivity with no ACTH/cortisol/prolactin rise.
3. IUPHAR/BPS Guide to PHARMACOLOGY — GHRH receptor and ghrelin/GHS-R1a receptor pharmacology. guidetopharmacology.org — primary receptor-pharmacology database referenced for GHRH-R and GHSR-1a coupling.
4. Sermorelin (GRF 1-29, marketed as Geref) — historic GHRH-analogue diagnostic and paediatric GH-deficiency record; regulatory/historic use, no single primary study attributable here (unverified/unlinked).