CJC-1295 vs Ipamorelin vs Tesamorelin: Mechanism, Half-Life, Evidence & FDA Status (2026)

Direct answer: CJC-1295, Ipamorelin, and Tesamorelin are three different growth-hormone secretagogues with different molecular identities, receptors, pharmacokinetics, and regulatory status. CJC-1295 and Tesamorelin are GHRH-receptor agonists, whereas Ipamorelin is a selective GHS-R1a agonist. Tesamorelin is the only FDA-approved drug among the three. CJC-1295 and Ipamorelin are not FDA-approved medicines.

The most important chemical distinction is within CJC-1295 itself: CJC-1295 with DAC is an albumin-binding modified GHRH analog, whereas “CJC-1295 without DAC” commonly refers to Modified GRF(1-29) — a distinct, shorter-acting molecule.

Research-use note: This is an educational comparison of published pharmacology for laboratory researchers. It is not medical advice. CJC-1295 and Ipamorelin are research peptides, not approved medicines. Tesamorelin is an FDA-approved prescription drug and should not be represented as an unapproved research chemical.


Key Findings

  1. Two receptors, one output. GHRH analogs (CJC-1295, Tesamorelin) signal through cAMP/PKA; the ghrelin-mimetic (Ipamorelin) signals through PLC/IP3/PKC. The two pathways show a GHRH–GHS-R1a pharmacological interaction at the pituitary.
  2. CJC-1295 is a GHRH(1-29) derivative, not a 44-mer. The DAC version is a 30-residue peptide conjugate whose Lys30 carries a maleimidopropionyl group that binds albumin, extending half-life from ~30 min to ~6 days.
  3. “CJC-1295 with DAC” and “without DAC” are different molecules. The “without DAC” form is chemically Modified GRF(1-29); the DAC form is a distinct albumin-binding conjugate.
  4. Regulatory status is not uniform. Tesamorelin (Egrifta) is FDA-approved (2010, HIV-associated lipodystrophy); CJC-1295 and Ipamorelin both reached Phase II before discontinuation.
  5. Half-life spans nearly two orders of magnitude — from Ipamorelin’s ~2 hours to CJC-1295 DAC’s ~6 days.

1. Entity Definition Table

EntityDefinitionKey identifier
CJC-1295 (DAC)Maleimido derivative of hGRF(1-29) with a Lys30-Nε-maleimidopropionyl albumin-binding moietyCAS 446262-90-4; PubChem CID 91971820
Modified GRF(1-29)The 29-residue peptide commonly marketed as “CJC-1295 without DAC”
IpamorelinPentapeptide GHS-R1a agonist / ghrelin mimetic (Aib-His-D-2-Nal-D-Phe-Lys-NH₂)CAS 170851-70-4; PubChem CID 20754357
Tesamorelin[trans-3-hexenoyl]GHRH(1-44) analogCAS 218949-48-5; PubChem CID 16137828
GHRH-RGrowth-hormone-releasing-hormone receptor
GHS-R1aGrowth hormone secretagogue receptor type 1a (ghrelin receptor)

Identification principle: Never identify a peptide solely by its commercial name. “CJC-1295 without DAC” is a common research-market name rather than a preferred chemical identifier — the more chemically descriptive designation is Modified GRF(1-29).


