Ipamorelin
& CJC-1295
Ipamorelin and CJC-1295 came out of two different research programmes. At Novo Nordisk, researchers were studying a small peptide that could prompt growth hormone release and asking which other signals came along with it. In Montreal, ConjuChem was working on a way to keep a GHRH analogue in circulation longer.[1][2]
The two paths meet at the pituitary, where growth hormone—GH—is released. Ipamorelin reaches those cells through the ghrelin receptor; CJC-1295 uses the GHRH receptor. That shared destination, reached through different receptors, is why the names so often appear together.[1][2][10]
Where did the two research paths begin?
In 1998, Novo Nordisk researchers published a peptide only five amino acids long that could prompt GH release. They called it ipamorelin; in the laboratory records it was NNC 26-0161. Raun and colleagues followed its activity from rat pituitary cells grown in the lab into animal experiments, where they could watch more of the endocrine response unfold.[1]
GH was only part of what they were measuring. They also followed ACTH, a pituitary signal involved in cortisol release, and cortisol itself. In their swine experiments, those two responses were not significantly different from the responses to GHRH. That is the experiment behind the selectivity finding so often attached to ipamorelin’s name.[1]
ConjuChem, in Montreal, was working on duration. Its researchers built a GHRH analogue with a chemical attachment that could bind to albumin in the bloodstream, giving the peptide a circulating carrier. Jetté and colleagues published that work in 2005. By 2006, Teichman’s team was reporting what happened to CJC-1295, GH and IGF-1 concentrations in human studies.[2][3]
How do the receptors differ?
The two compounds reach GH-releasing cells through different receptors. Ipamorelin activates GHS-R1a, better known as the ghrelin receptor, while CJC-1295 activates the GHRH receptor. Both pathways can signal to cells in the front part of the pituitary. Think of separate inputs reaching the same gland: the destination helps explain the pairing, while the receptor tells you how each molecule enters the conversation.[1][2][10]
That conversation unfolds over time. Ionescu and Frohman followed 12 participants who received CJC-1295 and found that GH continued to arrive in pulses. The frequency and magnitude of those pulses stayed unchanged in the study, while the low points between them and the average GH concentration increased. A longer-lasting receptor input could therefore sit alongside a pulsing GH record.[4][8]
The individual studies are where the measured findings come from. Our literature search found no primary human trial of ipamorelin and CJC-1295 together, so there is no combined human result to put alongside these separate receptor pathways.
Which molecule does “CJC-1295” name?
The name gets untidy here. ConjuChem’s CJC-1295 carries the albumin-binding DAC group, while “CJC-1295 without DAC” commonly refers to modified GRF(1-29). Even PubChem’s synonym lists contain conflicting labels. FDA’s chemistry review separates the structures, which gives us a way through the confusion: follow the amino-acid sequence and the group attached to its end.[6][7][8]
Ipamorelin
A five-residue synthetic peptide, also identified as NNC 26-0161.
- PubChem
- CID 9831659
- Formula
- C₃₈H₄₉N₉O₅
- Molar mass
- 711.9 g/mol
- CAS
- 170851-70-4
Free-molecule entry.[5]
CJC-1295 with DAC
A modified GHRH-derived sequence with an added terminal lysine carrying the albumin-binding group.
- PubChem
- CID 91971820
- Formula
- C₁₆₅H₂₆₉N₄₇O₄₆
- Molar mass
- 3647.2 g/mol
- CAS
- 446262-90-4
Mass as reported by PubChem.[6]
Read the sequences and identity notes
Ipamorelin: H-Aib-His-D-2-Nal-D-Phe-Lys-NH₂. Aib denotes α-aminoisobutyric acid; D-2-Nal denotes D-2-naphthylalanine. The D designations specify the configuration of those residues.[1][5]
Mod GRF(1-29): H-Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH₂.[7][8]
CJC-1295 with DAC: H-Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-Lys(DAC)-NH₂. The added lysine carries the Nε-3-maleimidopropionamide group described by Jetté. The modification must be specified along with the sequence.[2][6][8]
The formulas above describe the free molecules; a salt such as an acetate needs its own entry. There is also a small disagreement between the records: PubChem gives 3647.2 g/mol for the DAC structure, while FDA’s briefing prints 3647.95 g/mol beside the same formula. The card uses PubChem’s value, with both figures shown here so you can see where they came from.[6][8]
What changes when DAC is present?
DAC stands for drug affinity complex. Its reactive group forms a covalent bond with albumin at a site called Cys34—a cysteine residue with an available sulphur-containing group. That is the chemistry behind the hitchhiking analogy. Jetté’s team studied the peptide–albumin partnership and its activity at the GHRH receptor.[2]
In Teichman’s human work, the estimated half-life was 5.8–8.1 days. Once you know about the albumin attachment, you can see why the exact compound name belongs beside that number. Mod GRF(1-29) lacks the added binding modification, so the DAC study gives us no equivalent half-life estimate for that molecule.[3][8]
How much of the evidence comes from people?
