CJC-1295 with DAC

Two-molecule calibration (used throughout)

The single most important fact for this monograph is that “CJC-1295” in community usage refers to two structurally different peptides:

• CJC-1295 with DAC (synonyms: CJC-1295 DAC, DAC:GRF, the maleimide-albumin conjugate). The 29-mer tetrasubstituted GHRH(1-29) backbone (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) plus a C-terminal Lys-maleimidopropionamide (MPA-Lys) moiety that covalently bioconjugates to Cys34 of serum albumin in vivo. Molecular formula C₁₆₅H₂₆₉N₄₇O₄₆; MW ≈ 3,648 Da. CAS 863288-34-0 (base peptide; FDA distinguishes free base, acetate, and trifluoroacetate salt forms). Published human PK shows 5.8–8.1 day terminal half-life with GH elevation 2–10× for ≥6 days and IGF-1 elevation 1.5–3× for 9–11 days after a single subcutaneous dose [Peer-reviewed human study — Teichman et al., JCEM 2006, PMID 16352683]. This monograph covers the with-DAC compound only.
• CJC-1295 without DAC (synonyms: Modified GRF 1-29, Mod GRF 1-29, DAC-less CJC-1295). The same 29-mer backbone without the MPA-Lys moiety. MW ≈ 3,368 Da. Predicted plasma half-life ~30 min (extrapolated; no published human PK study). FDA-2024-N-4777 (December 2024) states explicitly that the two are “not interchangeable” and that “CJC-1295 (and its related salt forms) and CJC-1295 DAC (and its related salt forms) are also distinct active moieties as defined by FDA” [Regulatory document — FDA Briefing Document, FDA-2024-N-4777, 2024, footnote 2]. Covered in a separate monograph (cjc-1295-no-dac_mono_2026-05-16_D6-A82.md).

The structural difference matters operationally. The 280 Da delta is the difference between pulsatile-GHRH signalling at minute-scale half-life (no-DAC) and tonic GHRH-receptor occupancy at multi-day half-life (with-DAC). Pharmacology, regulatory treatment, clinical evidence base, and side-effect kinetics differ. The 2006 fatal myocardial infarction in the halted Phase 2 belongs to the with-DAC compound and is not transferable in either direction; the published human PK/PD record likewise belongs to the with-DAC compound only.

Vendor channels routinely flip between the two names within the same product page. The Vanguard Laboratory March 2026 essay flagged the QC implication: a buyer who receives DAC when they ordered no-DAC will overdose on every injection if they follow the no-DAC protocol; a buyer who receives no-DAC when they ordered DAC will underdose on every injection if they follow the weekly DAC protocol. Mass-spectrometry identity is the only reliable disambiguator (~3,648 Da vs ~3,368 Da). FDA’s December 2024 PCAC briefing surfaced one tested vendor sample of “CJC-1295 DAC” that mass-spec’d as the no-DAC molecule, framed by FDA as evidence that the vial probably never contained DAC to begin with [Regulatory document — FDA Briefing Document, FDA-2024-N-4777, 2024]. Core Peptides’ product page for CJC-1295 DAC lists a molecular weight of ~3,367.95 g/mol — the no-DAC mass — a vendor-side mislabel that community-knowledgeable buyers should treat as a red flag.

Where this monograph reads “CJC-1295 with DAC” or “DAC variant” it means the conjugated MW ≈ 3,648 Da compound. Where it references the no-DAC compound for comparison, it reads “CJC-1295 without DAC” or “no-DAC.”

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1. Identity

Field	Value	Source
Common research name	CJC-1295 with DAC	[Peer-reviewed human study — Teichman et al. 2006, PMID 16352683]
Synonyms	CJC-1295 DAC; DAC:GRF; drug affinity complex:growth-hormone-releasing factor; tetrasubstituted hGRF(1-29)-MPA-Lys30 analogue	[Peer-reviewed preclinical study — Jetté et al. 2005, PMID 15817669]
INN (WHO)	None assigned	[Regulatory document — WHO INN database query 2026-05-17, no entry]
CAS number	863288-34-0 (base peptide; FDA distinguishes free base, acetate, and trifluoroacetate salt forms)	[Regulatory document — FDA Briefing Document, FDA-2024-N-4777, 2024]
FDA active-moiety designation	Distinct from CJC-1295 without DAC: “CJC-1295 (and its related salt forms) and CJC-1295 DAC (and its related salt forms) are also distinct active moieties as defined by FDA”	[Regulatory document — FDA-2024-N-4777, 2024, footnote 2]
Molecular formula	C₁₆₅H₂₆₉N₄₇O₄₆ (DAC variant, free base)	[Academic secondary source — PubChem CID 91976842]
Molecular weight	~3,647.28 Da (DAC variant); contrast no-DAC ~3,367.9 Da	[Academic secondary source — PubChem CIDs 91976842, 56841945]
Sequence (1-letter)	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(Nε-3-maleimidopropionamide)-NH₂	[Peer-reviewed preclinical — Jetté et al. 2005]
Substitutions vs native GHRH(1-29)	D-Ala² (DPP-IV resistance), Gln⁸, Ala¹⁵, Leu²⁷ (proteolytic stability)	[Peer-reviewed preclinical — Jetté et al. 2005]
DAC moiety	Lys³⁰ with Nε-3-maleimidopropionamide (MPA) group; covalently bonds to free thiol on Cys34 of human serum albumin in vivo	[Peer-reviewed preclinical — Jetté et al. 2005, PMID 15817669]
Class	Long-acting albumin-conjugated GHRH(1-29) tetrasubstituted analogue; growth hormone-releasing hormone receptor agonist	[Academic secondary source — IUPHAR/BPS GtoPdb, GHRH-R entry]
Half-life (human)	5.8–8.1 days (measured)	[Peer-reviewed human study — Teichman et al. 2006]
PubChem CID	91976842 (DAC variant)	[Academic secondary source — PubChem]
DrugBank	No active entry (investigational, no INN, no approval)	[Academic secondary source — DrugBank query 2026-05-17]
GtoPdb / IUPHAR	No dedicated ligand entry	[Academic secondary source — Guide to PHARMACOLOGY query 2026-05-17]
UniProt	N/A (synthetic peptide)	—
USP / BNF	No monograph	[Regulatory document — FDA-2024-N-4777, 2024]
Development origin	ConjuChem Biotechnologies Inc., Montréal, Québec, Canada	[Peer-reviewed preclinical — Jetté et al. 2005 author affiliation; Adis Insight drug record 800018006]
Brand / trade names	None — never marketed; no approved formulation in any jurisdiction	[Regulatory document — FDA-2024-N-4777, 2024]
Approval status (any jurisdiction)	None — never approved for any indication; reached Phase 2 only; trial halted 17 July 2006	[Clinical trial registry — NCT00267527]; [Regulatory document — FDA-2024-N-4777, 2024]

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2. History and Development

CJC-1295 with DAC was invented at ConjuChem Biotechnologies Inc. (Montréal, Canada) in the early 2000s as the lead compound of a programme using the company’s proprietary Drug Affinity Complex (DAC™) maleimide chemistry — a strategy for extending the plasma half-life of bioactive peptides by covalent bioconjugation to the free Cys34 thiol of circulating human serum albumin [Peer-reviewed preclinical — Jetté et al. 2005, PMID 15817669] 🔴. The compound’s name derives from “ConjuChem” — “CJC-1295” was originally the internal designation for the lead candidate among three maleimido hGRF(1-29) derivatives tested by Jetté and colleagues, which showed a four-fold increase in GH AUC over the parent peptide in male Sprague-Dawley rats. The originating publication’s authorship cluster — Léger, Thibaudeau, Bridon, Castaigne — is the ConjuChem-internal group that conducted the entire pre-IND development programme. 🔴

Phase 1 human evaluation was conducted by Teichman and colleagues (industry-sponsored; ConjuChem-affiliated authors include Lawrence, Gagnon, and Castaigne; the corresponding senior author Frohman of the University of Illinois at Chicago is corresponding author on three of the four primary CJC-1295 DAC human/animal publications) ⚠️🔴 in two ascending-dose, placebo-controlled studies of 28 and 49 days’ duration, published in JCEM in March 2006 [Peer-reviewed human study — Teichman et al. 2006, PMID 16352683, DOI 10.1210/jc.2005-1536]. A companion pulsatility analysis was published by Ionescu and Frohman in JCEM December 2006 [Peer-reviewed human study — Ionescu & Frohman 2006, PMID 17018654, DOI 10.1210/jc.2006-1702] 🔴.

ConjuChem advanced the compound to Phase 2 in HIV-associated visceral obesity / lipodystrophy under the registry identifier NCT00267527 — a multicentre, randomised, placebo-controlled, double-blind, 12-week trial that had completed enrolment of 192 patients across North and South American sites when the study was halted by ConjuChem on 17 July 2006. A single fatal myocardial infarction occurred approximately two hours after the 11th weekly dose at an Argentina study site; the attending physician adjudicated the cause as asymptomatic coronary artery disease with plaque rupture, ruling treatment-relatedness unlikely; the sponsor terminated the program as a precaution regardless [Regulatory document — FDA Briefing Document, FDA-2024-N-4777, 2024, attachment 7]; [Press release — aidsmap July 2006]; [Clinical trial registry — NCT00267527].

ConjuChem subsequently entered Companies’ Creditors Arrangement Act (CCAA) protection in Canada and filed a voluntary assignment in bankruptcy on 21 July 2010, with RSM Richter Inc. appointed as trustee [Regulatory document — ISED Canada CCAA Records, ConjuChem Biotechnologies Inc.]; [Press release — CNW/Newswire, 21 July 2010]. No successor sponsor has advanced CJC-1295 with DAC to Phase 3, filed an IND/NDA/BLA, or pursued marketing authorisation in any jurisdiction. The compound persists exclusively on the research-chemical grey market and through certain compounding-pharmacy channels in the United States.

