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CJC-1295

CJC-1295

30-amino-acid GHRH analog with Drug Affinity Complex (DAC) albumin-binding modification more info
CJC-1295 with DAC is a synthetic 30-amino-acid analog of growth hormone-releasing hormone (GHRH 1-29) carrying four protease-resistance substitutions and a C-terminal maleimidopropionic acid (MPA) linker that covalently conjugates to cysteine-34 of circulating human serum albumin. The albumin tether confers a ~6-8 day plasma half-life. The without-DAC sequence sibling (Mod GRF 1-29) is a chemically distinct 29-amino-acid molecule with a half-life closer to thirty minutes; the two are routinely conflated in vendor catalogs. The published human pharmacology record consists of two papers from 2006.

Available for laboratory research use only.

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  • Identity
  • Purity (HPLC)
  • Endotoxin (USP <85>)
  • Sterility (USP <71>)
  • Heavy metals (ICP-MS per USP <233>)
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Biochemical Profile

CAS Number
863288-34-0
Molecular Formula
C165H269N47O46
Molecular Weight
3647.25 g/mol
Purity
≥98% (RP-HPLC-UV (220 nm) with LC-MS deconvolution for DAC integrity)
PubChem CID
91971820
Amino Acid Sequence
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(Nε-MPA)

Receptor Targets and Pharmacokinetic Design

CJC-1295 binds the growth hormone-releasing hormone receptor (GHRH-R, a Gαs-coupled receptor) on anterior pituitary somatotroph cells, where native GHRH triggers cyclic AMP elevation and pulsatile growth hormone (GH) release into systemic circulation. The molecule was derived from sermorelin (native GHRH 1-29, the bioactive N-terminal fragment of human GHRH 1-44, encoded at chromosome 20q11.23 and assigned UniProt P01286) by introducing four amino acid substitutions: D-Ala at position 2 (blocking DPP-IV N-terminal cleavage), Gln at position 8 (removing an asparagine deamidation hotspot), Ala at position 15 (stabilizing the backbone), and Leu at position 27 (eliminating the methionine oxidation pathway)[1]. These four substitutions are shared by the with-DAC and without-DAC forms and confer plasma protease resistance.

The Drug Affinity Complex (DAC) modification, present only in the with-DAC form, is a maleimidopropionic acid (MPA) group conjugated to the ε-amine of lysine-30. Following subcutaneous injection, the maleimide undergoes Michael addition to the free thiol of cysteine-34 on circulating human serum albumin, forming a stable thioether covalent bond. The peptide is now tethered to albumin and inherits albumin's natural 19-21 day plasma residence[1]. The result is a sustained, multi-day occupancy of the GHRH receptor, in contrast to the pulsatile signaling pattern of native hypothalamic GHRH.

The receptor-binding profile of the without-DAC form (Mod GRF 1-29) is identical at the GHRH-R level. The two forms differ in pharmacokinetic design, not in receptor pharmacology. The without-DAC form has an extrapolated plasma half-life closer to thirty minutes based on comparison to sermorelin and the four protease-resistance substitutions; no peer-reviewed primary human pharmacokinetic study has isolated the Mod GRF 1-29 form under any name in the published literature.

The published human pharmacology record for the with-DAC form consists of two papers in 2006: Teichman et al. reported two randomized controlled trials in healthy adults with subcutaneous administration over 28 and 49 days, observing a plasma half-life of 5.8 to 8.1 days, with GH and IGF-1 elevation persisting for several days per administration in the trial[2]. Ionescu and Frohman reported preservation of pulsatile GH secretion patterns over 7 days of continuous GHRH-R activation in 8 healthy young men[3]. The Teichman trial was authored by the ConjuChem chief medical officer with the ConjuChem chief executive as co-author; the molecule, the funding, and the trial conduct were all internal to the sponsor.

No independent replication of either 2006 paper has been published. ConjuChem Biotechnologies Inc. filed for bankruptcy in July 2010 following an asset sale; the subsequent ConjuChem LLC (operating within the Soon-Shiong portfolio from August 2011) pivoted to CJC-1134-PC, a DAC-modified GLP-1 analog for diabetes, and the GHRH program has not been resumed by any current sponsor[4]. The evidence base is structurally frozen at 2006.

Research Applications

Pituitary Endocrinology and Growth Hormone Axis Research

The GHRH receptor is expressed on anterior pituitary somatotroph cells and signals through the Gαs / adenylyl cyclase / cyclic AMP pathway to drive GH transcription and pulsatile release. Native hypothalamic GHRH is secreted into hypophyseal portal circulation in approximately 3 to 4 hour cycles, with somatostatin from periventricular nuclei providing counter-regulation. The integrated pulse pattern is the physiological signal that the GH / IGF-1 axis is tuned to interpret.