There are human studies, but the record takes some untangling. Small experiments followed peptide and hormone concentrations, ipamorelin went into a postoperative-ileus programme, and larger trials appear in registries without a full set of public results. Looking at each study separately lets us keep the people, the measurements and the findings together.[3][9][10][11][13]
Ipamorelin pharmacokinetics · 1999
Gobburu’s team followed ipamorelin and GH concentrations over time, reporting a terminal half-life of about two hours for ipamorelin in that experiment. The participant count is less tidy: the abstract describes five groups of eight, while FDA’s review says 48 enrolled and repeats the five-group description. The available accounts leave that discrepancy unresolved.[9][21]
Ipamorelin phase 2 · 2014 publication
Beck and colleagues reported a larger study in the postoperative-ileus programme: 117 people enrolled and 114 were included in the analyses. The principal and secondary comparisons did not reach statistical significance. This programme was asking a different clinical question from the earlier work tracking GH concentrations.[10]
Later ipamorelin phase 2 registry
The later registry entry, NCT01280344, lists 320 actual participants and marks the study completed. That is a substantial step up in size, but the registry has no results posted. We can see how many people took part without having that record’s findings to read.[11]
CJC-1295 early human studies · 2006
Teichman’s two studies followed GH, IGF-1 and the peptide’s time in circulation over 28 and 49 days. The first enrolled 42 people—35 received the compound and seven placebo—and the second enrolled 24, divided 20 and four. These are the early human studies behind the long-lasting endocrine and pharmacokinetic findings.[3][8]
CJC-1295 pulsatility and serum analysis
The 12 participants in Ionescu and Frohman’s pulsatility report also connect to a later paper. Sackmann-Sala’s team used samples from 11 of those same people to examine serum proteins. A second publication added another analytical view of the samples, so adding the two paper counts would count some people twice.[4][12]
The discontinued CJC-1295 programme
The later phase 2 story stops at a terminated registry entry, NCT00267527, with 120 in its enrolment field and no posted results. FDA’s review recounts a 2006 programme halt after a reported participant death, drawing on reports from the time. The registry does not establish whether the compound caused that death or how many participants completed an analysis.[13][8]
Where do the regulatory records stand?
For the Canadian record, we searched Health Canada’s Drug Product Database for ipamorelin, CJC and Mod GRF on 30 October 2026 and found no matching ingredient entries. Health Canada also names both ipamorelin and CJC-1295 in its April 2026 advisory on unauthorized peptide drugs. That advisory makes clear that a research-use label does not remove the product’s regulatory requirements.[18][19]
The FDA record is easier to follow once you separate its two compounding tracks. CJC-1295 and ipamorelin acetate appear among withdrawn nominations under 503A, while ipamorelin acetate also has a Category 2 entry under the separate 503B interim policy. That is why a bare reference to “Category 2” can leave out part of the story.[16]
The committee history goes back to 2024. FDA’s Pharmacy Compounding Advisory Committee recommended against including the evaluated ipamorelin forms that October and the evaluated CJC-1295 forms that December. Those votes advise the agency; they do not grant product approval. Neither compound appeared on the July 2026 meeting agenda.[14][15][17]
WADA names both compounds directly in the 2026 Prohibited List. CJC-1295 appears with the GHRH analogues and ipamorelin with GH secretagogues and mimetics, all under S2.2.4. Their prohibition applies at all times, including outside competition.[20]
Questions that follow the evidence
What is ipamorelin?
Ipamorelin is a synthetic chain of five amino acids, also called NNC 26-0161. It activates the ghrelin receptor, GHS-R1a, and researchers have followed both the resulting GH signal and the peptide’s own concentration over time.[1][5][9][10]
What is CJC-1295?
ConjuChem developed CJC-1295 as a modified GHRH analogue with an added DAC group. That group lets it bind to albumin in the bloodstream, giving it the extended time in circulation described in the original research. The exact name needs care because “CJC-1295” also appears on materials labelled “without DAC”.[2][8]
Where did the compounds originate?
Ipamorelin came from Novo Nordisk’s research programme and was described by Raun and colleagues in 1998. CJC-1295 came from ConjuChem in Montreal; its albumin-binding chemistry appeared in Jetté’s 2005 paper, followed by early human findings in 2006.[1][2][3]
How are their receptor pathways different?
Ipamorelin uses the ghrelin receptor, GHS-R1a, while CJC-1295 uses the GHRH receptor. Both pathways can reach GH-releasing pituitary cells. The separate receptors explain the interest in discussing them together, although our search identified no primary human trial of the pair.[1][2][10]
Is “CJC-1295 without DAC” the same molecule?
That label commonly refers to Mod GRF(1-29), which lacks the added albumin-binding modification. The shared CJC name can obscure the structural difference, so the sequence and terminal group are useful details to look for. The days-long half-life reported for the DAC compound belongs to that compound’s study.[3][6][7][8]
How much human research is there?