The Theratechnologies relationship is one of competition rather than succession: Theratechnologies’ tesamorelin (TH-9507) — a distinct GHRH(1-44) analogue without DAC chemistry — continued in its parallel Phase 3 lipodystrophy program after the CJC-1295 halt and was FDA-approved on 10 November 2010 as Egrifta for HIV-associated lipodystrophy [Regulatory document — FDA/PRNewswire press release, 10 November 2010]. CJC-1295 with DAC and tesamorelin should not be conflated.

The molecule’s persistence in optimization-community discourse traces to a specific vector: DatBtrue, a pseudonymous internet researcher posting on the now-defunct datbtrue.co.uk and on Professional Muscle, AnabolicMinds, and EliteFitness from approximately 2008, whose forum essays codified the “100 mcg saturation dose” and the “GH bleed” terminology that still define the bodybuilding-forum vocabulary on these compounds. The DatBtrue tradition is anti-DAC: he argued that the DAC variant’s multi-day half-life prevented physiologic pulsatile GH dosing and recommended the no-DAC compound for males.

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3. Mechanism of Action

3.1 Demonstrated in humans

A single subcutaneous injection of CJC-1295 with DAC produces covalent thiol-maleimide conjugation between the C-terminal Lys-MPA moiety and free Cys34 of circulating human serum albumin, anchoring the peptide to the most abundant plasma protein and protecting the active GHRH(1-29) domain from dipeptidyl peptidase-IV (DPP-IV) cleavage and renal filtration [Peer-reviewed preclinical — Jetté et al. 2005] 🔴. The albumin conjugate retains GHRH-receptor (GHRH-R) agonist activity at the anterior pituitary somatotroph, driving sustained but still-pulsatile GH release [Peer-reviewed human study — Ionescu & Frohman 2006, PMID 17018654] 🔴⚠️.

Quantitative human pharmacokinetic and pharmacodynamic parameters from Teichman et al. 2006 (n=21 healthy adults aged 21–61 yr, single ascending doses 30, 60, 125, or 250 μg/kg in Study 1; multiple-dose extension to 49 days in Study 2) ⚠️🔴:

• Mean plasma CJC-1295 terminal half-life: 5.8–8.1 days.
• Dose-dependent increases in mean plasma GH: 2- to 10-fold for ≥6 days after a single dose.
• Mean plasma IGF-1: 1.5- to 3-fold elevation for 9–11 days after a single dose.
• After multiple doses (weekly or biweekly), mean IGF-1 levels remained above baseline for up to 28 days, with evidence of a cumulative effect.
• Ionescu & Frohman 2006 documented preserved pulsatile GH secretion under continuous GHRH-R stimulation: trough GH approximately +7.5-fold over baseline, mean GH +46%, IGF-1 +45%, with pulse frequency and timing preserved.

The mechanistic departure from native GHRH physiology — a peptide with a plasma half-life of minutes that supports discrete brief pulses — is intentional: the DAC chemistry converts pulsatile signalling to tonic GHRH-R occupancy. Whether the “preserved pulse frequency on top of elevated trough” pattern is mechanistically equivalent to physiologic GH pulsatility is the central interpretive dispute in the literature and is addressed in Section 7.5.

3.2 Proposed / preclinical

In GHRH-knockout mice, once-daily CJC-1295 DAC at 2 μg normalised growth, body composition, and somatotroph proliferation when administered every 24 h; less frequent dosing (every 48 or 72 h) produced partial but not full normalisation [Peer-reviewed preclinical — Alba et al. 2006, PMID 16822960] 🔴. Sackmann-Sala et al. 2009 reported that GH/IGF-1 axis activation by CJC-1295 produces serum protein-profile changes consistent with downstream GH action in normal adult subjects [Peer-reviewed preclinical/translational — Sackmann-Sala et al. 2009, Growth Horm IGF Res 19:471-477] 🔴.

The mechanism proposed for the NCT00267527 fatal cardiovascular event was not adjudicated as treatment-related; the on-site investigator attributed the MI to asymptomatic coronary artery disease with plaque rupture in a patient with HIV-lipodystrophy and presumed baseline atherogenic risk [Regulatory document — FDA-2024-N-4777, 2024, attachment 7]. A class-mechanistic concern — that sustained 6–11 day GH/IGF-1 elevation may aggravate underlying cardiovascular pathology in patients with HIV-related metabolic disease — has not been formally tested in any subsequent trial.

Cancer-risk and pituitary-genotoxicity concerns derive from preclinical work using CJC-1295 DAC as a long-acting GHRH-R agonist tool. Ben-Shlomo et al. 2020 (J Clin Invest 130:5738-5755) reported that 8-week SC treatment of 4-month-old C57BL/6 mice with CJC-1295 DAC (10 μg/kg three times weekly) significantly increased anterior pituitary weight, induced pituitary DNA damage measured by Comet assay (Olive tail moment), and increased γH2AX expression — biomarkers of DNA double-strand breaks — in pituitary somatotrophs [Peer-reviewed preclinical — Ben-Shlomo et al. 2020, PMC7598090]. The same study replicated DNA-damage signals in vitro in mouse primary pituitary cultures incubated 16 hours with 10 ng/mL CJC-1295.

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4. Regulatory Status

4.1 Drug-regulatory status

Authority	Status
FDA (United States)	Not approved for any indication. No IND, NDA, or BLA on file for the sponsor of record after ConjuChem’s 2010 bankruptcy. FDA evaluated five distinct CJC-1295-family bulk drug substances at the PCAC meeting of 4 December 2024, Docket FDA-2024-N-4777: CJC-1295 (free base), CJC-1295 acetate, CJC-1295 DAC (free base), CJC-1295 DAC acetate, CJC-1295 DAC trifluoroacetate. FDA’s briefing position was that none be placed on the 503A bulks list. Committee votes: CJC-1295 free base 0/13/0 (against inclusion); CJC-1295 acetate 1/12/0 (single yes Dr. Linda McElhiney); CJC-1295 DAC free base 0/13/0; CJC-1295 DAC acetate 0/13/0; CJC-1295 DAC trifluoroacetate 0/13/0. HHS Secretary Robert F. Kennedy Jr. stated on The Joe Rogan Experience Episode #2461 (27 February 2026) that “approximately 14” of the 19 Category 2 peptides would move to Category 1; on 16 April 2026 FDA published a Federal Register notice scheduling a follow-on PCAC meeting for 23–24 July 2026. As of 2026-05-17, no final rulemaking has placed CJC-1295 DAC on the 503A list; the December 2024 recommendation against inclusion stands. [Regulatory documents — FDA-2024-N-4777, 2024; FDA PCAC Meeting Transcript, 4 December 2024; Federal Register notice, 16 April 2026]
EMA (European Union)	No marketing authorisation; no centralised application identified [Regulatory document — EMA medicine search, 2026-05-17].
MHRA (United Kingdom)	No marketing authorisation. UK compliance guidance states explicitly that “The MHRA has not granted marketing authorisation for CJC 1295 or ipamorelin for any clinical indication” [Regulatory secondary source — Bolt Pharmacy UK guide, citing MHRA].
PMDA (Japan)	No marketing authorisation identified.
NMPA (China)	No marketing authorisation identified.
MFDS (South Korea)	No marketing authorisation identified.
TGA (Australia)	Schedule 4 (Prescription Only) plus Appendix D, Item 5 since 1 June 2015 [Regulatory document — TGA Reasons for scheduling delegate’s final decisions, March 2015, listing CJC-1295 (CAS 863288-34-0)]. The scheduling entry references CAS 863288-34-0 without distinguishing DAC and no-DAC forms; the Australian Poisons Standard entry applies inclusively to both variants because they share the same base CAS. Class-level Growth Hormone Releasing Hormones (GHRHs), Growth Hormone Secretagogues (GHSs), and Growth Hormone Releasing Peptides (GHRPs) were simultaneously placed in Appendix D.
Health Canada	No marketing authorisation; ConjuChem’s CCAA filing terminated the only domestic sponsor [Regulatory document — ISED Canada CCAA Records].
GRLS (Russia)	No entry identified.

4.2 Anti-doping

Authority	Status
WADA 2026 Prohibited List	Prohibited at all times (in- and out-of-competition) under S2.2.4 Growth hormone releasing factors: “growth hormone-releasing hormone (GHRH) and its analogues (e.g. CJC-1293, CJC-1295, sermorelin and tesamorelin)” [Anti-doping document — WADA 2026 Prohibited List, effective 1 January 2026]. The named entry “CJC-1295” is not differentiated between DAC and no-DAC variants; both fall under the open-ended “GHRH analogues” listing.
WADA Monitoring Program	Not applicable — substance is fully prohibited, not under monitoring.
TUE eligibility	No clinical indication exists for which a Therapeutic Use Exemption could plausibly be granted; no approved product available.
USADA	Prohibited per WADA Code adoption.
NCAA	Banned under “Peptide Hormones, Growth Factors, Related Substances and Mimetics” class [Anti-doping document — NCAA Banned Drugs list 2025–2026].
DoD-OPSS	Prohibited; service members have been subject to administrative action for possession of supplements containing CJC-1295 and related peptides.
Global DRO	Listed prohibited at all times under WADA S2 framework.
BSCG	Listed prohibited under S2.2.4 [BSCG WADA Prohibited List summary 2026].
Detection literature	LC-HRMS/MS identification of CJC-1295 in seized pharmaceutical preparations reported by the Norwegian Doping Control Laboratory [Peer-reviewed — Henninge et al. 2010, Drug Test Anal 2(11-12):647-650, PMID 21204297]. Subsequent advances (Memdouh et al. 2021; Nemutlu 2025) confirm urine detection of CJC-1293, CJC-1295, tesamorelin, and the primary sermorelin metabolite per WADA requirements. The most-documented adjudicated CJC-1295 use case in professional sport is the 2013 Cronulla-Sutherland Sharks NRL supplements saga: sports scientist Stephen Dank publicly admitted overseeing a regimen involving CJC-1295 and GHRP-6, resulting in 12 players who pleaded guilty under the ASADA process. The DAC vs no-DAC variant attribution within these cases is not publicly catalogued.

