CJC-1295 and ipamorelin are constantly compared, but they are not really rivals: they are partners. One tells the body to release more growth hormone; the other sharpens each pulse. Together they produce a stronger, cleaner release than either on its own, which is why our pen carries both.
Pluma de inyección multidosis con 20 mg de CJC-1295 e ipamorelina. Análogo de GHRH combinado con un secretagogo selectivo de la hormona del crecimiento, para inyección subcutánea. Exclusivamente con fines de investigación y análisis.
This comparison reflects our reading of the growth hormone peptide literature published in 2026. We assess each compound by its mechanism on the GH axis and explain the rationale behind the standard stack.
CJC-1295 and ipamorelin target two different receptors on the somatotroph cell: 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. Used together they act as two separate levers on the GH axis and produce a release profile that, on mechanistic reasoning, sits closer to natural pulsatility than either peptide alone, because the two receptors activate independent intracellular cascades that converge on the same secretory machinery.
The honest caveat that is rarely stated plainly: in the set of sources reviewed for this comparison, no randomised controlled trial of the combination in healthy adults has been identified. This article separates receptor pharmacology from marketing and grades the quality of the evidence at each level.
For tonic, sustained stimulation of the GH axis, CJC-1295 with DAC leads on duration of action (a 6–8-day half-life through albumin binding [1]); for clean, selective pulse activation, ipamorelin wins as a ghrelin receptor agonist with no knock-on effect on cortisol or prolactin [2]; sermorelin, the oldest and best-studied GHRH analogue, suits research that needs a short-acting GHRH signal (around 10–20 min) closer to natural pulsatility. The decisive distinguishing features are mechanism and duration of action: CJC-1295 and sermorelin are both GHRH receptor agonists (long-acting versus short-acting), whereas ipamorelin works on an entirely different receptor (GHSR-1a). That is why a GHRH analogue is combined with ipamorelin rather than replaced by it.
CJC-1295 is a 30-amino-acid synthetic GHRH analogue, usually supplied with a Drug Affinity Complex (DAC) modification that binds covalently to endogenous albumin and extends the circulating half-life to around 6–8 days [1]. The Body Pharm pen carries the DAC form, which is why its reference schedule is a single daily dose rather than several. Ipamorelin is a selective pentapeptide agonist of the ghrelin receptor (GHSR-1a) with a half-life of around 2 hours [8], designed to trigger GH release without measurable effects on prolactin, adrenocorticotropic hormone (ACTH) or cortisol [2]. Neither compound is authorised as a medicine; both are supplied solely for laboratory research use.
The mechanistic separation matters for protocol design. CJC-1295 (with DAC) provides continuous, low-threshold tonic stimulation of the GHRH receptor on the somatotroph and raises the ceiling of every endogenous GH pulse, without generating discrete pulses of its own. Ipamorelin works on a different receptor (GHSR-1a) and produces a sharp, brief secretagogue spike that mimics ghrelin's pulse-triggering role. The two pathways converge on the same somatotroph cell but use independent intracellular cascades (Gs/cyclic adenosine monophosphate (cAMP) for GHRH-R; Gq/phospholipase C (PLC) for GHSR-1a, according to standard receptor pharmacology [3]), which is the mechanistic basis for the supra-additive release seen in rodent and in vitro work.
Receptor pharmacology (the coupling of GHRH-R and GHSR-1a) is well characterised in vitro and in animal models, because these receptor families have been studied extensively since the 1990s. The secondary clinical sources reviewed here describe them consistently, but they are no substitute for the primary entries of the International Union of Basic and Clinical Pharmacology / British Pharmacological Society (IUPHAR/BPS) [3].
The half-life of CJC-1295 DAC (around 6–8 days) is widely cited in the secondary literature, because the prolonged albumin-binding profile is the defining feature of the DAC modification. The original pharmacokinetic data come from Teichman et al. 2006, who estimated a half-life of 5.8 to 8.1 days [1].
Ipamorelin's half-life (around 2 hours) and its selectivity are described in commercial and clinical-practice sources, because the short duration of action and the absence of cortisol and prolactin co-secretion are the decisive differences from earlier growth hormone-releasing peptides (GHRPs). The selectivity comes from the primary work of Raun et al. 1998 [2]; the human half-life of around 2 hours, from the pharmacokinetic modelling by Gobburu et al. 1999 in healthy volunteers [8].