2. Molecular Identity

PropertyModified GRF(1-29)CJC-1295 (DAC)IpamorelinTesamorelin
ClassGHRH analogGHRH analog + albumin binderGHS-R1a agonist / ghrelin mimeticGHRH analog
Peptide residues2930544
DAC modificationNoneLys30 Nε-maleimidopropionylNoneNone
Albumin bindingNoYesNoNo
SequenceH-Tyr-D-Ala²-Asp-Ala-Ile-Phe-Thr-Gln⁸-Ser-Tyr-Arg-Lys-Val-Leu-Ala¹⁵-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu²⁷-Ser-Arg-NH₂(29-mer above) + Lys30(Nε-maleimidopropionyl)Aib-His-D-2-Nal-D-Phe-Lys-NH₂[trans-3-hexenoyl]GHRH(1-44)-NH₂
Molecular weight≈ 3.4 kDa3,647 Da711.87 Da≈ 5,136 Da
Molecular formula— (29-mer)C₁₆₅H₂₆₉N₄₇O₄₆C₃₈H₄₉N₉O₅C₂₂₁H₃₆₆N₇₂O₆₇S
CAS446262-90-4170851-70-4218949-48-5
PubChem CID919718202075435716137828
Half-life (human)~30 min~6 days (5.8–8.1 d)~2 hFormulation-dependent (see §5)
ReceptorGHRH-RGHRH-RGHS-R1aGHRH-R
Regulatory statusResearch peptideResearch peptide (Phase II discontinued)Research peptide (Phase II discontinued)FDA-approved (Egrifta)

Note: Molecular weights above are for the free-base forms indexed in PubChem. Actual molecular mass can differ depending on the salt/counterion form (e.g., acetate or TFA) specified by the supplier — a distinction that matters for molar concentration calculations.


3. CJC-1295: The Long-Acting GHRH Analog

3.1 Structure

CJC-1295 is a modified form of GHRH(1-29) (sermorelin) carrying four substitutions — D-Ala², Gln⁸, Ala¹⁵, Leu²⁷ — that reduce proteolytic degradation. It was developed by ConjuChem Biotechnologies. PubChem (CID 91971820) describes the DAC form as a maleimido derivative of hGRF(1-29).

3.2 The DAC Mechanism

The long half-life comes from a Drug Affinity Complex (DAC) — a maleimidopropionyl-based albumin-binding modification — not from the peptide sequence itself:

  1. A maleimide-containing linker is attached to the C-terminus (Lys30).
  2. The maleimide forms a covalent bond with cysteine-34 of serum albumin.
  3. The peptide circulates with albumin, releasing active peptide gradually.
  4. Result: human half-life ≈ 5.8–8.1 days (vs ~30 min without the DAC moiety).

3.3 Pharmacokinetics & Clinical History

In a single human study (Teichman et al. 2006), a single CJC-1295 DAC dose raised GH approximately 2- to 10-fold and IGF-1 approximately 1.5- to 3-fold. These figures come from one small study and should be read as illustrative, not definitive.

CJC-1295 reached Phase II for lipodystrophy and GH deficiency. The program was halted after a participant died: contemporary reporting indicated the attending physician considered previously undiagnosed coronary artery disease with plaque rupture the most likely cause and did not attribute the event to CJC-1295; the sponsor nevertheless terminated development as a precaution.

3.4 Why “with DAC” vs “without DAC” Matters

The two forms are chemically distinct and not interchangeable:

Modified GRF(1-29)CJC-1295 (DAC)
C-terminalSer-Arg-NH₂Ser-Arg-Lys30(Nε-maleimidopropionyl)-NH₂
Half-life~30 min5.8–8.1 days
Dosing frequency in researchFrequentInfrequent

A research buyer should confirm which form is being supplied — the commercial name “CJC-1295” alone does not specify this, and the two forms have materially different pharmacokinetics.


4. Ipamorelin: The Selective GHS-R1a Agonist

4.1 Structure

Ipamorelin (Novo Nordisk; development code NNC 26-0161) is a pentapeptideAib-His-D-2-Nal-D-Phe-Lys-NH₂ — derived from GHRP-1. It is a selective agonist of the growth hormone secretagogue receptor type 1a (GHS-R1a).

4.2 Mechanism

GHS-R1a activation couples to Gq/11 → PLC → IP3/DAG → Ca²⁺ release + PKC → GH exocytosis. GHS-R1a activation provides a signaling route that is pharmacologically distinct from GHRH receptor activation and can interact with the somatostatin-regulated GH axis — a different entry point than the cAMP/PKA pathway used by GHRH analogs.