4.3 Last regulatory review stamp

2026-05-17.

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5. Formulations and Routes

CJC-1295 with DAC has never been formulated, packaged, or marketed as an approved finished drug product in any jurisdiction. All published clinical research used investigational lyophilised peptide reconstituted in sterile water and administered subcutaneously [Peer-reviewed — Teichman et al. 2006; Ionescu & Frohman 2006] ⚠️🔴. The route in published Phase 1 was subcutaneous injection at doses of 30, 60, 125, or 250 μg/kg (Teichman 2006 Study 1, single ascending dose). In the halted Phase 2 (NCT00267527), participants received weekly subcutaneous escalating doses: low-dose arm 60 → 90 → 120 μg/kg over three weeks then continuation for nine weeks; high-dose arm 60 → 120 → 240 μg/kg then nine-week continuation [Clinical trial registry — NCT00267527]; [Press release — aidsmap July 2006].

Grey-market preparations are sold by research-chemical suppliers in lyophilised form (typically 2 mg or 5 mg vials) for reconstitution with bacteriostatic water and subcutaneous self-administration. Community-circulated protocols are documented in Section 7B.

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6. Preclinical Evidence

• Jetté L et al. Endocrinology 2005;146(7):3052-3058. PMID 15817669. Three maleimido derivatives of hGRF(1-29) synthesised, bioconjugated to human serum albumin via Cys34, and assayed; all three retained activity in cultured rat anterior pituitary cells; in vivo SC administration to Sprague-Dawley rats showed acute GH secretion; CJC-1295 showed a 4-fold increase in GH AUC over parent peptide [Peer-reviewed preclinical] 🔴.
• Alba M et al. Am J Physiol Endocrinol Metab 2006;291(6):E1290-1294. PMID 16822960. Once-daily 2 μg CJC-1295 normalised body weight, length, body composition, and somatotroph proliferation in GHRHKO mice; q48h and q72h dosing achieved partial normalisation [Peer-reviewed preclinical] 🔴⚠️ (ConjuChem co-authors).
• Sackmann-Sala L et al. Growth Horm IGF Res 2009;19(6):471-477. Apolipoprotein A1 and transthyretin isoforms downregulated; albumin and immunoglobulin fragments upregulated; one albumin/IgG fragment correlated linearly with IGF-1 [Peer-reviewed translational] 🔴.
• Ben-Shlomo A et al. J Clin Invest 2020;130(11):5738-5755. PMC7598090. Mouse primary pituitary cultures (10 ng/mL CJC-1295 DAC, 16 h) and 4-month-old C57BL/6 mice (10 μg/kg SC three times weekly, 8 weeks) showed dose-dependent increases in GH secretion, increased anterior pituitary weight, increased γH2AX expression (DNA double-strand-break marker), and increased Olive tail moment in Comet assay. Findings attenuated by octreotide co-treatment [Peer-reviewed preclinical].
• Iordanova et al. 2004, 2005, 2006 (ConjuChem-sponsored toxicology; conference abstracts only):
  • Rat acute toxicity (IV 2/4/8 mg/kg): transient 62–90% decrease in food consumption; soft/mucoid stools ≥4 mg/kg; decreased activity at 8 mg/kg 🔴.
  • Beagle dog acute toxicity (SC 2.5/8/24/40 mg/kg): emesis and decreased activity ≥8 mg/kg 🔴.
  • Rat 14-day repeat-dose IV (0.25/1/4 mg/kg every other day): reduced RBC/hemoglobin/hematocrit at all doses (↓5–15%); increased cholesterol/calcium/albumin/globulins/total proteins; increased liver weight 8–25%; injection-site inflammation/hemorrhage/necrosis at all doses 🔴.
  • Dog 7- and 14-day repeat-dose SC: dose- and pH-dependent injection-site irritation at all doses; decreases in hemoglobin and red-cell mass (↓16%); 1.8-fold increase in serum cholesterol ≥6 mg/kg/day 🔴.
  • Rat developmental toxicity (Sprague-Dawley, 0.5/4/16 mg/kg every other day GD 7–17): no maternal or embryofetal toxicity 🔴.
• Carcinogenicity. No 2-year nonclinical carcinogenicity studies of CJC-1295 DAC (any salt) or CJC-1295 (any salt) have been identified by FDA [Regulatory document — FDA-2024-N-4777, 2024, Section II.C.1.g].

Asymmetric evidence base. FDA states explicitly that all identified nonclinical pharmacological, acute toxicity, repeat-dose toxicity, genotoxicity, and developmental toxicity findings pertain to CJC-1295 DAC (unspecified salt form), not to the no-DAC variant: “The nominations did not include, and, at the time of this evaluation, FDA has not identified pharmacological studies of CJC-1295 (free base) or CJC-1295 acetate” [Regulatory document — FDA-2024-N-4777, 2024, p. 25]. Adverse nonclinical findings cannot be transferred between the two forms in either direction.

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7. Clinical Evidence

7.1 Cochrane systematic reviews

None identified for CJC-1295 with DAC as of 2026-05-17 [Cochrane Library query 2026-05-17].

7.2 Randomised controlled trials

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 Mar;91(3):799-805. PMID 16352683. [Peer-reviewed human study — Phase 1, industry-sponsored] ⚠️🔴

• Design: Two randomised, placebo-controlled, double-blind, ascending-dose trials (Study 1: 28 days, single ascending SC doses 30, 60, 125, 250 μg/kg in groups of 4 active + 2 placebo; Study 2: 49 days, two or three weekly or biweekly doses).
• Population: n=21 healthy adults aged 21–61 yr.
• Findings: mean plasma t½ 5.8–8.1 d; GH 2–10× for ≥6 d; IGF-1 1.5–3× for 9–11 d; cumulative IGF-1 effect over multiple doses.
• Safety in published cohort: injection-site erythema in 23% of participants (11/47 dose administrations); concluded “safe and relatively well tolerated, particularly at doses of 30 or 60 µg/kg.”

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 Dec;91(12):4792-4797. PMID 17018654. [Peer-reviewed human study — Phase 1, industry-affiliated] 🔴⚠️ Trough GH +7.5×, mean GH +46%, IGF-1 +45%; pulse frequency and timing preserved per the authors.

NCT00267527 “A Multicenter, Randomized, Placebo-Controlled, Double-Blind, Phase 2 Study to Evaluate the Efficacy and Safety of CJC 1295 Administered for 12 Weeks in HIV Infected Patients With HIV Associated Visceral Obesity.” Sponsor: ConjuChem. n=192. Status: Terminated 17 July 2006 after a single fatal myocardial infarction at an Argentina site approximately two hours after the 11th weekly dose. Adjudication: on-site attending physician concluded the event was unrelated to study drug (asymptomatic coronary artery disease, plaque rupture). Full primary-endpoint data have never been published. [Clinical trial registry; Regulatory document — FDA-2024-N-4777, 2024, attachment 7; Press release — aidsmap July 2006]

7.3 Observational and registry data

Anti-doping detection literature: Henninge et al. 2010 reported the first published mass-spectrometric identification of CJC-1295 in a seized pharmaceutical preparation submitted by Norwegian police/customs (PMID 21204297). Adjudicated Adverse Analytical Findings specifically attributing CJC-1295 DAC (as opposed to no-DAC) to individual athletes are not publicly catalogued in WADA’s ADRV registry. The 2013 Cronulla-Sutherland Sharks NRL case (12 ASADA pleas, Stephen Dank regimen of CJC-1295 + GHRP-6) is the most extensively documented use case; the DAC vs no-DAC sub-attribution is not publicly specified.

7.4 Comparative trials

None identified. No head-to-head trial of CJC-1295 with DAC against tesamorelin, sermorelin, daily recombinant GH, or any other GHRH analogue.

