CJC-1295 with DAC
What the Research Actually Shows
Human: 2 studies, 3 groups · Animal: 1 · In Vitro: 0
The growth hormone secretagogue that binds to your blood proteins and works for a week per injection—and why the company that made it no longer exists
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BLUF: Bottom Line Up Front
CJC-1295 with DAC is the only growth hormone secretagogue that works for nearly a week from a single injection. Two published human studies show it raises growth hormone 2–10-fold and IGF-1 1.5–3-fold—with effects lasting 6–11 days per dose. But the company that developed it, ConjuChem Biotechnologies, terminated its largest trial after a patient died three hours after an injection, then went bankrupt. No new human data has been published since 2006. The science is real. The compound works. And it has been abandoned by every pharmaceutical entity that touched it.
CJC-1295 with DAC is a study in pharmaceutical ingenuity and pharmaceutical abandonment. The science behind it is genuinely clever: take a GHRH analog, attach a reactive chemical linker that covalently bonds to albumin in the bloodstream, and transform a 30-minute peptide into a week-long growth hormone stimulant. One injection per week instead of one or more per day. The human data confirms the concept works—growth hormone and IGF-1 rise substantially and stay elevated for days.
And then the story falls apart. A patient in a Phase II trial in Argentina died three hours after their eleventh injection. The attending physician attributed the death to pre-existing asymptomatic coronary artery disease, not to the drug itself. But the trial was terminated, never completed, and never published. ConjuChem Biotechnologies ran out of money and filed for bankruptcy in 2010. Patrick Soon-Shiong acquired the company's assets and did nothing with them.
The result is a compound that has real Phase I/II data, an elegant pharmacological mechanism, and zero active pharmaceutical development. The evidence is frozen at 2006. No academic group, no pharmaceutical company, no government agency has published a new human study on CJC-1295 with DAC in twenty years. It remains available through specialty peptide vendors, used by a community that is working from the same two published papers the rest of us are.
This article covers the with-DAC version specifically. For the no-DAC version (Mod GRF 1-29)—a pharmacologically different compound with a 30-minute half-life and no human clinical data—see the CJC-1295 (no DAC) article (forthcoming Platinum version).
Quick Facts: CJC-1295 with DAC at a Glance
TYPE
Synthetic GHRH analog with Drug Affinity Complex (maleimido albumin-binding linker at Lys³⁰)
ALSO KNOWN AS
CJC-1295-DAC, DAC:GRF, Modified GRF(1-29)-DAC
MOLECULAR WEIGHT
~3647 Da (peptide + linker); ~70 kDa when bound to albumin
ROUTE
Subcutaneous injection. Weekly dosing.
COMMUNITY INTEREST
Weekly GH optimization, sustained IGF-1 elevation, convenience over injectable peptide secretagogues requiring daily dosing.
DAC TECHNOLOGY
Maleimido linker covalently binds Cys³⁴ on serum albumin within minutes of injection. Irreversible binding. Creates a stable peptide-albumin complex with a half-life of 5.8–8.1 days.
HALF-LIFE
5.8–8.1 days (human data, Teichman 2006). Longest in Cluster D. ~700× longer than no-DAC version (~30 min). >1,000× longer than native GHRH (~10 min).
PRIMARY MOLECULAR FUNCTION
GHRHR agonism → sustained GH/IGF-1 elevation via irreversible albumin binding. Pulsatile GH secretion preserved despite continuous stimulation (Ionescu 2006).
WEEKLY DOSING
The most convenient dosing schedule in the cluster. One injection per week at 30–60 µg/kg produced sustained GH/IGF-1 elevation in clinical trials.
ABANDONED COMPOUND
No pharmaceutical company is developing CJC-1295 with DAC. No new human data since 2006. The compound was abandoned due to corporate failure—not proven inefficacy.
DEVELOPER
ConjuChem Biotechnologies (Montreal). Phase II trial terminated 2006. Bankruptcy 2010. Assets acquired by Patrick Soon-Shiong. No further development.
CLINICAL PROGRAMS
2 published Phase I studies (2006). Phase II HIV lipodystrophy trial terminated after patient death. No active clinical programs. Developer bankrupt.
FDA STATUS
Not FDA-approved. Category 2 (removed Sept 2024). Never completed Phase II. No active IND.
WADA STATUS
Prohibited—S2. Banned in- and out-of-competition.