Randomised trial data for the combination in healthy adults: none identified, because no such study has been published in the indexed literature.
Regulatory status: at the time of writing (2026), no marketing authorisation as a medicine has been identified for either peptide. It is worth checking their status directly with the competent authorities.
If your next step is to work through the dosing logic, you will find it in the CJC-1295 + ipamorelin dosing protocol; for comparison with the closest authorised GHRH analogue, the tesamorelin dosing protocol is the natural reference point.
CJC-1295 and ipamorelin act on two structurally unrelated G protein-coupled receptors with orthogonal downstream cascades. That makes the stack mechanistically non-redundant rather than merely additive in a trivial sense. CJC-1295 binds the GHRH receptor (GHRH-R) on somatotroph cells of the anterior pituitary and signals through Gs/adenylate cyclase. Ipamorelin binds the growth hormone secretagogue receptor (GHSR-1a) and signals through Gq/phospholipase C [3]. Both cascades converge on GH exocytosis, but they get there via independent second messengers.
With CJC-1295, GHRH-R activation raises intracellular cAMP through adenylate cyclase, which activates protein kinase A (PKA). PKA phosphorylates substrates that trigger vesicular GH release and drives CREB-mediated (cAMP response element-binding protein) transcription of the GH1 gene, thereby enlarging the releasable pool. The mechanistic consensus dates back to Mayo's cloning and characterisation of GHRH-R in Molecular Endocrinology (1992) [5] and remains the standard interpretation in the current secondary literature, because the cAMP/PKA pathway has been confirmed across several cell types and species. The functional consequence is a reinforcement of pulse amplitude: when an endogenous GHRH pulse fires, more GH is released per pulse.
With ipamorelin, GHSR-1a activation couples to Gq and stimulates phospholipase C, which cleaves phosphatidylinositol-4,5-bisphosphate (PIP2) into inositol-1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 mobilises Ca²⁺ from the endoplasmic reticulum stores. The rise in cytosolic Ca²⁺ triggers the immediate exocytosis of pre-formed GH vesicles. This is the cascade described by Howard et al. in Science (1996) [6] for what was then the orphan GHS receptor, and it has been replicated in later characterisation work, because the IP3/calcium mechanism is fundamental to ghrelin receptor biology. The functional consequence is a discrete, short-lived GH spike that, in practice, triggers a pulse rather than enlarging an existing one.
| Peptide | Receptor | G protein / pathway | Main effect on the GH profile |
|---|---|---|---|
| CJC-1295 (with or without DAC) | GHRH-R | Gs → adenylate cyclase → cAMP ↑ → PKA → GH transcription + exocytosis | Increases pulse amplitude; raises the somatotroph's baseline availability |
| Ipamorelin | GHSR-1a (ghrelin receptor) | Gq → PLC → IP3/DAG → intracellular Ca²⁺ ↑ → vesicular exocytosis | Increases pulse frequency; triggers brief, discrete GH spikes |
Because cAMP/PKA and Ca²⁺/PLC act as parallel inputs to the same secretory machinery, co-administration recruits two independent control levers within a single cell. That is the pharmacological rationale behind the CJC-1295 + ipamorelin dosing protocol. It is also what separates CJC-1295 from the authorised comparator in the tesamorelin dosing protocol: tesamorelin is itself a GHRH-R agonist and is therefore not orthogonal to CJC-1295. It is worth cross-checking the receptor identifiers and canonical coupling against the IUPHAR/BPS Guide to Pharmacology database (2025) [3] before finalising a protocol document.