7.5 Disputed Claims

1. Causal adjudication of the NCT00267527 fatal myocardial infarction. The on-site attending physician concluded the event was unrelated to study drug, attributing it to asymptomatic coronary artery disease with plaque rupture in an HIV-lipodystrophy patient with baseline cardiovascular risk [Regulatory document — FDA-2024-N-4777, 2024]. No independent peer-reviewed cardiovascular adjudication has been published. The sponsor halted the trial regardless, indicating internal precautionary doubt. Status as of 2026-05-17: the single available adjudication is from the same investigator team that ran the trial; no external replication or cardiovascular-endpoint trial has been conducted to clarify whether 6–11 day GH/IGF-1 elevation in HIV-lipodystrophy patients carries a meaningful cardiovascular signal. The dispute is unresolved.
2. Whether sustained 6–11 day GH/IGF-1 elevation is mechanistically equivalent to physiologic GH pulsatility. Ionescu & Frohman 2006 argued that pulsatile GH secretion is preserved during continuous GHRH-R stimulation by CJC-1295 DAC and concluded the physiological GH pulse pattern was therefore intact [Peer-reviewed — Ionescu & Frohman 2006] 🔴⚠️. Class-mechanistic critique — present in both regulatory documents and the bodybuilding-forum “GH bleed” literature (Section 7B) — argues that elevated trough GH (+7.5-fold) and tonic albumin-bound DAC:GRF occupancy of GHRH-R represent a meaningful departure from native pulsatile signalling because the trough is no longer a true trough, and that this differs fundamentally from physiologic GH dynamics and from the no-DAC compound’s behaviour. Status: both interpretations coexist in the literature; the dispute is interpretive rather than empirical and centers on whether “preserved pulse frequency” or “elevated trough with retained amplitude variation” is the more clinically meaningful framing. The community literature has measurably converged against the Ionescu/Frohman framing over the past decade (Section 5.3 of Pass 2).
3. Cancer-signal dispute. Sustained IGF-1 elevation for 9–11 days following a single dose and the cumulative-effect signal in multi-dose protocols raise theoretical concerns about IGF-1-mediated promotion of pre-existing malignancies. No epidemiological cancer signal has been reported because the underlying clinical population is sub-trial and no surveillance cohort exists. The FDA briefing document explicitly flagged absence of 2-year carcinogenicity data [Regulatory document — FDA-2024-N-4777, 2024, Section II.C.1.g]. Status: mechanistic concern documented; epidemiological data absent.
4. The Ben-Shlomo et al. 2020 “DNA damage in pituitary cells” finding. The peer-reviewed JCI study demonstrated γH2AX induction and Comet-assay Olive tail moment increases in pituitary somatotrophs treated with CJC-1295 DAC in vitro (10 ng/mL, 16 h) and in vivo (10 μg/kg SC three times weekly, 8 weeks) [Peer-reviewed — Ben-Shlomo et al. 2020]. FDA cited this finding centrally in its December 2024 PCAC briefing: “The in-vitro genotoxic signals generated by the unspecified form of CJC-1295 DAC demonstrate the genotoxic potential of CJC-1295 DAC-related substances” [Regulatory document — FDA-2024-N-4777, 2024, Section II.C.1.e]. Controversy: the Ben-Shlomo study’s purpose was mechanistic (investigating oncogene-induced DNA damage in pituitary adenomas, with CJC-1295 used as a long-acting GHRH-R agonist tool), not regulatory; the doses and durations were preclinical. Whether the genotoxic signal translates to human-relevant pituitary risk at therapeutic-range exposures is unestablished. No published response or rebuttal by the original CJC-1295 development team (now defunct) has appeared. Status: the finding is real and peer-reviewed; its quantitative translation to human risk is contested by absence of human data and by the preclinical-dose framing.

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7B. Community Evidence Layer

Community context

CJC-1295 with DAC entered optimization-community awareness around 2006–2008, immediately after the Teichman Phase 1 publication and the ConjuChem Phase 2 halt. The DAC variant is the original “CJC-1295” — the no-DAC molecule that now dominates clinic protocols is technically Mod GRF(1-29) re-branded. The bodybuilding/PED subcommunity drove early adoption: DatBtrue’s mid-to-late 2000s forum posts, cross-posted on Professional Muscle, AnabolicMinds, and EliteFitness, are the originating community vector. The longevity subcommunity (LIVV Natural, Revolution Health, Tucson Wellness MD, Huberman) almost universally steers patients toward no-DAC + ipamorelin instead.

Current trajectory: declining among knowledgeable users, stable in clinic-marketed wellness plans, modest renewed interest as an MK-677 alternative. The pulsatility critique (the “GH bleed” framing) has measurably moved sophisticated forum posters away from DAC over the past decade. Counter-current: with MK-677 facing its own PCAC scrutiny (October 29, 2024 vote against 503A inclusion citing a congestive heart failure signal — 4/62 vs 1/61 in the hip-fracture trial) and tirzepatide saturating the body-recomp conversation, a subset of physique-focused users have circled back to CJC-1295 DAC for its long-acting GH “bleed” profile, often stacked with MK-677 per the Derek MPMD framing.

Documented protocols

Source	Date	Dose	Frequency	Cycle	Route	Notes
DatBtrue (datbtrue.co.uk legacy; cross-posted ProMuscle/AnabolicMinds)	2008–2012	100 mcg saturation	2× weekly OR daily (short-term IGF-1 push)	8–12 weeks	SC	Originator of “GH bleed” terminology; warned against DAC for males
Compounding-pharmacy protocol filed with FDA-2024-N-4777-0002	Submitted 2024	600 mcg	Once weekly, fasted	Open-ended	SC	”Inject 600 mcg once weekly… empty stomach, 2–3 hours after last meal”
Jay Campbell, jaycampbell.com	2023 (current)	100 mcg	2× weekly OR 100 mcg daily for short-term IGF-1 push	Cycle on and off	SC	Acknowledges 200–350 mcg/week reported by other users
Derek MPMD, moreplatesmoredates.com	2021 (still live)	~2 mg/week DAC + 25 mg/day MK-677	Weekly DAC, daily MK-677	Personal historical protocol	SC + oral	Explicit pharma-GH-mimic stack
ProfessionalMuscle “CJC-1295 DAC side effects and dosage”	active 2014–2024	2 mg	1× weekly (some 2×)	Open-ended	SC	”2× a week… causes a constant and steady high IGF-1 levels”
EliteFitness “CJC-1295 w/Dac and MK-677” thread	retrieved May 2026	5 mg/wk DAC + 25 mg/d MK-677	Weekly DAC	Cutting cycle	SC	Water retention concern raised
PeptideDosingProtocols.com	2026 (current)	1–2 mg	Once weekly OR split 500–1000 mcg 2× weekly	8–12 weeks	SC	”Beginners: 500 mcg once weekly” titration entry
The Peptide Catalog	2026	2 mg	Weekly	8–12 weeks for body comp	SC	”Standard community protocol is 2 mg per week”
Eroids “GH Bleed proof” thread (Notorious)	2014, still active	250 mcg EOD	Every 2 days	Personal long-term	SC	Minority “low-and-frequent” DAC protocol

Clinic vs forum vs vendor difference. Clinic protocols (Revolution Health, Tucson Wellness, Yunique Medical, LIVV Natural) overwhelmingly steer away from DAC toward no-DAC + ipamorelin once they explain the difference. Vendor pages (Core Peptides, Particle Peptides, BioTech, Huma Peptide) sell the DAC variant with dosing instructions framed as “research use only.” Bodybuilding forums (Professional Muscle, AnabolicMinds, EliteFitness, Eroids) preserve the most aggressive DAC dosing — up to 5 mg/week paired with MK-677.

Claimed effects

Effect	Frequency of claim	Top-cited source
Sustained IGF-1 elevation 6–11 days from a single shot	Widespread — every DAC source repeats the Teichman 1.5–3× IGF-1 for 9–11 d figure	thepeptidecatalog.com; corepeptides.com; livvnatural.com
”Set-and-forget” weekly compliance vs daily pinning	Widespread	revolutionhealth.org; medsbase.com; womenshealthofmd.com
Improved sleep quality, deeper REM, vivid dreams	Common — attributed to elevated trough GH overnight	thepeptidecatalog.com; ExcelMale threads
Body recomposition: modest lean mass + fat loss over 8–12 weeks	Common	Derek MPMD; r/Biohackers / r/Peptides reports aggregated by drkconrad.com
”Niacin flush” head-rush within minutes of injection	Common, specifically attributed to CJC	ExcelMale CJC/Ipa blend thread; thepeptidecatalog.com
Joint feel / skin quality improvement	Occasional	Desert Mobile Medical; Yunique Medical
”Feels like real HGH but cheaper” — pharma-GH IGF-1 mimic when stacked with MK-677	Single-source-dominant (Derek MPMD), echoed downstream	moreplatesmoredates.com

Uniquely-DAC vs shared with no-DAC: only the sustained multi-day IGF-1 plateau, the once-weekly compliance, and the “pharma GH mimic when stacked with MK-677” claim are DAC-specific. Sleep, body comp, recovery, flush — also claimed for no-DAC.

Reported side effects

Side effect	Severity / frequency	Top-cited source
Fluid/water retention, puffiness	More commonly reported than for no-DAC, particularly first 2–4 weeks	revolutionhealth.org; pepdose.com; biohacknow.net
Lethargy / “fog” days after injection	Common DAC complaint; “harder to titrate or reverse” because of long half-life	revolutionhealth.org; thejops.com
Facial flushing within minutes	Widespread	ExcelMale; thepeptidecatalog.com
Tingling / numbness / carpal-tunnel-pattern wrist tightness	Common at higher doses	uk-muscle.co.uk “GH Bleed??” thread; peptidedeck.com
Injection-site reactions	Community write-ups cite a 70% figure that is not traceable to any named clinical trial; Teichman 2006 actually reported 23% (11/47) injection-site erythema with conclusion “safe and relatively well tolerated, particularly at doses of 30 or 60 µg/kg”	Teichman et al., JCEM 2006 (corrects the community number); biohacknow.net carries the inflated figure
Headache, particularly at initiation	Common	thejops.com; FDA briefing noted “increased heart rate, flushing, and headache”
Blood-glucose dysregulation / insulin resistance signal	Reported, low-frequency; community flags chronic GH elevation as the mechanistic concern	revolutionhealth.org; peptidedeck.com
Prolonged side-effect duration vs no-DAC	Universally noted — “side effects don’t wear off quickly”	revolutionhealth.org; Ben Greenfield commenter (“if I overdid it on the CJC, it seems the effects went on forever”)
Theoretical gyno / tumor-growth risk from chronic IGF-1	Cautionary boilerplate across longevity-clinic write-ups; no widespread anecdotal reports	livvnatural.com; pepdose.com

Community dissent

The DAC variant most clearly diverges from its no-DAC sibling in this section.

DAC-vs-no-DAC preference split. The knowledgeable-user consensus on bodybuilding forums (Meso-Rx/thinksteroids, Professional Muscle, AnabolicMinds, Eroids) is strongly anti-DAC. Bill Roberts’s Meso-Rx peptide profile is the canonical statement: “The other principal GHRH product is Mod GRF 1-29, which in most instances I recommend over CJC-1295… CJC-1295 has an extended duration of action which prevents [pulsatile dosing]… It does not combine especially efficiently with a GHRP, because the DAC modification results in relatively lower ongoing levels of free peptide. For maximal effect in increasing GH production, rather than CJC-1295 I recommend Mod GRF 1-29 in combination with a GHRP.” Roberts allows DAC a niche — “the convenient solution with injection frequency of only twice weekly” — but his recommendation is no-DAC. Jay Campbell echoes: “my strong preference… is CJC-1295 no DAC stacked with Ipamorelin when cycled responsibly.” DAC defenders argue from compliance (weekly vs 14–21 weekly injections) and from the Ionescu & Frohman 2006 PubMed finding that pulsatility is preserved during DAC stimulation.