NOT INTERCHANGEABLE
CJC-1295 with DAC and CJC-1295 without DAC are pharmacologically different compounds. Half-life differs by ~700-fold. GH profiles are fundamentally different (sustained vs. pulsatile). Data from one does NOT apply to the other.
LONG HALF-LIFE RISK
If adverse effects occur, they persist for nearly a week. Unlike short-acting peptides where you can simply stop dosing, the albumin-bound complex cannot be removed or neutralized once injected.
Evidence Tier
2 Clinical Trials
EVIDENCE TIER
2 Clinical Trials
VERDICT
Reasonable Bet
Verdict
Reasonable Bet
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Subscribe to Peptidings WeeklyWhat Is CJC-1295 (with DAC)?
Pronunciation: see-jay-see-twelve-ninety-five (with dack) (also known as CJC-1295-DAC, DAC:GRF, ConjuChem CJC-1295)
Albumin is the most abundant protein in your blood—a molecular workhorse that transports hormones, fatty acids, and drugs through the circulation. It has a half-life of approximately 19 days. If you could attach a peptide drug to albumin, the peptide would ride along for the duration—surviving for days instead of minutes. CJC-1295 with DAC is a compound designed to do exactly that.
The base molecule is the same tetrasubstituted GRF(1-29) found in CJC-1295 (no DAC)—a GHRH analog with four amino acid substitutions for enzymatic stability. The DAC modification adds a reactive maleimidopropionic acid linker at position 30 (lysine). Within minutes of subcutaneous injection, this linker forms a covalent thioether bond with cysteine-34 on circulating serum albumin. The bond is irreversible. Once attached, the peptide-albumin complex circulates for nearly a week, continuously presenting the GHRH analog to pituitary GHRH receptors.
The result: a single weekly injection that elevates growth hormone and IGF-1 for 6–11 days. This is not a sustained-release formulation—the peptide itself is not slowly released from a depot. It is actively bound to albumin and continuously stimulating the GHRH receptor for the entire duration of the albumin complex's circulation.
PLAIN ENGLISH
This compound works by hitching a ride on the most common protein in your bloodstream. Once injected, a chemical hook permanently attaches the growth hormone-releasing peptide to albumin, and it keeps working for nearly a week until the albumin naturally breaks down. One shot per week instead of one or more per day.
Origins and Discovery
ConjuChem Biotechnologies, founded in Montreal in 1996, specialized in Drug Affinity Complex technology—a platform for extending the half-life of therapeutic peptides by conjugating them to albumin-binding linkers. Their pipeline included DAC-modified versions of GLP-1 (for diabetes), interferon-alpha (for hepatitis C), and GRF(1-29) (for growth hormone deficiency).
CJC-1295 was ConjuChem's most advanced GRF program. The company conducted two Phase I studies published by Teichman et al. and Ionescu & Frohman in 2006, demonstrating the pharmacological proof of concept in healthy adults. They then launched a Phase II trial (NCT00267527) for HIV-associated visceral obesity—approximately 192 patients receiving weekly subcutaneous injections for 12 weeks.
In July 2006, a patient in the Argentina arm of the HIV trial died approximately three hours after receiving their eleventh weekly injection. The attending physician attributed the death to acute myocardial infarction secondary to pre-existing asymptomatic coronary artery disease—not to CJC-1295. However, the trial was terminated, the data were never published, and the FDA investigated.
ConjuChem's financial position deteriorated through 2007–2009, and the company filed for bankruptcy protection in 2010. Patrick Soon-Shiong—the billionaire physician known for developing Abraxane and later acquiring the Los Angeles Times—acquired ConjuChem's assets in 2010–2011. No new CJC-1295 development has been initiated under any successor entity.
Mechanism of Action
The base peptide operates through identical GHRHR pharmacology as CJC-1295 (no DAC) and sermorelin: Gs → cAMP → PKA → calcium mobilization → GH granule exocytosis. The four amino acid substitutions (D-Ala², Gln⁸, Ala¹⁵, Nle²⁷) provide DPP-IV resistance.