4.3 Selectivity Profile (reported)

Ipamorelin’s defining feature is reported selectivity — in original characterization studies (Raun et al. 1998) it stimulated GH without significant effect on prolactin, ACTH, cortisol, FSH, LH, or TSH. The following is a qualitative summary, not a quantitative ranking:

ParameterIpamorelinGHRP-2GHRP-6Hexarelin
GH releaseHighHighHighHigh
CortisolMinimalModerateModerateModerate
ProlactinMinimalLowLowLow
AppetiteLowModerateHighModerate

Its elimination half-life is ~2 hours (Gobburu et al. 1999). Clinical development for postoperative ileus was discontinued after Phase II studies failed to demonstrate sufficient efficacy (Beck et al. 2014).


5. Tesamorelin: The Approved GHRH Analog

Tesamorelin is GHRH(1-44) carrying a trans-3-hexenoyl group at the N-terminal tyrosine. It activates the GHRH receptor and promotes endogenous GH secretion, with downstream increases in IGF-1. It is the only compound in this comparison with an FDA-approved drug product: Egrifta (tesamorelin for injection) was approved November 10, 2010 for reduction of excess abdominal fat in adults with HIV-associated lipodystrophy, on the basis of Phase 3 data (Falutz et al. 2007).

Half-life note: Tesamorelin pharmacokinetics vary by formulation and study population. Earlier EGRIFTA labeling reported mean elimination half-lives of approximately 26 minutes in healthy subjects and 38 minutes in HIV-infected patients, while the current EGRIFTA WR label reports approximately 11 minutes after a single 1.28 mg subcutaneous dose. A single generic half-life should not be applied across all tesamorelin formulations.

Regulatory note: Tesamorelin’s approval is indication-specific (HIV-associated lipodystrophy). Approval does not extend to other uses. Any commercial or research handling should comply with applicable drug and local regulatory requirements.


6. Head-to-Head Comparison

DimensionCJC-1295 DACIpamorelinTesamorelin
ReceptorGHRH-RGHS-R1aGHRH-R
SignalingcAMP/PKAPLC/IP3/PKCcAMP/PKA
Half-life5.8–8.1 days~2 hFormulation-dependent (11–38 min)
GH patternProlonged elevationPulsatileEndogenous secretion
IGF-1 inductionSustained (days)ModerateSustained
SelectivityGH axisRelatively selective for GHGH axis
RegulatoryPhase II discontinuedPhase II discontinuedFDA-approved (Egrifta)

6.1 The GHRH–GHS-R1a Pharmacological Interaction

Experimental studies have demonstrated supra-additive GH responses when GHRH and GHRP/GHS-R agonism are combined (Veldhuis & Bowers 2003). This is a laboratory observation about pituitary signaling, not a therapeutic recommendation — combination research investigates mechanism, not clinical benefit.


7. Clinical Evidence Snapshot

CompoundHuman PK/PDClinical trialsCompleted efficacy evidenceFDA approval
CJC-1295 DACYesPhase IINo (discontinued)No
IpamorelinYesPhase IINegative/insufficient (POI)No
TesamorelinYesPhase IIIYes (HIV lipodystrophy)Yes

This table separates pharmacology (human PK/PD data exist for all three) from efficacy evidence (only Tesamorelin has a completed pivotal program). The two research peptides reached early clinical stages but do not have approved indications.


8. Evidence Type Framework

RPL Peptides Evidence Framework. The levels below are an editorial framework used in this article and are not equivalent to GRADE, Oxford CEBM, FDA evidence classifications, or any other formal regulatory evidence system. Chemical identity data (sequence, molecular weight, formula) are drawn from authoritative databases (PubChem, CAS, FDA records) rather than from an evidence tier.