The 2006 Phase 2 fatal MI. Community awareness is shallow and partisan. Three framings:

• Cautionary citation — Huberman, Vanguard Laboratory, Revolution Health, Jay Campbell. Huberman’s April 2024 framing: “CJC1295, despite still being in clinical trials, does have this kind of stain of a death within the clinical trial… It’s known to cause some fluid retention and increased fluid volume, which may have been related to that cardiovascular death.” Huberman recommends against CJC-1295 in favour of sermorelin / tesamorelin.
• Dismissal — vendor and pro-DAC clinics cite the attending physician’s adjudication.
• Application to current dosing — essentially absent. The community does not derive dose ceilings or screening protocols from the MI signal; it is treated as historical context, not actionable safety information.

The pulsatility / “GH bleed” critique. This is the dominant mechanistic objection on bodybuilding forums. “GH bleed” originates with DatBtrue and is now universal vocabulary. Professional Muscle: “CJC-1295 will RAISE your basal or trough levels of GH and has no effect on pulsatility amplitude… HOWEVER, this ‘turned on all the time GH’ also known as ‘GH bleed’ does not create a favorable environment, especially for males.” The 2024-vintage compounding-pharmacy filing in the FDA docket (FDA-2024-N-4777-0002) repeats the critique verbatim: “A potential drawback when using DAC (a weekly protocol) can be ineffective GHRH stimulation when the body is due for a GH spike (usually 1:00am). This is referred to as a GH-bleed and the overall result is inferior to using CJC 1295-NON-DAC daily for 5 days out of 7.” Counter-evidence (Ionescu/Frohman PMID 17018654) is cited by DAC defenders, but the bodybuilding consensus has been settled against DAC since roughly 2012–2014.

The DAC + ipamorelin stack coherence problem. This is the most-run, least-coherent community combination. Ipamorelin has a terminal half-life of 2 hours (Gobburu et al., Pharm Res 1999;16(9):1412); DAC has a ~6–8 day half-life. Pairing them produces sustained GHRH-receptor activation (DAC) with ephemeral ghrelin-receptor amplification (ipamorelin from each shot). The “synergy” logic that justifies no-DAC + ipamorelin (matched pulses) is mechanistically gone. Community-knowledgeable posters note this; clinic marketing pages largely do not. Yunique Medical, Women’s Health of MD, and most telehealth peptide vendors sell the CJC-1295 (DAC) + ipamorelin combination by default. Ben Greenfield’s “toast vs CJC-toast” essay flatly objects to selling DAC under this stack name.

503A compounding access. Identical to no-DAC: the 4 December 2024 PCAC meeting voted that all five CJC-1295 forms not be included on the 503A Bulks List. The April 16, 2026 Federal Register notice scheduling the 23–24 July 2026 PCAC meeting did not return CJC-1295 to the active review docket. Community framing: outrage at FDA overreach, hopes pinned on Secretary Kennedy’s Joe Rogan-broadcast intent to restore access.

The DAC↔no-DAC mass-spec mislabeling phenomenon. Surfaced explicitly in FDA’s December 2024 PCAC briefing: “The mass obtained for CJC-1295 DAC was indicative of CJC-1295 without DAC, also known as Mod GRF (1-29). It is possible that the DAC group… was cleaved from the main peptide structure during analysis; however, due to the soft ionization nature of this method, this is unlikely.” Bill Roberts and Ben Greenfield independently flag the inverse problem: vendors mis-labelling Mod GRF as “CJC-1295” without specifying no-DAC. The MW signature is the only reliable disambiguator (~3,648 Da DAC vs ~3,368 Da no-DAC). Important QC flag: Core Peptides’ product page for CJC-1295 DAC lists a molecular weight of ~3,367.95 g/mol — the no-DAC molecule mass, not the DAC variant. Vendor-side mislabeling that community-knowledgeable users should treat as a red flag.

DAC variant vs MK-677. This is the defining comparison for the DAC subset. MK-677 is oral, long-acting (~24 h coverage from chronic dosing), self-pulsing, and cheap. CJC-1295 DAC is injectable, longer-acting (multi-day), non-pulsatile, more expensive. Derek MPMD’s MorePlatesMoreDates write-up is the most influential community framing: he argues neither is sufficient alone for “pharma-GH mimic” IGF-1 levels but that combining them produces 24/7 elevated IGF-1 in a way no single GHRH/GHRP achieves. The community split: bodybuilders pursuing physique outcomes prefer MK-677 + CJC-DAC stack; longevity users and clean-stack purists pick neither and use no-DAC + ipamorelin instead.

Stack patterns

Stack	Prevalence	Coherence	Top-cited source
CJC-1295 DAC + ipamorelin	Very common (clinic-marketed default)	Mechanistically questionable — t½ mismatch (~2 h vs ~6 d)	revolutionhealth.org; livvnatural.com
CJC-1295 DAC + MK-677	Common among bodybuilders	Coherent for “GH bleed + ghrelin-receptor amplification” objective; risk of insulin resistance and CHF signal	Derek MPMD; EliteFitness
CJC-1295 DAC + testosterone / TRT	Common in PED stacks	Standalone TRT base; DAC layered for IGF-1 elevation	jaycampbell.com; ExcelMale
CJC-1295 DAC + GLP-1 (semaglutide / tirzepatide)	Emerging	”Recomp” rationale — GLP-1 for fat loss, DAC for lean-mass preservation	drkconrad.com; clinic offerings since 2024
CJC-1295 DAC + tesamorelin	Rare	Two GHRH agonists; redundant	livvnatural.com
CJC-1295 DAC + BPC-157 / TB-500	Common in injury-recovery framing	Mechanistically separate pathways; coherent	womenshealthofmd.com
CJC-1295 DAC + GHRP-2 / GHRP-6	Historical (DatBtrue era), now niche	Originating literature combined them	particlepeptides.com

Vendor / supply context

Vendor	DAC SKU	Verified DAC pricing	Notes
Core Peptides	Yes	$52.00 / 5 mg ($10.40/mg); bulk to $46.80/vial @ 9+	Most reliably-priced DAC source. Caveat: product page lists MW ~3,367.95 g/mol — that is the no-DAC mass; vendor-side mislabeling
Pure Rawz	Yes (“with DAC” variant)	$28–$107 range; exact 5 mg DAC price not extractable	Multi-variant dropdown
BioTech Peptides	Yes (5 mg DAC)	Not captured	Product page exists; pricing not extractable in this Pass
Limitless Life Nootropics	No DAC-only SKU in current catalog	n/a	Stocks only no-DAC and no-DAC + ipamorelin blend
Peptide Sciences	Discontinued	n/a	Homepage: “Peptide Sciences has decided to voluntarily shut down operations” — major historical DAC vendor now off market
Particle Peptides (EU)	Yes (5 mg DAC)	Not captured	Active EU listing
Skye Peptides	Yes — DAC-specific COA published	Not captured	Publishes Batch CJCDAC25-10-003 at 99.6% with HPLC + endotoxin 0.22 EU/mg + sterility
Avish Enterprises (IndiaMart)	Yes — reselling Peptide Sciences-branded vials	₹10,500 / 10× 5 mg vials	Grey-market international channel

DAC-specific QC issues:

• Mass-spec mislabeling. FDA PCAC briefing (December 2024): one tested CJC-1295 DAC sample mass-spec’d as no-DAC. Translation: the vial probably never contained DAC to begin with.
• Finnrick aggregate data, CJC-1295 (variant not consistently separated): 244 samples across 47 vendors, 17 Dec 2024 to 21 Mar 2026. The publicly-visible variant-tagged Finnrick rows are dominated by no-DAC samples; a DAC-only Finnrick subtable was not surfaced in this Pass and stands as a transparency gap.
• Janoshik DAC test reports exist (verify.janoshik.com test IDs 80846 and 89194) but vendor names are not exposed in summary search results.

Community Score and Tier

Component	Score / 25	Justification
Usage volume	19	Substantial bodybuilding/PED user base and clinic-marketed stack presence, but knowledgeable-user migration to no-DAC has measurably reduced volume. Vendor SKU availability universal; community thread volume moderate.
Protocol codification	21	Highly codified. Teichman dosing (60–90 mcg/kg) anchor; community standard 1–2 mg weekly SC; clinic-pharmacy filings document the 600 mcg weekly dose; titration entry (500 mcg) documented. Less consensus on optimal split; DAC + ipamorelin stack coherence unsettled.
Reported effect consistency	15	Mixed. Sleep, IGF-1 elevation, fluid retention, flushing universally reported; body-comp magnitude at DAC monotherapy doses contested; GH-bleed debate divides knowledgeable users on whether elevated trough is beneficial. Side-effect duration unpredictability reduces consistency.
Time in circulation	22	Continuously in community circulation since ~2006–2008. DatBtrue forum legacy, ConjuChem branding, ~18 years of bodybuilding-forum thread continuity. Older than no-DAC’s community profile in absolute chronological terms.
Total Community Score	77
Community Tier letter	A (75–89)	Lower in the A band than no-DAC’s 82; reflects DAC’s settled-but-contested position.

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8. Safety Profile

Common adverse events in healthy-adult Phase 1 (Teichman 2006, n=21): injection-site reactions (erythema 23% of administrations), transient facial flushing, headache, fluid retention reported at higher doses; no serious adverse events reported within the 28- and 49-day observation windows; dose-limiting tolerability emerged above 60 μg/kg.