The published human pharmacology of CJC-1295 with DAC is concentrated in the GH and IGF-1 endpoint domain. Teichman et al. (2006) reported GH excursions in healthy adult volunteers over multi-day windows following single subcutaneous administration of the with-DAC form, with cumulative IGF-1 elevation measured up to 28 days under multidose conditions[2]. The two trials were conducted in 30 healthy adults across the 28-day and 49-day study arms.

Ionescu and Frohman (2006) reported that pulsatile GH secretion was preserved over 7 days of continuous GHRH-R activation by the with-DAC form in 8 healthy young men[3]. This finding is the load-bearing observation for the commercial framing of CJC-1295 as compatible with pulsatile signaling. The finding rests on 8 subjects over 7 days; generalization to chronic multi-month administration has not been characterized in the peer-reviewed literature.

Albumin Conjugation and Drug Affinity Complex Chemistry

The DAC linker chemistry is the entire mechanism by which the with-DAC form achieves its multi-day half-life. The maleimide group on the lysine-30 side chain undergoes Michael addition with the free Cys34 thiol of human serum albumin, the only readily reactive thiol present in human plasma. The resulting thioether bond is stable, and the peptide inherits albumin's natural plasma residence of approximately 19 to 21 days. Jetté et al. (2005) reported the underlying conjugation chemistry and antibody-response characterization in the ConjuChem development program[1].

The critical product-stability failure mode is maleimide hydrolysis. In aqueous solution at neutral pH, maleimides ring-open to the corresponding maleamic acid (mass increase of 18 daltons) with a half-life of hours to days. The ring-opened form no longer Michael-adds to albumin. A reconstituted batch can be 99% pure by peptide HPLC and still be 50 to 70% functionally inactive DAC after extended storage above 4 degrees Celsius. Reversed-phase HPLC at 220 nm cannot distinguish intact from ring-opened maleimide; LC-MS deconvolution paired with a thiol-reactivity assay is the diagnostic test that quantifies the three product isoforms (intact M, ring-opened M+18, and decoupled M-151).

Most research-use vendor Certificates of Analysis report peptide HPLC purity and total mass alone. Both measurements are blind to the ring-opened maleimide. Per-batch LC-MS deconvolution plus a thiol-reactivity readout is the QC test most diagnostic of DAC integrity for this peptide and is absent from competitor product disclosure across the comparable laboratory commerce category.

Pulsatile Versus Sustained Signaling Design Comparison

Two FDA-approved GHRH analogs exist; CJC-1295 is not one of them. Sermorelin (native GHRH 1-29) received FDA approval as a diagnostic in 1990 and for chronic pediatric GH deficiency in 1997; it was withdrawn in 2008 for commercial reasons unrelated to safety or efficacy[5]. Tesamorelin received FDA approval in 2010 for a narrow HIV-associated indication[6]. Both approved members of the GHRH-analog class are short-half-life molecules that preserve pulsatile GHRH-R signaling by design.

The with-DAC form of CJC-1295 takes the opposite pharmacokinetic path. By tethering to albumin, it converts the natural pulsatile GHRH signal into sustained, multi-day GHRH-R occupancy. Ionescu and Frohman (2006) reported preservation of GH pulsatility over 7 days in 8 healthy men[3]; whether this preservation extends to chronic multi-month signaling has not been characterized in published human studies. The pharmacological question of whether sustained GHRH-R signaling phenocopies pulsatile signaling at chronic timescales remains open in the peer-reviewed record.

The approved indications of these distinct molecules do not transfer to CJC-1295. Importing sermorelin or tesamorelin safety or efficacy data to CJC-1295 is not supported by published comparison studies. The class is regulable, as the existence of two approved members demonstrates; the with-DAC molecule is not approved by any major regulatory authority for any indication.

GHRH Receptor Splice Variants and Tumor Biology

GHRH-R splice variants, notably SV1, are documented on multiple human cancer cell lines including pancreatic (MIA PaCa-2), prostate, breast, lung, renal, ovarian, and bone cancer preparations. Rekasi et al. (2002) reported the SV1 splice variant characterization across human cancer cell lines, and subsequent work from the Schally laboratory at Tulane and Miami extended these observations across additional tumor types[7]. Cells transfected with SV1 gain mitogenic responsiveness to GHRH agonists.

Andrew Schally received the 1977 Nobel Prize in Physiology or Medicine for the discovery of hypothalamic regulatory peptides including GHRH. The post-Nobel academic program from the Schally laboratory has spent more than 25 years developing GHRH antagonists (JV-1-36, JV-1-38, MIA-602, MZ-J-7-138, and related compounds) as anti-tumor agents, specifically because GHRH-R-positive tumors expand under agonist exposure[8].