CJC-1295 is a long-acting GHRH analogue that increases pulse amplitude. Ipamorelin is a selective ghrelin receptor agonist (a GHS, or growth hormone secretagogue) that increases pulse frequency, without the cortisol or prolactin co-secretion seen with earlier GHRPs. Anyone who regards off-target hormonal effects as critical should bear in mind that ipamorelin's selectivity profile is the main reason it has displaced the older secretagogues in current protocols.
| Characteristic | CJC-1295 (with DAC) | Ipamorelin | Sermorelin |
|---|---|---|---|
| Peptide class | GHRH analogue (modified GHRH 1-29) | Pentapeptide GHRP / GHSR-1a agonist | GHRH analogue (GHRH 1-29) |
| Target receptor | GHRH-R | GHSR-1a (ghrelin receptor) | GHRH-R |
| Intracellular pathway | Gs → cAMP → PKA | Gq → PLC → IP3/DAG → Ca²⁺ | Gs → cAMP → PKA |
| Main effect on GH | Pulse amplitude ↑; greater baseline availability in the somatotroph | Pulse frequency ↑; brief, discrete GH spikes | Pulse amplitude ↑; short-acting GHRH tone closer to natural pulsatility |
| Half-life | Approx. 6–8 days with DAC (albumin-bound); approx. 30 min without DAC (Mod GRF 1-29) | Approx. 2 hours in humans | Approx. 10–20 min; considerably shorter than CJC-1295 with DAC |
| Selectivity | High; no clinically relevant effect on prolactin or ACTH reported in the early human dose-finding studies, because the GHRH-R pathway does not touch the prolactin or ACTH axes | High; Raun et al. (1998) reported no rises in ACTH, cortisol or prolactin in swine, even at doses more than 200-fold above the ED50 for GH release, unlike GHRP-6 [2] | High; GHRH-R-selective, does not touch the prolactin or ACTH axes |
| Level of evidence | Phase I/II human pharmacokinetics/pharmacodynamics (PK/PD) (Teichman et al., 2006: 30–60 µg/kg produced 2- to 10-fold GH increases over baseline) [1]; no randomised trial identified after 2006 | Rodent mechanistic data [2] plus limited human pharmacokinetics [8]; no randomised trial identified in healthy adults | The oldest and best-studied GHRH analogue; its historical diagnostic and paediatric use in GH deficiency (marketed as Geref) gives it the broadest human track record among the GHRH analogues |
| Dose in the Body Pharm pen | Around 100 mcg per administration, once daily in the evening (DAC form) | Around 100 mcg per administration, once daily in the evening, in the same cartridge as the CJC-1295 | Not supplied; the literature uses 100–500 µg per administration, normally daily |
| Route of administration | Subcutaneous injection | Subcutaneous injection | Subcutaneous injection |
Ipamorelin's selectivity is the practical reason it has displaced GHRP-6 and GHRP-2 in research protocols. The older GHRPs reliably raised prolactin and ACTH/cortisol alongside GH, which interfered with any measurement that depended on a clean somatotroph signal. CJC-1295, as a GHRH-R agonist, competes more directly with tesamorelin than with ipamorelin. For the logic of the combined protocol and weight-based dose planning, see the CJC-1295 + ipamorelin dosing protocol.
Sermorelin is the third compound most people weigh up 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 that signals through the same Gs/cAMP/PKA cascade as CJC-1295 and reinforces GH pulse amplitude. The decisive difference is duration of action: sermorelin's half-life is around 10–20 minutes, radically shorter than the 6–8 days of albumin-bound CJC-1295 with DAC [1] and shorter even than the roughly 30 minutes of Mod GRF 1-29. That short action produces an acute, transient GHRH signal that lets the endogenous axis return to baseline between doses, which is why sermorelin is often described as closer to natural pulsatility than the multi-day tonic receptor occupancy of the DAC variant.
Sermorelin is also the oldest and most widely studied member of the GHRH analogue class, with a longer human track record (used historically in diagnostics and in paediatric GH deficiency research under the Geref brand) than CJC-1295. For the researcher, the practical distinction is three-way: sermorelin and CJC-1295 are both GHRH-R agonists that differ chiefly in half-life (short-acting versus long-acting), whereas ipamorelin is not a GHRH analogue at all but 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 stacked with ipamorelin rather than swapped for it: the two receptor arms are not redundant. Body Pharm does not offer sermorelin in its catalogue; it is included here as comparative context, because it is the standard reference point for this class.