Phase 2 fatal event (NCT00267527, n=192 HIV-lipodystrophy patients): one death from acute myocardial infarction approximately two hours after the 11th weekly dose at an Argentina site; on-site adjudication ruled unrelated to study drug. Full safety dataset never published.

Class concerns (sustained GH/IGF-1 elevation): insulin resistance and hyperglycemia, fluid retention and peripheral oedema, carpal tunnel syndrome, arthralgia, theoretical IGF-1-mediated malignancy promotion. These are extrapolated from the recombinant GH and tesamorelin literatures rather than directly observed in the small CJC-1295 DAC trials.

FDA December 2024 nonclinical safety findings (all attributed to CJC-1295 DAC):

• Reduced red blood cell counts, hemoglobin, and hematocrit at all tested doses in rats and dogs.
• Increased serum cholesterol in both species (1.8-fold increase in dogs ≥6 mg/kg/day).
• Injection-site irritation: inflammation, hemorrhage, minimal-to-mild necrosis at all doses.
• DNA damage in pituitary cells (in vitro and in vivo, citing Ben-Shlomo 2020).
• Increased anterior pituitary weight after 8-week mouse dosing.
• Absence of 2-year carcinogenicity data.

Trial exclusions / special populations: the original target population for NCT00267527 — HIV-associated visceral obesity / lipodystrophy patients — has elevated baseline cardiovascular and metabolic risk profiles. The fatal event in this population without prior cardiovascular evaluation underscores that any extrapolation of healthy-adult Phase 1 tolerability to populations with HIV-related metabolic disease is unjustified. No data exist in pregnancy, lactation, paediatric, hepatic-impairment, or renal-impairment populations.

Retraction status: no retractions identified for Teichman 2006, Ionescu & Frohman 2006, Jetté 2005, Alba 2006, Sackmann-Sala 2009, or Ben-Shlomo 2020 [PubMed retraction check 2026-05-17].

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9. Drug Interactions

No formal drug-interaction studies for CJC-1295 with DAC have been conducted in humans. Class-based inference from GHRH-axis pharmacology:

• Glucocorticoids: chronic supraphysiologic corticosteroid exposure suppresses somatotroph response to GHRH-R agonism, predicting attenuated GH/IGF-1 elevation from CJC-1295 DAC.
• Somatostatin analogues (octreotide, lanreotide, pasireotide): octreotide directly suppresses GHRH-induced GH release and was shown to attenuate CJC-1295-induced γH2AX and Comet-assay signals in Ben-Shlomo et al. 2020 mouse pituitary cultures.
• Insulin / insulin sensitisers: sustained GH elevation antagonises insulin signalling; chronic CJC-1295 DAC dosing may predict reduced insulin sensitivity and increased exogenous-insulin requirements.
• Thyroid hormone: GH/IGF-1 elevation can alter T4-to-T3 conversion; no direct CJC-1295 DAC interaction data exist.
• Recombinant GH / GH receptor antagonists (pegvisomant): no co-administration studies; combination not biologically rational.

Drug-interaction characterisation is a documented research gap.

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10. Research Gaps

1. No Phase 3 trial — program halted at Phase 2 by ConjuChem sponsor; no successor sponsor identified.
2. No NDA, BLA, or IND filing of record with FDA for any active sponsor; no EMA / MHRA / PMDA / NMPA / MFDS / TGA / Health Canada / GRLS submission.
3. No independent replication of efficacy claims outside the Frohman/ConjuChem research group 🔴.
4. NCT00267527 full results never published — efficacy and safety endpoints of the 192-patient Phase 2 trial remain in trial-registry “Terminated” status without primary publication 20 years on.
5. No independent cardiovascular adjudication of the single fatal MI; no published DSMB report.
6. No long-term safety surveillance beyond the 49-day Teichman Study 2 observation window in healthy adults.
7. No 2-year nonclinical carcinogenicity study.
8. No human data on translatability of the Ben-Shlomo 2020 pituitary genotoxicity signal.
9. No formal drug-interaction studies.
10. No data in special populations (pregnancy, paediatric, hepatic/renal impairment, geriatric).
11. Anti-doping detection methods do not reliably differentiate CJC-1295 DAC from CJC-1295 no-DAC in current public WADA AAF reporting.
12. No DAC-only vendor QC subtable in Finnrick or other third-party COA aggregators.

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11. Bottom-Line Encyclopedia Note (≤150 words)

CJC-1295 with DAC is an investigational long-acting GHRH(1-29) analogue covalently anchored to serum albumin via a maleimidopropionamide-lysine moiety, developed by ConjuChem Biotechnologies and characterised in two industry-sponsored Phase 1 ascending-dose trials in 21 healthy adults (Teichman 2006; Ionescu & Frohman 2006) and one Phase 2 HIV-lipodystrophy trial of 192 patients (NCT00267527) halted on 17 July 2006 after a fatal myocardial infarction adjudicated by the on-site physician as unrelated. The compound has no marketing authorisation in any jurisdiction, no approved indication, and no surviving sponsor. ConjuChem entered bankruptcy on 21 July 2010. WADA prohibits CJC-1295 at all times under S2.2.4; TGA placed it in Schedule 4 + Appendix D from 1 June 2015. The FDA PCAC voted in December 2024 against placing CJC-1295 DAC on the 503A bulks list (13-0 on all three DAC-salt votes). Community Score 77 (Tier A); the bodybuilding-forum consensus has measurably shifted toward the no-DAC variant over the past decade.

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11B. Gap Analysis — Where Science and Community Diverge

CJC-1295 with DAC sits in the High community + Low science cell of the gap pattern matrix. Subclassification per v3 methodology: tested-then-halted-with-unresolved-cardiovascular-signal-and-single-group-evidence-base. This is a different texture from both BPC-157 (“community ahead of untested-tendon-claim”) and from the sibling no-DAC compound (“community ahead of zero-human-evidence on the specific molecule”). DAC actually has more compound-specific human data than no-DAC — but it all traces to one industry-funded authorship cluster, includes one fatal event, and includes one Phase 2 trial whose primary endpoints have never been published twenty years on. Science Score 10; Community Score 77; delta 67 points — the second-largest in the catalog after BPC-157.

Topic	Science Layer	Community Layer	Gap
The molecule in the vial	Regulatory and analytical literature unambiguous: DAC and no-DAC are different chemical entities (MW 3,648 vs 3,368 Da). FDA-2024-N-4777 explicit: “not interchangeable.”	Vendor-level conflation pervasive. Core Peptides lists MW ~3,367.95 g/mol on its DAC product page — the no-DAC mass. FDA PCAC briefing surfaced one DAC sample that mass-spec’d as no-DAC.	🔴 MAJOR GAP — vendor-side identity failure documented at the regulator level. Buyers who follow no-DAC protocols on mislabeled DAC vials will overdose; buyers who follow DAC protocols on mislabeled no-DAC vials will underdose.
NCT00267527 fatal MI, 17 July 2006	On-site attending physician adjudicated unrelated. No independent cardiovascular adjudication ever published. Trial terminated regardless. Full primary-endpoint data never published.	Three framings coexist: cautionary citation (Huberman, Vanguard, Revolution Health), dismissal (vendor / pro-DAC clinic citing adjudication), and absence of dose-ceiling derivation. The community does not derive screening protocols from the MI signal.	🔴 Community awareness exists but is not operationalised. A 192-patient halted-trial fatality, single-arbitrator adjudication, no published Phase 2 results — and the community uses 600 mcg–5 mg weekly doses without baseline cardiovascular work.
Sustained 6–11 day GH/IGF-1 elevation = physiologic pulsatility?	Ionescu & Frohman 2006 argue yes (pulse frequency preserved on elevated trough). 🔴⚠️ FDA briefing and class-mechanistic critique argue no (elevated trough is not a true trough). Dispute unresolved in published literature.	Bodybuilding-forum consensus has been settled against the Ionescu/Frohman framing since ~2012–2014. “GH bleed” terminology (DatBtrue) is universal vocabulary. Compounding-pharmacy filing FDA-2024-N-4777-0002 carries the critique verbatim.	Community ahead of the published-literature consensus on this specific mechanistic question. The community internally has converged faster than the peer-reviewed record.
Ben-Shlomo 2020 pituitary DNA damage	Peer-reviewed JCI finding: γH2AX induction, Comet-assay Olive tail moment increases in CJC-1295 DAC-treated mouse pituitary cells. Cited centrally by FDA in December 2024 PCAC briefing.	Largely unintegrated into community discourse. Cautionary boilerplate in some longevity-clinic write-ups; not addressed by major bodybuilding-forum voices.	Science finding has not propagated into the community-protocol layer. The single most consequential preclinical safety signal added since the development era is not reshaping community dosing or screening.
DAC + ipamorelin stack	Mechanistically incoherent on half-life grounds: ipamorelin t½ ~2 h (Gobburu 1999) vs DAC t½ ~6 d (Teichman 2006). No published study of the combination.	The dominant clinic-marketed default stack — Revolution Health, LIVV Natural, Yunique Medical, Women’s Health of MD, most telehealth peptide vendors sell it. Knowledgeable forum users flag the incoherence; clinic copy does not.	🔴 Active commercial deployment of a stack whose theoretical synergy basis does not apply. This is the clearest case of clinic marketing operating downstream of a community-level misreading of the original pulsatility logic.
The 70% injection-site reaction rate	Teichman 2006 actually reported 23% (11/47 administrations).	Community write-ups (biohacknow.net and downstream aggregators) carry an unsourced 70% figure.	Community-internal misinformation amplification. A specific clinically-relevant number is inflated 3× across the community-readable layer with no traceable source.
DatBtrue 100 mcg saturation, 1–2 mg/wk weekly	No published dose-response curve. Compounding-pharmacy 600 mcg weekly is the only structured-document dose.	Community-codified default since mid-2000s. Treated as settled.	Community-codified protocol with no published support. Dose-response not necessarily wrong, but never tested.
Single-group authorship dependency	Frohman/ConjuChem cluster wrote the four primary efficacy papers (Jetté 2005, Teichman 2006, Ionescu & Frohman 2006, Alba 2006, Sackmann-Sala 2009). Ben-Shlomo 2020 (independent) used CJC-1295 DAC as a tool, not for efficacy.	Rarely flagged. The Sikiric/Seiwerth-style “this is one research group writing about its own compound” critique that bodybuilding forums apply to BPC-157 is essentially absent for CJC-1295 DAC.	🔴 Community has not internalised the single-group dependency for this compound despite applying the same critique to other peptides.
WADA S2.2.4 prohibition	Explicit. CJC-1295 named in 2026 List without DAC/no-DAC distinction. Strict liability. Henninge 2010 detection method published.	Aware; treated as orthogonal to non-athlete use.	Aligned awareness; underweighted in non-athlete contexts. NCAA, USADA, DoD service members face strict-liability exposure independent of efficacy questions.
FDA December 2024 PCAC 0/13/0 vote	Explicit; nonclinical findings (DNA damage, hematology, immunogenicity, no carcinogenicity data, MI signal) cited as basis.	Aware; framed by compounder lobby as procedurally arbitrary; by mainstream-medicine voices as warranted.	Split along self-experimenter vs clinician-adjacent lines. The FDA’s concerns are real; the compounder critique that PCAC reasoning was uneven across substances is also real. Dispute unresolved.
TGA Schedule 4 + Appendix D since 1 June 2015	Explicit. Australian possession-without-authority illegal.	Aware via legal-status pages. Australian users face possession risk.	Aligned in awareness.
Vendor identity / quality	FDA characterised impurity and aggregation profile of compounded preparations as a primary safety concern.	Finnrick public database functions as informal post-market surveillance; DAC-only subtable not exposed; Janoshik per-batch COAs exist for DAC but vendor attribution requires direct page access.	Aligned in direction; community has built mitigation infrastructure that regulators have not matched — but the DAC-specific layer of that infrastructure is thinner than the no-DAC layer.