The chronic-GHRH-R-agonism question for the with-DAC form of CJC-1295 has not been engaged in any peer-reviewed publication. The Teichman 2006 cohort (approximately 30 healthy adults over 49 days) and the Ionescu 2006 cohort (8 healthy men over 7 days) are not powered to detect a cancer-acceleration signal in patients with occult GHRH-R-positive tumors. The ConjuChem Phase 2 trial in HIV-associated visceral adiposity (NCT00267527) might in principle have provided some longer-term signal at the n=192 planned cohort, but the trial halted at first dose for most enrolled participants and the data were never published. The honest framing in the peer-reviewed record is unanswered, not answered safely.

Stability, Quality Testing, and Storage Considerations

The dominant aqueous degradation pathway for the with-DAC form is maleimide hydrolysis at the lysine-30 conjugation site. Lyophilized storage at minus 20 degrees Celsius preserves the intact maleimide for 18 to 24 months under sealed dry conditions with desiccant. Once placed into aqueous solution, the maleimide hydrolysis clock is running; the ring-opened maleamic acid form (mass increase 18 daltons) accumulates over hours to days at neutral pH and is no longer thiol-reactive.

Secondary stability concerns include aspartimide formation at the asparagine and aspartate residues at positions 3 and 25 during synthesis and storage, racemization of D-alanine at position 2 under prolonged base exposure, and hygroscopicity of the acetate counter-ion form. Karl Fischer water content and counter-ion identity (acetate versus trifluoroacetate) are standard COA fields; both affect the reported molecular mass.

A defensible quality panel for the with-DAC form includes RP-HPLC at 220 nm with greater than 98% area, ESI-MS or LC-MS confirmation of the M plus H envelope, LC-MS deconvolution to quantify the three DAC isoforms, a thiol-reactivity stoichiometric readout (using N-acetylcysteine or glutathione consumption), and Marfey's reagent chiral analysis to confirm the D-alanine-2 configuration. Endotoxin testing by Limulus Amebocyte Lysate, bioburden, residual solvents, and heavy metals per ICH Q3D round out the panel for research-grade laboratory material.

Independent Replication, Clinical Status, and Regulatory Posture

The peer-reviewed human pharmacology record for CJC-1295 in either form is two papers from 2006 (Teichman et al. and Ionescu and Frohman), both involving ConjuChem-supplied molecule, with the trial conduct internal to the sponsor[2][3]. No independent replication of either paper has been published. The corresponding PubMed corpus for CJC-1295 across all topics is approximately 30 to 50 indexed papers, making it the smallest catalog entry by published volume.

ConjuChem Biotechnologies Inc. (founded 1997, Montreal; TSX-listed November 2000) terminated its Phase 2 HIV-associated visceral adiposity trial (NCT00267527, n=192 planned, multicenter) following a participant death at the Argentina site on July 17, 2006, after the eleventh weekly subcutaneous dose of CJC-1295 with DAC. The attending physician's clinical impression was acute myocardial infarction attributed to asymptomatic pre-existing coronary artery disease unrelated to study drug; no autopsy, no Data Safety Monitoring Board minutes, and no FDA or regulator report have surfaced in the public record. The trial was halted and the company filed for Canadian bankruptcy on July 21, 2010. The relaunched ConjuChem LLC (Los Angeles, August 2011) within the Soon-Shiong portfolio pivoted to a DAC-modified GLP-1 program and never resumed GHRH development[4].

The regulatory posture closed in late 2024. Both forms of CJC-1295 were placed on FDA 503A Category 2 (Do-Not-Compound) in September 2023. On December 4, 2024, the FDA Pharmacy Compounding Advisory Committee voted against 503A bulks-list inclusion for all five SKU variants (free base, acetate, DAC free base, DAC acetate, DAC trifluoroacetate)[9]. CJC-1295 was not in the April 22, 2026 RFK Jr. 12-peptide reclassification batch and was not on the July 23-24, 2026 PCAC docket. The World Anti-Doping Agency lists CJC-1295 explicitly under S2.2.4 (Growth Hormone Releasing Factors) as a non-specified substance prohibited at all times with no Therapeutic Use Exemption pathway; Henninge et al. (2010) reported the first analytical detection method[10]. The Australian Therapeutic Goods Administration scheduled CJC-1295 as Schedule 4 plus Appendix D Item 5 in June 2015. The Tailor Made Compounding plea (2022 to 2023, $1.79 million forfeiture) explicitly named CJC-1295[11]; the United States versus Watkins indictment (April 1, 2026, District of Utah, 1:26-cr-00015-DBB) explicitly named CJC-1295 alongside other compounding peptides[12].