The DAC modification fundamentally alters pharmacokinetics without changing pharmacodynamics at the receptor level:
Albumin binding kinetics: The maleimido linker reacts with cysteine-34 on serum albumin within 15 minutes of injection (Jetté 2005). The thioether bond is covalent and irreversible—the peptide cannot detach from albumin. The complex circulates with albumin's natural half-life (~19 days), but the peptide's biological activity degrades faster than albumin itself, yielding an effective half-life of 5.8–8.1 days (Teichman 2006).
Sustained GHRHR stimulation: The albumin-bound complex continuously presents the GHRH analog to pituitary somatotroph GHRH receptors. This is sustained stimulation—not pulsatile—yet the Ionescu 2006 study demonstrated that pulsatile GH secretion was preserved. The mechanism: GHRH receptor downregulation and somatostatin negative feedback create an oscillatory system even under continuous input. The somatostatin-mediated troughs still occur, though they are elevated above baseline (trough GH +7.5-fold, mean GH +46%).
The safety implication of irreversibility: Unlike short-acting peptides where adverse effects resolve within hours of discontinuation, the albumin-bound CJC-1295-DAC complex persists for days. If an adverse reaction occurs—injection site reaction, cardiovascular event, allergic response—the drug cannot be cleared, neutralized, or dialyzed out. The patient must wait for the complex to degrade naturally. This is the pharmacological trade-off for weekly dosing convenience.
PLAIN ENGLISH
The DAC linker permanently hooks the peptide onto a blood protein called albumin. This means it keeps working for a week—great for convenience, but it also means if something goes wrong, you cannot turn it off. The peptide keeps stimulating growth hormone release until the albumin naturally breaks down, which takes nearly a week.
Key Research Areas and Studies
GH and IGF-1 Stimulation (Teichman et al. 2006)
The Teichman study is the foundational efficacy dataset. In two double-blind, placebo-controlled, ascending-dose RCTs in healthy adults aged 21–61: - Single injection of 30–60 µg/kg SC produced GH increases of 2–10-fold lasting 6+ days - IGF-1 increased 1.5–3-fold with effects lasting 9–11 days - Cumulative effect observed with repeated weekly dosing - Well tolerated at therapeutic doses (30–60 µg/kg) - Dose-limiting toxicities at higher doses included injection site reactions
This is clean Phase I data demonstrating proof of concept: the DAC modification works as designed, and the GHRH analog remains biologically active when bound to albumin.
Pulsatile GH Preservation (Ionescu & Frohman 2006)
The Ionescu study addressed the most important mechanistic concern: does continuous GHRH receptor stimulation flatten GH pulsatility? Answer: no, at least in the short term. In healthy young males receiving CJC-1295-DAC at 60 or 90 µg/kg, overnight frequent blood sampling (every 20 minutes) showed that GH pulsatility was preserved. Trough GH increased 7.5-fold (meaning the "valleys" between pulses were substantially elevated above normal). Mean GH increased 46%. IGF-1 increased 45%.
The preservation of pulsatility under sustained GHRH input is consistent with the oscillatory nature of the somatostatin feedback system—somatostatin periodically inhibits GH release even when GHRH stimulation is continuous. However, the study was small and short-term—whether pulsatility is preserved during chronic weekly dosing over months is unknown.
The HIV Lipodystrophy Trial (NCT00267527)
ConjuChem's Phase II trial enrolled approximately 192 HIV patients with visceral obesity for 12 weeks of weekly subcutaneous CJC-1295-DAC. The trial was terminated in July 2006 after a patient in Argentina died approximately three hours after receiving their eleventh weekly injection. The attending physician attributed the death to acute myocardial infarction secondary to pre-existing asymptomatic coronary artery disease.
This trial was never completed and never published in peer-reviewed literature. The ClinicalTrials.gov record shows termination. The data that were collected—including any safety signals from 192 patients over up to 11 weeks—are proprietary and unpublished.
The editorial framing: this death did not prove CJC-1295-DAC caused the MI. Pre-existing CAD is a common cause of acute MI, and temporal proximity to an injection does not establish causation. However, the trial was terminated (not merely paused), the data were never published (raising questions about whether there were other signals), and the company ceased to exist within four years. The community cannot assess this event because the data are sealed.
The DAC Modification — How It Works
This compound-specific section provides the technical deep dive into the Drug Affinity Complex technology that defines this compound.
What DAC is: A maleimidopropionic acid (MPA) linker attached to lysine at position 30 of the GHRH(1-29) analog. The maleimido group is a thiol-reactive Michael acceptor—it forms a covalent thioether bond with the free sulfhydryl group of cysteine-34 on serum albumin.