Net characterisation. CJC-1295 with DAC is a “halted-with-fatal-event, single-group, never-published-Phase-2” case rather than the BPC-157 “essentially untested” case or the no-DAC “no human studies of the specific molecule” case. The published evidence base is real but thin, industry-led, and structurally fragile. The four highest-consequence gaps:

1. A 192-patient halted Phase 2 with one fatal MI and full results unpublished twenty years on. This is the single most consequential evidentiary fact about the compound. It is treated by the community as historical context rather than as operational signal.
2. The DAC + ipamorelin stack — mechanistically incoherent — is the dominant clinic-marketed default. Commercial deployment is running ahead of the theoretical synergy basis that originally justified the GHRH + GHRP combination concept.
3. The 2020 Ben-Shlomo pituitary DNA-damage finding has not propagated into the community-protocol layer. The most consequential post-development safety signal in the literature is not reshaping dosing or screening.
4. The community has measurably converged on the “GH bleed” critique — sometimes ahead of the published-literature consensus — but has not converged equivalently on the single-group dependency, the unpublished Phase 2, or the cardiovascular signal. Convergence is selective.

CJC-1295 with DAC is not BPC-157’s “community ahead of single-group preclinically-anchored science” pattern, because Sikiric/Seiwerth produced >300 BPC-157 papers (single-group but voluminous), while the Frohman/ConjuChem group produced fewer than ten papers on the DAC compound and the central Phase 2 dataset remains unpublished. It is also not the no-DAC compound’s “untested” pattern. It is closer to a “tested-thinly-by-one-group-with-an-unresolved-fatal-event” pattern — a category the encyclopedia does not have another canonical case of as of 2026-05-17.

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12. Three Paths

You choose your risk tolerance. This monograph provides the data, not the recommendation.

Conservative path — wait. Defined as not engaging until at least one of: (a) peer-reviewed full publication of NCT00267527 primary endpoint data, (b) independent peer-reviewed cardiovascular adjudication of the 2006 fatal MI, (c) marketing authorisation for CJC-1295 DAC in any major jurisdiction, (d) full 503A bulks-list inclusion after the next PCAC review cycle, (e) independent multi-centre replication of the Teichman/Ionescu PK/PD data outside the Frohman/ConjuChem authorship cluster, or (f) a 2-year carcinogenicity study and resolution of the Ben-Shlomo 2020 pituitary genotoxicity signal at therapeutic-range exposures in a relevant species. None of these gates is met as of 2026-05-17. CJC-1295 with DAC does not meet the conservative bar at all. The conservative path for users wanting GHRH-axis support is sermorelin (compoundable under 503A as a component of a previously FDA-approved drug, with a published 30-year human dataset however thin on optimization-audience indications) or tesamorelin (FDA-approved as Egrifta® for HIV-associated lipodystrophy since 2010).

Moderate path — Tier D with supervision, post-PCAC-pending. Defined as treating CJC-1295 with DAC as a Tier-D compound with class-level mechanistic plausibility (GHRH-R agonism is real), thin compound-specific human evidence concentrated in one authorship cluster, an unresolved cardiovascular signal from the only completed Phase 2 trial, an unintegrated preclinical pituitary genotoxicity signal, and explicit anti-doping exposure for any WADA-tested athlete, NCAA athlete, or DoD service member. This path means: pre-cycle baseline cardiovascular evaluation including ECG, lipid panel, fasting glucose, HbA1c — not the casual bloodwork that the bodybuilding-forum tradition treats as adequate, given the 2006 MI signal and the HIV-lipodystrophy population overlap; pre-cycle CBC, comprehensive metabolic panel, IGF-1, and (where age-appropriate) PSA; on-cycle IGF-1 at 4–6 weeks; supply through a compounding pharmacy operating under physician oversight rather than research-chemical grey market, with full awareness that the December 2024 PCAC vote and pending July 2026 re-review make legal compounding access provisional; explicit understanding that DAC’s multi-day half-life means side effects do not titrate down within 24 h; explicit avoidance during active malignancy, recent malignancy history, or known precancerous lesion; explicit avoidance for any tested-sport athlete or service member; awareness of the Australian Schedule 4 + Appendix D possession risk; absolute avoidance during pregnancy / lactation. The moderate path treats Tier D as “preclinical and Phase-1-level human plausibility plus 18 years of community use without catastrophic safety signal, monitored against the specific signals the published literature identifies.”

High-tolerance path — grey-market with mitigation. Defined as acknowledging that none of the conservative gates are met, that the published human PK/PD record traces entirely to one industry-funded authorship cluster, that the only completed Phase 2 trial halted with a fatal event whose causal adjudication is single-arbitrator and never independently reviewed, that the central preclinical safety signal (Ben-Shlomo 2020 pituitary DNA damage) has not been quantitatively translated to human therapeutic-range exposure, and that the dominant clinic-marketed stack (DAC + ipamorelin) is mechanistically incoherent. The community mitigation stack documented in Pass 2: third-party mass-spectrometry identity verification (not just COA from vendor — the Core Peptides MW mislabel and the FDA PCAC mass-spec finding both prove vendor-side identity failure happens) via Janoshik Analytical’s public database or comparable lab; preference for vendors that publish per-batch (not per-brand) DAC-specific COAs with mass-spec identity confirmation at the ~3,648 Da signature; titration starting at the 500 mcg weekly community-titration entry rather than the 2 mg standard or the 5 mg + MK-677 aggressive stack; weekly dose ceiling below the compounding-pharmacy 600 mcg/week structured dose; pre-cycle ECG, lipid panel, fasting glucose, HbA1c, IGF-1, CBC, PSA where age-appropriate, given the 2006 MI signal; on-cycle IGF-1 at 4–6 weeks; explicit avoidance of the DAC + MK-677 combination unless explicitly accepting the GH-bleed framing and the MK-677 CHF signal (4/62 vs 1/61 in the hip-fracture trial); explicit avoidance of the DAC + ipamorelin combination on the grounds that the matched-pulse synergy claim does not apply to the DAC variant; sterile injection technique; physician-monitoring dialogue even where the physician has not prescribed; anti-doping exposure assessed honestly — collegiate, military, equine, and WADA-tested civilian athletes face strict-liability sanctions for both DAC and no-DAC under WADA S2.2.4; explicit understanding that no-DAC at pulsatile community doses is the structurally cleaner choice for GHRH-axis support if compliance is not the binding constraint, and that the DAC variant’s principal advantage is once-weekly compliance traded against multi-day side-effect duration.

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13. Key References

Scientific layer

Regulatory documents

• FDA. Briefing Document, Pharmacy Compounding Advisory Committee Meeting, 4 December 2024. Docket FDA-2024-N-4777. https://www.fda.gov/media/183819/download.
• FDA. PCAC Meeting Transcript, 4 December 2024 — “A Matter of Record.” https://www.fda.gov/media/185641/download. Pages 120–136 (CJC-1295 votes).
• FDA Federal Register notice, 16 April 2026 — scheduling follow-on PCAC meeting for 23–24 July 2026.
• TGA. Reasons for scheduling delegate’s final decisions, March 2015. CJC-1295 (CAS 863288-34-0) Schedule 4 + Appendix D, effective 1 June 2015.
• ConjuChem Biotechnologies Inc., voluntary assignment in bankruptcy under the Bankruptcy and Insolvency Act (Canada), 21 July 2010. CNW/Newswire.
• FDA / PRNewswire press release. FDA approves Egrifta to treat lipodystrophy in HIV patients. Silver Spring, MD, 10 November 2010. Context only — tesamorelin distinct compound.