Research Literature

Published literature reviews from the Peerless research desk that reference CJC-1295.

Reconstitution & Storage

Recommended Diluent
Sterile water
Storage (lyophilized)
-20°C, dry, dark, 18-24 months
Storage (reconstituted)
2-8°C, use promptly (maleimide hydrolysis clock runs in aqueous solution)
Shelf Life
18-24 months lyophilized

Research References

  1. [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. Endocrinology. 2005;146(7):3052-3058. PMID:15817669
  2. [2] Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. 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;91(3):799-805. PMID:16352683
  3. [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. J Clin Endocrinol Metab. 2006;91(12):4792-4797. PMID:17018654
  4. [4] ConjuChem Biotechnologies Inc. corporate filings. TSX delisting and Canadian bankruptcy proceedings July 21, 2010; ConjuChem LLC relaunch within the Soon-Shiong portfolio, Los Angeles, August 30, 2011 (verified 2026-05-19 from public corporate records and aidsmap contemporaneous reporting on NCT00267527 trial halt).
  5. [5] EMD Serono / Merck Serono. Sermorelin acetate for injection prescribing information and withdrawal notice. FDA confirmation that withdrawal was for commercial reasons, not safety or efficacy. December 2008.
  6. [6] Falutz J, Mamputu JC, Potvin D, et al. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010;95(9):4291-4304. PMID:20554713
  7. [7] Rekasi Z, Czompoly T, Schally AV, Halmos G. Isolation and sequencing of cDNAs for splice variants of growth hormone-releasing hormone receptors from human cancers. Proc Natl Acad Sci USA. 2000;97(19):10561-10566. PMID:10984545
  8. [8] Schally AV, Varga JL, Engel JB. Antagonists of growth-hormone-releasing hormone: an emerging new therapy for cancer. Nat Clin Pract Endocrinol Metab. 2008;4(1):33-43. PMID:18084344
  9. [9] FDA Pharmacy Compounding Advisory Committee (PCAC). Meeting transcript and voting record, December 4, 2024. Vote against 503A bulks-list inclusion for CJC-1295 (all five SKU variants) and Ipamorelin (October 29, 2024 vote). FDA Briefing Document recommended against inclusion.
  10. [10] Henninge J, Pepaj M, Hullstein I, Hemmersbach P. Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation. Drug Test Anal. 2010;2(11-12):647-650. PMID:21204297
  11. [11] United States v. Tailor Made Compounding LLC, et al. Plea agreement and $1.79 million forfeiture record, 2022-2023. CJC-1295 explicitly named in charging documents alongside Ipamorelin.
  12. [12] United States v. Justin Bradley Watkins. United States District Court, District of Utah, Case No. 1:26-cr-00015-DBB. Indictment filed April 1, 2026. CJC-1295 explicitly named alongside additional compounding peptides; first federal indictment of a US-licensed physician for selling misbranded peptides.
  13. [13] Frohman LA, Kineman RD. Growth hormone-releasing hormone and pituitary development, hyperplasia and tumorigenesis. Trends Endocrinol Metab. 2002;13(7):299-303. PMID:12114112
  14. [14] Cunha SR, Mayo KE. Ghrelin and growth hormone (GH) secretagogues potentiate GH-releasing hormone (GHRH)-induced cyclic adenosine 3',5'-monophosphate production in cells expressing transfected GHRH and GH secretagogue receptors. Endocrinology. 2002;143(12):4570-4582. PMID:12446584
  15. [15] Alba M, Fintini D, Bowers CY, Parlow AF, Salvatori R. Effects of long-term treatment with growth hormone-releasing peptide-2 in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(5):E929-E936. PMID:16822960
  16. [16] Sackmann-Sala L, Ding J, Frohman LA, Kopchick JJ. 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. Growth Horm IGF Res. 2009;19(6):471-477. PMID:19505838

Scientific Journal Author

Lawrence A. Frohman, MD

Section of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago College of Medicine

Landmark Publications

  • Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. 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;91(3):799-805. (PMID 16352683)
  • Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792-4797. (PMID 17018654)
  • Frohman LA, Kineman RD. Growth hormone-releasing hormone and pituitary development, hyperplasia and tumorigenesis. Trends Endocrinol Metab. 2002;13(7):299-303. (PMID 12114112)

Dr. Frohman is independently cited here as the external academic co-author of the two 2006 human pharmacology papers on CJC-1295. There is no affiliation or commercial relationship between Dr. Frohman, the University of Illinois at Chicago, or any associated commercial entity, and Peerless Peptides.

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