LevelDefinition
ARegulatory / approved-product evidence
BHuman randomized / controlled clinical evidence
CHuman PK/PD evidence
DReplicated preclinical / biochemical evidence
ELimited or single-group preclinical evidence
ClaimEvidence level
Tesamorelin FDA approval (indication-specific)A
Tesamorelin Phase 3 efficacy (HIV lipodystrophy)B
CJC-1295 half-life 5.8–8.1 days; GH/IGF-1 elevationC
Ipamorelin half-life ~2 hC
Ipamorelin selectivity (no cortisol/ACTH)D
GHRH–GHS-R1a supra-additive GH responseD
CJC-1295 / Ipamorelin Phase II discontinuationA–B (trial/company records)

Regulatory status is treated as a separate dimension from biological evidence — approval reflects a regulatory determination, not a scientific efficacy claim.


9. Quality Specifications (Typical Targets, Not Universal Standards)

The values below are typical supplier targets for research-grade material, not universal regulatory standards. Thresholds vary by supplier, application, and analytical method — verify against each product’s Certificate of Analysis (COA).

ParameterTypical approachMethod
Purity≥ 99% (commonly requested)RP-HPLC (214 nm)
Mass identityConsistent with theoretical/expected mass within method-specific toleranceLC-MS / HRMS / MALDI-TOF as appropriate
Peptide content70–90% net peptideAmino acid analysis
Water< 5%Karl Fischer
EndotoxinApplication-specific acceptance limitLAL or recombinant Factor C

Purity ≠ peptide content. HPLC purity and net peptide content are different measurements. Net peptide content is lower than chromatographic purity because the gross powder weight includes counterions (acetate/TFA), residual water, and residual solvents — a distinction that matters when calculating molar concentrations.

For interpretation guidance: COA interpretation guide · HPLC interpretation guide · white paper on reading a COA.


10. Buyer Checklist: What to Ask the Manufacturer

  1. Exact molecule — confirm whether CJC-1295 is the DAC or “without DAC” (Modified GRF 1-29) form; they are different products with different half-lives.
  2. Sequence and molecular weight — request MS-confirmed identity consistent with the theoretical mass, and the salt/counterion form (especially the Ipamorelin pentapeptide).
  3. Purity result and method — ask for the actual chromatographic purity result and method; ≥ 99% is a commonly requested research-grade specification, but the appropriate acceptance criterion depends on the application.
  4. Peptide content vs. gross weight — account for counterion (TFA/acetate), residual water, and residual solvents; HPLC purity is not net peptide content.
  5. Endotoxin result — ask for the actual value and confirm it meets the requirements of the intended experimental system.
  6. Lot traceability — a unique lot number through synthesis → purification → QC.
  7. Storage — compound-specific: confirm the recommended temperature per the product COA (lyophilized material is commonly stored at −20 °C, but verify per compound).
  8. Regulatory framing — confirm “research use only” labeling for unapproved compounds; reject any therapeutic representation.

11. Frequently Asked Questions

What is the difference between GHRH analogs and GHRP?
GHRH analogs (CJC-1295, Tesamorelin) act at the pituitary GHRH receptor via cAMP/PKA. GHRPs (Ipamorelin) act at the ghrelin receptor (GHS-R1a) via PLC/IP3/PKC. The two systems interact pharmacologically.

What does DAC mean in CJC-1295?
DAC (Drug Affinity Complex) is a maleimidopropionyl-based albumin-binding modification on Lys30 that extends half-life from ~30 min to ~6 days.

Is CJC-1295 a 44-amino-acid peptide?
No. CJC-1295 is a modified GHRH(1-29) — a 29-residue peptide (or a 30-residue conjugate with the DAC moiety). The 44-amino-acid peptide is Tesamorelin (GHRH 1-44).

Is “CJC-1295 without DAC” the same as Modified GRF(1-29)?
Yes in market practice, but the preferred chemical identifier is Modified GRF(1-29); “CJC-1295 without DAC” is a common research-market name.