Why Cys-34 specifically: Human serum albumin has a single free cysteine residue at position 34 (Cys³⁴). This is the only thiol on albumin that is accessible for conjugation. The DAC linker is engineered to react specifically with this site, creating a defined 1:1 peptide-albumin complex.
The binding timeline: Within 15 minutes of subcutaneous injection, the majority of CJC-1295-DAC molecules have bound to circulating albumin (Jetté 2005). Unbound peptide is rapidly cleared (as with the no-DAC version). Only the albumin-bound fraction persists.
Why this matters for understanding the compound: The CJC-1295-DAC you inject is not what stimulates your GHRH receptors. What stimulates your receptors is the CJC-1295-DAC-albumin complex—a ~70 kDa macromolecule. The pharmacological properties of this complex (tissue distribution, receptor access, half-life) are fundamentally different from the free peptide.
The irreversibility problem: The thioether bond between DAC and albumin is covalent and non-hydrolyzable under physiological conditions. There is no enzyme that cleaves it, no drug that reverses it, and dialysis does not remove it (the complex is too large and too tightly bound to albumin). Once injected, the compound is committed. This is the trade-off for the week-long half-life.
PLAIN ENGLISH
The DAC modification is a chemical hook that permanently attaches to a blood protein. Think of it as a parasite latching onto a whale—the peptide rides albumin's circulation for nearly a week. The bond cannot be broken. This is what makes the once-a-week dosing possible, and it is also what makes the compound irreversible once injected.
Claims vs. Evidence
| Claim | What the Evidence Shows | Verdict |
|---|---|---|
| “"CJC-1295 with DAC raises GH and IGF-1 for a week per injection"” | Confirmed by Teichman 2006. GH elevated 2–10-fold for 6+ days. IGF-1 elevated 1.5–3-fold for 9–11 days. This is the strongest finding. | Strong Foundation |
| “"CJC-1295 with DAC preserves pulsatile GH secretion"” | Ionescu 2006 showed pulsatility preserved in overnight sampling. But trough GH was 7.5× above normal—meaning "pulsatile" does not mean "normal." Small study, short-term only. | Reasonable Bet |
| “"CJC-1295 with DAC is safer because it requires only weekly dosing"” | Less frequent injection = fewer injection site reactions. But: irreversible binding means adverse effects persist for days. The HIV trial death—regardless of causation—occurred 3 hours post-injection with no ability to reverse drug exposure. Convenience ≠ safety. | Eyes Open |
| “"CJC-1295 with DAC improves body composition"” | No body composition data from published trials. GH/IGF-1 elevation was demonstrated, but clinical outcomes (lean mass, fat mass, strength) were not measured. The terminated HIV trial may have had body composition data—unpublished. | Thin Ice |
| “"CJC-1295 with DAC is the same as CJC-1295 (no DAC) but longer-lasting"” | FALSE. The DAC modification changes half-life by ~700-fold, changes the GH profile from pulsatile to sustained, changes the molecular species from free peptide (~3.4 kDa) to albumin complex (~70 kDa), and changes the safety profile (irreversible vs. rapidly cleared). These are pharmacologically different compounds. | Thin Ice |
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The Human Evidence Landscape
Teichman et al. 2006 — The Dose-Escalation Study
Design: Two randomized, double-blind, placebo-controlled, ascending-dose studies. N: Healthy adults aged 21–61 (exact N not specified in abstract). Duration: Single-dose and multi-dose weekly injections. Key findings: Half-life 5.8–8.1 days. GH increased 2–10-fold for 6+ days. IGF-1 increased 1.5–3-fold for 9–11 days. Cumulative effect with weekly dosing. Well tolerated at 30–60 µg/kg. Limitations: Phase I—safety and PK focus, not efficacy. Healthy volunteers—not a disease population. Exact sample sizes not reported in abstract. PMID: 16352683
Ionescu & Frohman 2006 — The Pulsatility Study
Design: Clinical trial with overnight frequent blood sampling (q20 min). N: ~8–12 healthy males, aged 20–40. Duration: Single dose + overnight observation. Key findings: Pulsatile GH secretion preserved despite continuous GHRHR stimulation. Trough GH +7.5-fold. Mean GH +46%. IGF-1 +45%. No dose difference between 60 and 90 µg/kg (ceiling effect). Limitations: Very small sample. Single overnight observation—chronic pulsatility preservation unknown. Healthy young men only. PMID: 17018654
NCT00267527 — The Terminated HIV Trial (UNPUBLISHED)
Design: Phase II, weekly SC injection, 12 weeks. N: ~192 HIV patients with visceral obesity. Status: Terminated July 2006 after patient death (acute MI, Argentina, ~3 hours after 11th injection). Outcome: Never completed. Never published. Data proprietary. Editorial significance: The termination and non-publication create an evidence gap—the community cannot assess whether there were other safety signals in 192 patients over up to 11 weeks of treatment.