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 cell. CJC-1295 binds the GHRH receptor, raises intracellular cAMP via Gαs and upregulates GH gene transcription and pool availability. Ipamorelin binds GHSR-1a and drives Gq/phospholipase C signalling and the IP3-mediated calcium transient that triggers vesicular exocytosis. One peptide loads the gun and the other pulls the trigger.
That is not a marketing analogy. Endogenous GH pulses themselves are generated by hypothalamic GHRH release together with near-simultaneous gastric and hypothalamic ghrelin spikes acting on the same cell population. Co-administering 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 from the early 1990s showed synergistic GH release when GHRH was given alongside a ghrelin receptor agonist (GHRP-6; Bowers et al., 1990) [7]. 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.
Neither CJC-1295 nor ipamorelin suppresses somatostatin (SST), the inhibitory arm of the GH axis. SST tone fluctuates over the day and largely sets the ceiling on what a GH secretagogue can produce, because somatostatin acts on a separate receptor (the somatostatin receptor, SSTR) that directly inhibits somatotroph firing. The best-described SST trough coincides with early sleep, which is why the reference schedule for the DAC pen places the single daily dose in the evening.
Co-stimulation does not override negative feedback. IGF-1 rises after sustained GH exposure still feed back on the pituitary and the hypothalamus, because the IGF-1 receptor is expressed on both somatotroph cells and hypothalamic neurons. The multi-day receptor occupancy of DAC-modified CJC-1295 can flatten the pulsatile profile if ipamorelin is dosed too infrequently to restore frequency. The physiological advantage of the stack depends on preserving the pulse architecture, which is a question of dose and timing and not a question of "more is more". Weight-based planning for the combination is set out in the CJC-1295 + ipamorelin dosing protocol. If you are comparing GHRH analogues head-to-head, use the tesamorelin dosing protocol as the authorised-analogue reference.
The evidence base for the CJC-1295 + ipamorelin combination is mechanistically defensible but clinically thin. Each peptide has its own primary literature, no published randomised human trial of the combination exists, and most of the stack-specific claims circulating online are extrapolations from the pharmacology of each compound on its own, not direct study data.
The phase I work of Teichman et al. 2006, published in The Journal of Clinical Endocrinology & Metabolism, remains the reference citation [1]. In healthy adults given single subcutaneous injections of CJC-1295 with DAC at doses of 30 to 60 µg/kg, GH rose 2- to 10-fold for 6 days or more and IGF-1 rose 1.5- to 3-fold for 9 to 11 days, with an estimated half-life of 5.8 to 8.1 days, because the DAC modification prolongs the circulating half-life. That dataset is now twenty years old, was not designed to assess long-term safety or pulse-architecture endpoints, and has not been replicated at scale. Treat it as the best available human signal, not as confirmation of safety under chronic administration.
Ipamorelin's primary pharmacology comes from Raun et al. 1998 in the European Journal of Endocrinology, who established an effective dose 50 (ED50) of around 80 nmol/kg intravenously (i.v.) for GH release in anaesthetised rats and demonstrated selectivity against the cortisol and prolactin axes in swine [2], because the GHSR-1a receptor does not couple to the ACTH or prolactin pathways. Human data are limited to a single-dose pharmacokinetic-pharmacodynamic study in healthy volunteers (Gobburu et al., 1999) [8] and to small tolerability studies, mostly unpublished or internal to industry. Recent searches of the published literature have found no large randomised trial in healthy adults. The mechanism is well characterised at the ghrelin receptor, but human dose-response curves and chronic-exposure endpoints remain undefined.
A search of the indexed literature has returned no randomised controlled trial of CJC-1295 combined with ipamorelin in human subjects. What exists is the pharmacology of each peptide described 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 "proven" superior in humans to either peptide alone is, on current evidence, a conclusion derived from receptor pharmacology and not a study result.
If you want to turn that conclusion into a working protocol, the CJC-1295 + ipamorelin dosing protocol sets out the timing logic. The tesamorelin dosing protocol provides the authorised-analogue reference against which the plausibility of any GHRH-based design should be checked.