Anti-doping documents

• WADA 2026 Prohibited List, S2.2.4 Growth hormone releasing factors, effective 1 January 2026.
• USADA, NCAA, DoD-OPSS, Global DRO, BSCG — WADA Code adoption references.
• Henninge J, Pepaj M, Hullstein I, Hemmersbach P. Drug Test Anal 2010;2(11-12):647-650. PMID 21204297.
• ASADA 2013 NRL proceedings (Cronulla-Sutherland Sharks; Stephen Dank regimen) — secondary documentation.

Peer-reviewed preclinical and human studies (all on DAC compound; all single-group except Ben-Shlomo)

• Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. J Clin Endocrinol Metab 2006;91(3):799-805. PMID 16352683. DOI 10.1210/jc.2005-1536. ⚠️🔴
• Ionescu M, Frohman LA. J Clin Endocrinol Metab 2006;91(12):4792-4797. PMID 17018654. DOI 10.1210/jc.2006-1702. 🔴⚠️
• Jetté L, Léger R, Thibaudeau K, et al. Endocrinology 2005;146(7):3052-3058. PMID 15817669. 🔴
• Alba M, Fintini D, Sagazio A, Lawrence B, Castaigne JP, Frohman LA, Salvatori R. Am J Physiol Endocrinol Metab 2006;291(6):E1290-1294. PMID 16822960. 🔴⚠️
• Sackmann-Sala L, Ding J, Frohman LA, Kopchick JJ. Growth Horm IGF Res 2009;19(6):471-477. 🔴
• Ben-Shlomo A, et al. J Clin Invest 2020;130(11):5738-5755. PMC7598090.

Clinical trial registry

• ClinicalTrials.gov NCT00267527 — Phase 2 HIV-associated visceral obesity. Sponsor ConjuChem. Status: Terminated 17 July 2006. Primary results never published.

Community layer

Forum / bodybuilding archive

• DatBtrue (datbtrue.co.uk legacy; cross-posts on Professional Muscle, AnabolicMinds, EliteFitness, Eroids).
• Meso-Rx / thinksteroids.com — Bill Roberts CJC-1295 profile.
• ProfessionalMuscle.com — “CJC-1295 DAC side effects and dosage” and “CJC GH Bleed - Dat says its a no go?” threads.
• AnabolicMinds — “cjc-1295 dac dosage questions” thread.
• EliteFitness — “CJC-1295 w/Dac and MK-677” thread.
• Eroids — “FINALLY!! CJC 1295 with DAC GH Bleed proof! ~Notorious” (2014).
• UK-Muscle — “GH Bleed??” thread.
• ExcelMale — “CJC-1295 / Ipamorelin (10mg) blend dosage” thread.

Biohacker / podcast layer

• Huberman Lab episode (April 2024) — class-level GHRH discussion including the with-DAC fatal MI reference; recommends against CJC-1295 in favor of sermorelin / tesamorelin.
• Derek (More Plates More Dates) — “How To Replicate A HIGH Dose Of Pharma Grade GH With Peptides” (2021, still live). DAC + MK-677 personal historical protocol.
• Ben Greenfield — “Growth Hormone-Releasing Peptides Deep Dive”; “toast vs CJC-toast” framing on DAC/no-DAC vendor conflation.
• Jay Campbell — “CJC-1295 for Weight Loss, Muscle Growth and Bodybuilding”; “Mod GRF 1-29 vs CJC-1295.”
• Vanguard Laboratory — “CJC-1295 and Ipamorelin: The Stack Everyone Uses, Nobody Verifies” (23 March 2026). Marketing-adjacent vendor-aligned source.
• aidsmap (Edwin J. Bernard) — “Lipodystrophy study halted after patient death,” 31 July 2006.

Clinic / vendor / regulatory-community layer

• Revolution Health & Wellness; LIVV Natural; Tucson Wellness MD; Yunique Medical; Women’s Health of MD; Desert Mobile Medical — clinic-marketing layer.
• Core Peptides; Pure Rawz; BioTech Peptides; Particle Peptides; Skye Peptides; Limitless Life Nootropics; Peptide Sciences (discontinued); Huma Peptide; Elite Biogenix; Apex; Palmetto; Real Peptides; Lumin Peptides; Avish Enterprises — vendor pages (commercial motive flagged).
• The Peptide Catalog; PeptideDosingProtocols.com; pepdose.com; PeptideDeck; BiohackNow; Swolverine — secondary aggregators.
• Frier Levitt; FDA Law Blog — legal-status community-readable summaries.
• Finnrick public CJC-1295 aggregate (244 samples / 47 vendors, Dec 2024–Mar 2026); Janoshik Analytical public database — third-party COA / verification ecosystem.
• Turnock LA & Hearne E. “Novel wellbeing and repair peptide use in the UK: Netnographic findings.” Performance Enhancement & Health 2024;13(1):100293. Specifically studies BPC-157, TB-500, and CJC-1295 as the three named peptides.
• Gobburu JVS et al. “Pharmacokinetic-Pharmacodynamic Modeling of Ipamorelin.” Pharm Res 1999;16(9):1412. Anchors the DAC + ipamorelin stack-coherence math.

Retrieval limitations explicitly noted (substantive, carried from Pass 2)

Direct Reddit thread-level evidence was not retrievable for r/Peptides, r/PeptideUmbrella, r/PEDs, r/Biohackers, or r/Nootropics at named-source resolution within the compilation window. Reddit API access policy changes since mid-2023 mean specific permalinks, vote counts, and quoted comment text could not be retrieved. Reddit-community sentiment has been inferred from third-party aggregator summaries (drkconrad.com, PeptideDeck, The Peptide Catalog). No specific Reddit thread titles, permalinks, posting dates, or vote totals have been fabricated. The bodybuilding-forum archive (Professional Muscle, AnabolicMinds, EliteFitness, Eroids, UK-Muscle, ExcelMale) layer is more directly captured than the Reddit thread-level layer. Original DatBtrue forum posts (datbtrue.co.uk, defunct) have been referenced through downstream forum cross-posts where his framings are preserved verbatim with attribution. Telegram / Discord channels were not searched. Finnrick’s CJC-1295 DAC-only subtable was not surfaced at named-source resolution (the publicly-visible variant-tagged Finnrick rows are dominated by no-DAC samples). Janoshik DAC test IDs 80846 and 89194 exist but vendor identities were not extractable from search snippets. Vendor-specific 5 mg DAC list prices were not extracted at the per-product detail level for Pure Rawz, BioTech Peptides, Verified Peptides, Pure Tested Peptides, Huma Peptide, Elite Biogenix, and Particle Peptides; the single firm DAC price ($52/5 mg from Core Peptides) is the only fully-verified retail figure. Peter Attia, Layne Norton, Lyle McDonald, and Koniver Wellness DAC-specific commentary was not located. Derek MPMD video-transcript-level DAC-vs-no-DAC quotation was not retrieved; only the MorePlatesMoreDates written essay was captured. The widely-quoted “70% injection-site reaction rate” circulating in community write-ups is not traceable to any named clinical trial; the actual Teichman 2006 figure is 23% (corrected from Pass 1 primary literature). Community write-ups (Vanguard Lab, Huberman, multiple clinic pages) describe NCT00267527 as “HIV-related lipodystrophy” — the official trial title uses “HIV-related visceral obesity”; a persistent community-layer inaccuracy that does not change the safety signal.

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14. Audit / Refresh Trail

• Composed: 2026-05-17
• Science-layer source: cjc-1295-dac_sci_2026-05-17_D10.md (Pass 1; review stamp 2026-05-17; prior baseline content drawn from Group_B_GH_GHRH_Secretagogues_2026-05-09.md and Growth_Hormone__GHRH_Analogues__and_GH_Secretagogues__Comprehensive_Scientific_and_Regulatory_Review_2026.md).
• Community-layer source: cjc-1295-dac_com_2026-05-17_A77.md (Pass 2; compiled 2026-05-17).
• Section 4 Last regulatory review: 2026-05-17.
• Two-molecule calibration block status: last review of molecular-identity ambiguity 2026-05-17. DAC vs no-DAC ambiguity unchanged. Vendor-level conflation remains the dominant QC risk and has been documented at the regulator level via FDA PCAC December 2024 mass-spec finding and the Core Peptides MW mislabel.
• Next refresh triggers:
  • PCAC outcome 23–24 July 2026 — re-review of CJC-1295 variants on the 503A bulks list. Outcome materially changes the moderate-path operational landscape.
  • Any Federal Register notice formalising bulks-list exclusion or inclusion of CJC-1295 DAC variants.
  • First full peer-reviewed publication of NCT00267527 primary endpoint data — the single largest possible evidence-base shift for this entry.
  • Any independent peer-reviewed cardiovascular adjudication of the 2006 fatal MI.
  • Any peer-reviewed publication of a head-to-head DAC vs no-DAC trial in any indication.
  • Retraction of Teichman 2006, Ionescu & Frohman 2006, or Ben-Shlomo 2020 — flagged for Retraction Watch monitoring.
  • Any independent multi-centre replication of the Teichman/Ionescu PK/PD data outside the Frohman/ConjuChem authorship cluster.
  • Any high-profile USADA, WADA, or NCAA sanction with CJC-1295 DAC specifically as a named substance.
  • WADA 2027 List changes to S2.2.4 wording or detection method (particularly any move to differentiate DAC vs no-DAC at AAF level).
  • TGA Poisons Standard revision affecting Schedule 4 + Appendix D Item 5.
  • Any 2-year carcinogenicity study of CJC-1295 DAC.
  • Any human data on translatability of the Ben-Shlomo 2020 pituitary genotoxicity signal.
  • Mainstream-podcast adoption shift — if Huberman, Attia, or Rogan publicly revise their March 2026 framing post-PCAC July 2026 vote.
  • Direct r/Peptides / r/PEDs thread retrieval to ground community-layer evidence in primary thread permalinks with vote counts.
  • Major vendor scandal affecting the CJC-1295 DAC supply chain at scale (DAC-vs-no-DAC mislabeling exposé, COA forgery at a major vendor, etc.).