The record ranges from small studies of hormone concentrations to the published 117-person ipamorelin postoperative-ileus study. A later ipamorelin registry lists 320 participants without posted results, and the later CJC-1295 phase 2 record is terminated. There is also overlap between some CJC papers because researchers returned to samples from the same people; adding every paper’s count would overstate the number of participants.[3][10][11][12][13]
What is their WADA status?
WADA names both in S2.2.4 of its 2026 Prohibited List, with a prohibition that applies in and out of competition. CJC-1295 sits with the GHRH analogues, while ipamorelin sits with GH secretagogues and mimetics.[20]
Are either authorized by Health Canada?
Our 30 October 2026 Drug Product Database searches found no matching ingredient records for ipamorelin, CJC or Mod GRF. Health Canada also names both compounds in its April 2026 advisory on unauthorized peptide drugs and explains that a research-use label does not create an exemption.[18][19]
What should a storage statement specify?
A useful storage statement names the exact material and form, its container condition, a temperature and the period backed by stability testing. The papers reviewed here do not give us one temperature or shelf life that applies to all three materials. A COA records what the lab found at the test date; to establish shelf life, someone has to follow how the material changes over time.[8][21]
Abbreviations and Terms
GH and IGF-1
GH is growth hormone; IGF-1 is insulin-like growth factor 1. The CJC-1295 human studies followed their concentrations as part of the endocrine record.[3]
GHRH and its receptor
GHRH stands for growth hormone-releasing hormone. CJC-1295 is an analogue—a modified version—that acts at the GHRH receptor.[2]
GHS-R1a
This is the ghrelin receptor, the receptor activated by ipamorelin. It provides a different input to GH-releasing pituitary cells from the GHRH-receptor pathway.[1][10]
DAC and albumin
DAC means drug affinity complex. In CJC-1295, this added group allows the peptide to attach to albumin, a circulating protein that acts as its carrier.[2]
Mod GRF(1-29)
This is the modified 29-amino-acid sequence commonly labelled “CJC-1295 without DAC”. It lacks the added albumin-binding modification of the DAC compound.[7][8]
Half-life
Half-life describes the time for a measured concentration to fall by half during a stated phase of its decline. The estimate belongs to the molecule and experimental conditions being studied.[3][9]
Pulses, troughs and mean GH
Pulses are the bursts in the GH record, and troughs are the low points between them. Mean GH is the average concentration across the measurement period; it describes a different feature of the record from pulse frequency or magnitude.[4]
COA
A certificate of analysis records the tests and results reported for a sample. The compound name and lot number help connect that report to the material you are reading about; the COA guide explains the fields.
References
Primary papers, molecular records, trial registries and official regulatory sources. Checked 30 October 2026.
- Raun et al. (1998). Ipamorelin, the first selective growth hormone secretagogue. PMID 9849822.
- Jetté et al. (2005). hGRF(1-29)–albumin bioconjugates and the identification of CJC-1295. PMID 15817669. Descriptive short title.
- Teichman et al. (2006). Prolonged stimulation of GH and IGF-I secretion by CJC-1295 in healthy adults. PMID 16352683. Short title.
- Ionescu & Frohman (2006). Pulsatile secretion of GH persists during continuous stimulation by CJC-1295. PMID 17018654. Short title.
- PubChem. Ipamorelin, CID 9831659. Formula, molar mass, identifiers and sequence.
- PubChem. CJC-1295, CID 91971820. DAC structure record.
- PubChem. CID 56841945. Defined 29-residue structure; conflicting synonyms noted in the text.
- FDA. CJC-1295-related bulk substances: December 2024 briefing document. Chemistry, human-study review and development history.
- Gobburu et al. (1999). Pharmacokinetic–pharmacodynamic modelling of ipamorelin in human volunteers. PMID 10496658. Short title.
- Beck et al. (2014). Randomized ipamorelin study in postoperative ileus. PMID 25331030. Descriptive short title.
- ClinicalTrials.gov. NCT01280344. Ipamorelin phase 2 registry; 320 actual participants; no posted results.
- Sackmann-Sala et al. (2009). CJC-1295 and serum-protein profiles. PMID 19386527. Descriptive short title; cohort overlap stated in Methods.
- ClinicalTrials.gov. NCT00267527. Terminated CJC-1295 phase 2 record.
- FDA. Final minutes, PCAC, 29 October 2024. Ipamorelin votes.
- FDA. Final minutes, PCAC, 4 December 2024. CJC-1295 votes.
- FDA. Current bulk-substance risk notices. Separate active Category 2 and withdrawn-nomination tables.
- FDA. PCAC meeting agenda, 23–24 July 2026.
- Health Canada. Drug Product Database API. Active-ingredient searches: IPAMORELIN, CJC and MOD GRF; no matches on the check date.
- Health Canada. Peptide advisory RA-81874, 9 April 2026.
- WADA. 2026 Prohibited List. S2.2.4.
- FDA. Ipamorelin-related bulk substances: October 2024 briefing document. Chemistry, stability and human-study review.