Use CJC-1295 alone when the research question concerns a sustained elevation of baseline GH/IGF-1, because its long half-life produces tonic GHRH-R stimulation. Use ipamorelin alone when the question concerns acute, selective pulse activation, because its short half-life allows discrete dosing windows. Use the combination when the aim is to model a more physiological pulsatile profile through non-redundant activation of GHRH-R plus GHSR-1a. The three options are not interchangeable, and the half-life arithmetic matters more than most forum discussions admit.
CJC-1295 with DAC has a plasma half-life in the 6- to 8-day range and produces a tonic stimulus at the GHRH receptor rather than a discrete pulse [1]. That suits low-frequency dosing schedules and amplitude-dominated designs; Ionescu and Frohman (2006) observed that pulsatile GH secretion is preserved during that continuous stimulation, with pulse frequency and magnitude unaltered and a marked rise in basal (trough) GH levels [4]. Effects on IGF-1 appear more slowly and persist between injections.
Ipamorelin alone behaves very differently. Its short half-life (around two hours in healthy volunteers [8], with effective ghrelin receptor occupancy considerably briefer) means each administration produces a discrete GH pulse with minimal knock-on effect on cortisol or prolactin [2]. That selectivity is the main reason it is preferred over older secretagogues such as GHRP-6, but it forces a more frequent dosing schedule if sustained effects are wanted.
This distinction is routinely confused online. CJC-1295 without DAC, often sold as Mod GRF 1-29, is the same tetra-substituted GHRH(1-29) sequence without the maleimide linker that binds albumin. Its half-life drops to around 30 minutes, because the unconjugated peptide is rapidly degraded by proteolysis. That puts it in the same dosing-frequency category as ipamorelin and makes it the GHRH component of choice when pulse-coupled co-administration is wanted rather than tonic GHRH tone beneath intermittent ghrelin receptor pulses.
The combined protocol exploits the independent pathways of the two receptors. 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 CJC-1295 + Ipamorelin 20 mg combination pen is a single pre-filled pen, not two paired devices. It carries a 3 ml cartridge with 20 mg of total peptide and the two active compounds co-dissolved in a 50:50 split, and it is supplied solely for research and analytical purposes. It arrives ready to use: there is nothing to mix and nothing to prepare.
What matters for comparative work is how the dose is read. There is a single dose dial, marked directly in milligrams, and the figure you dial is the dose of each of the two peptides. The GHRH-R agonist and the GHSR-1a agonist therefore arrive in a constant ratio on every administration, and any signal in the output data can be attributed more cleanly to dose or timing than to a preparation artefact.
The 20 mg total is designed to cover an extended research cycle from a single device, with subcutaneous administration in line with the pharmacokinetic assumptions discussed above. The arithmetic follows directly from that reading rule: dialling 0.1 mg delivers 0.1 mg of each peptide, 0.2 mg of the mixture per injection, so the 20 mg cartridge yields 100 doses. Because the GHRH component is the DAC form, the reference schedule is a single daily administration in the evening. For the timing logic, see the CJC-1295 + ipamorelin dosing protocol.
The pen is stored between 2 and 8 °C, protected from light, with a 24-month shelf life unopened and 12 months from the first puncture; it will tolerate up to 30 days at room temperature (30 °C maximum) if you have no fridge available. Let it reach room temperature before injecting and do not freeze it. If you are defining endpoints around lean mass or recovery markers, the muscle growth peptides category will be relevant. If your focus is tissue repair and recovery endpoints, have a look at the recovery peptides category.
The combination pen is in stock and can be ordered from the CJC-1295 + Ipamorelin 20 product page; shipping is within Spain.
Notice: this product is supplied solely for in vitro research and analytical purposes. It is not a medicine, it is not intended for administration to humans or animals and it is not intended for any diagnostic or therapeutic purpose.
The CJC-1295 + ipamorelin stack is the only common research combination that preserves endogenous pulsatile GH secretion by acting on two upstream receptors at once. 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 in the order of minutes, rather than the multi-day exposure of CJC-1295 with DAC. Its GH curve looks more like a sharp natural pulse than a tonic elevation, because the shorter half-life lets the endogenous GH axis return to baseline between doses. In the United States it has an authorised indication for HIV-associated lipodystrophy (FDA approval in 2010). In Spain it is not authorised as a medicine and is handled as a research compound. For the pharmacokinetic contrast with CJC-1295, the tesamorelin dosing protocol sets out the logic of short-acting administration.