Is any of these FDA-approved?
Tesamorelin (Egrifta) is FDA-approved for HIV-associated lipodystrophy. CJC-1295 and Ipamorelin are unapproved research peptides whose clinical programs were discontinued.

What is Ipamorelin’s half-life?
~2 hours — suitable for pulsatile GH protocols with low desensitization risk.

Can CJC-1295 and Ipamorelin be combined?
Their mechanisms show a supra-additive GH interaction in experimental studies; combination research investigates this mechanism. This is a laboratory observation, not a therapeutic recommendation.


12. Research Materials & Documentation

Product and reference pages, separated from the mechanism discussion above:

Cornerstone & guides (main site):

Related research comparisons:

Product & data pages:


References

  1. Jetté L, Léger R, Thibaudeau K, et al. “Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog.” Endocrinology. 2005;146(7):3052–3058. PMID: 15817669.
  2. Teichman SL, Neale A, Lawrence B, 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.” Journal of Clinical Endocrinology & Metabolism. 2006;91(3):799–805. PMID: 16352683.
  3. Ionescu M, Frohman LA. “Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog.” Journal of Clinical Endocrinology & Metabolism. 2006;91(12):4792–4797. PMID: 17018654.
  4. Alba M, Fintini D, Sagazio A, et al. “Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse.” American Journal of Physiology — Endocrinology and Metabolism. 2006;291(6):E1290–1294. PMID: 16822960.
  5. Raun K, Hansen BS, Johansen NL, et al. “Ipamorelin, the first selective growth hormone secretagogue.” European Journal of Endocrinology. 1998;139(5):552–561. PMID: 9849822.
  6. Gobburu JV, Agersø H, Jusko WJ, Ynddal L. “Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers.” Pharmaceutical Research. 1999;16(9):1412–1416. PMID: 10496658.
  7. Johansen PB, Nowak J, Skjaerbaek C, et al. “Ipamorelin, a new growth-hormone-releasing peptide, induces longitudinal bone growth in rats.” Growth Hormone & IGF Research. 1999;9(2):106–113. PMID: 10373343.
  8. Beck DE, Sweeney WB, McCarter MD. “Prospective, randomized, controlled, proof-of-concept study of the ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients.” International Journal of Colorectal Disease. 2014;29(12):1527–1534. PMID: 25331030.
  9. Falutz J, Allas S, Blot K, et al. “Metabolic effects of a growth hormone-releasing factor in patients with HIV.” New England Journal of Medicine. 2007;357(23):2359–2370. PMID: 18057338.
  10. Bowers CY. “Growth hormone-releasing peptide (GHRP).” Cellular and Molecular Life Sciences. 2012;69(13):2145–2157.
  11. Veldhuis JD, Bowers CY. “Determinants of GH-releasing hormone and GH-releasing peptide synergy in men.” Journal of Clinical Endocrinology & Metabolism. 2003;88(6):2820–2828.
  12. Kojima M, Kangawa K. “Ghrelin: structure and function.” Physiological Reviews. 2005;85(2):495–522.
  13. Alaiha M, Aschner P. “Tesamorelin: a review of clinical experience.” Expert Opinion on Biological Therapy. 2019;19(6):537–545.
  14. U.S. Food and Drug Administration. Egrifta (tesamorelin for injection) approval (November 10, 2010) and current DailyMed labeling.
  15. National Center for Biotechnology Information. PubChem CID 91971820 (CJC-1295); CID 20754357 (Ipamorelin); CID 16137828 (Tesamorelin). Accessed 2026-08-30.

For laboratory sourcing or OEM supply of research peptides, contact RPL Peptide.

Disclaimer: This article is for informational and research-context purposes only. It is not medical advice. CJC-1295 and Ipamorelin are research peptides not evaluated by the FDA for safety or efficacy. Tesamorelin (Egrifta) is an FDA-approved prescription drug; statements about its clinical use reflect published trial data and labeling. All mechanistic statements reflect published pharmacology and carry the evidence-level caveats noted above.

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