Somatropin (recombinant human GH) bypasses the hypothalamic-pituitary axis altogether. There is no binding to GHRH-R or GHSR-1a, no pulse architecture and no modulation of negative feedback by somatostatin, because the exogenous hormone does not engage the normal feedback circuits. The dose is the exposure. That removes the safety margin that pulsatile secretagogues retain through endogenous feedback and alters the IGF-1 response curve. The somatropin dosing protocol covers that distinct pharmacokinetic 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 touch off-target pathways. Both drive measurable cortisol and prolactin co-secretion alongside GH, precisely the weakness ipamorelin was developed to eliminate. For anyone choosing a GHSR-1a arm to combine with a GHRH-R agonist, that difference in selectivity is the reason ipamorelin has displaced the older GHRPs in current protocols. The rationale for combined dosing is detailed in the CJC-1295 + ipamorelin dosing protocol.
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 and extends the half-life to around 6–8 days [1], because the albumin-peptide conjugate is too large for renal filtration. Mod GRF 1-29 (often called CJC-1295 without DAC) is the unconjugated tetra-substituted GRF(1-29) sequence and degrades within around 30 minutes, because the bare peptide is rapidly proteolysed. Both share the same active GHRH-R binding sequence. The DAC group changes the pharmacokinetics, not the receptor pharmacology.
Ipamorelin does not produce a significant rise in cortisol or prolactin at research doses in the original characterisation work [2], because the GHSR-1a receptor does not couple to the ACTH or prolactin axes. That is the specific reason it was developed as a selective GHSR-1a agonist, in contrast to GHRP-6. The older ghrelin-mimetic peptides drive measurable co-secretion of ACTH-cortisol and prolactin. Ipamorelin's selectivity profile is the main argument for including it in a modern stack.
Yes. The characterisation by Raun et al. 1998 reported no significant rises in ACTH, cortisol or prolactin with ipamorelin at doses that produced robust GH release [2], because its pentapeptide structure confers GHSR-1a selectivity. GHRP-6, at comparable doses, raised both cortisol and prolactin, because its hexapeptide structure touches off-target receptors. That selectivity difference is the standard reason the secondary literature gives for preferring ipamorelin in research protocols where a clean somatotroph signal is needed.
Yes, and in the Body Pharm pen they already come combined: the two peptides are co-dissolved in the same cartridge, so a single administration delivers both. They are chemically compatible and neither reacts with the other under standard storage conditions. Combining them does not alter the receptor pharmacology of either. The CJC-1295 + ipamorelin dosing protocol sets out the dialled doses and timing.
GHRH analogues (CJC-1295, sermorelin, tesamorelin) bind the GHRH receptor on pituitary somatotroph cells and reinforce 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 help trigger the pulse, because GHSR-1a activation causes IP3-mediated calcium release and immediate vesicular exocytosis. The receptors are different, the intracellular cascades differ and the two classes act synergistically when given together [7]. The tesamorelin dosing protocol covers the authorised GHRH analogue as a comparator in detail.
Neither peptide is authorised as a medicine. They are supplied solely for in vitro research and analytical purposes. They are not authorised for administration to humans. It is worth checking their legal status directly with the competent authorities before buying.
The Body Pharm CJC-1295 + Ipamorelin 20 mg combination pen is the fixed-ratio research format this article refers to. It is supplied solely for in vitro research and can be ordered from its product page. The list price is €149.
If your protocol design is already settled, order the Body Pharm CJC-1295 + Ipamorelin 20 mg combination pen from its product page. If you are still fixing doses and timing, work through the CJC-1295 + ipamorelin dosing protocol and check its plausibility, before buying, against the tesamorelin dosing protocol as the authorised-analogue reference.
Buying from the UK? See CJC-1295 vs ipamorelin on the UK store, which ships within the UK.
Buying from Germany? See CJC-1295 vs ipamorelin on the German store, which ships within Germany and Austria.
Buying from Czechia? See CJC-1295 vs ipamorelin on the Czech store, which ships within Czechia.
Buying from another EU country? See CJC-1295 vs ipamorelin on the European store, which ships across the EU.
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