What the Landscape Reveals
The human evidence for CJC-1295 with DAC is thin but genuine. Two published studies demonstrate pharmacological proof of concept. A Phase II trial existed but was terminated and never published. The total published human experience amounts to perhaps 30–50 subjects in short-term studies. No clinical outcome endpoints (body composition, strength, sleep, quality of life) were measured. The evidence base has been frozen since 2006—twenty years without new data.
Safety, Risks, and Limitations
Irreversibility
The most important safety consideration unique to this compound. Once injected, CJC-1295-DAC binds irreversibly to albumin. If an adverse reaction occurs, the drug persists for 5.8–8.1 days. No antidote. No reversal agent. No removal mechanism. For short-acting peptides, "stop dosing and wait a few hours" is a viable safety response. For CJC-1295-DAC, "stop dosing and wait a week" is the only option.
The HIV Trial Death
A patient died approximately 3 hours after their 11th weekly injection. The attending physician attributed the death to pre-existing asymptomatic coronary artery disease. Without published trial data, the community cannot independently assess: how many other adverse cardiovascular events occurred in the trial; whether there was a pattern of cardiovascular signals; what the overall safety profile looked like in 192 patients. The termination and non-publication are themselves concerning—not because they prove the drug caused the death, but because the data needed to make that assessment is sealed.
Antibody Formation
The DAC linker is a non-endogenous chemical modification. The albumin-peptide complex presents non-native epitopes to the immune system. Immunogenicity rates were presumably measured in ConjuChem's trials but were never published. Antibody formation could neutralize the compound's activity over repeated dosing cycles.
Sustained Insulin/Glucose Effects
GH is a counter-regulatory hormone. Sustained GH elevation over a week may produce more persistent insulin resistance than pulsatile stimulation. No published metabolic data exist for CJC-1295-DAC.
Compounding and Quality
CJC-1295-DAC is more complex to synthesize than the no-DAC version because of the DAC linker conjugation step. Manufacturing variability—incorrect conjugation, free linker contamination, incomplete binding—adds quality risk beyond what exists for simpler peptides.
What Is NOT Known
- Long-term safety at any dose
- Cardiovascular safety (the only relevant data is sealed in an unpublished terminated trial)
- Metabolic effects (glucose, insulin) during chronic weekly dosing
- Immunogenicity rates (antibody formation)
- Effects in populations with renal, hepatic, or cardiac compromise
- Drug interactions
- Cancer risk from sustained IGF-1 elevation
Legal and Regulatory Status
- FDA status: Not FDA-approved. Never completed Phase II. Category 2 (placed 2023–2024, removed September 2024 following nominator withdrawal). Regulatory status in flux (2026). HHS announced intent to lift peptide bans.
- DEA: Not a controlled substance.
- WADA: Prohibited under S2. Banned in- and out-of-competition.
- Commercial status: ConjuChem bankrupt. No manufacturer holds an IND. No pharmaceutical-grade product exists. Available through specialty peptide vendors.
Research Protocols and Formulation Considerations
CJC-1295-DAC is available from specialty peptide vendors as lyophilized powder for reconstitution. The DAC modification makes it more complex to manufacture and more expensive than the no-DAC version.
Storage: Lyophilized powder should be stored refrigerated or frozen. Reconstituted solution should be refrigerated (2–8°C / 36–46°F). The maleimido linker may be reactive with other thiol-containing compounds in solution—reconstitution and storage conditions matter more than for simple peptides.
Dosing in Published Research
| Study | Population | Dose | Route | Frequency | Duration | Key Outcome |
|---|---|---|---|---|---|---|
| Teichman et al. 2006 | Healthy adults, 21–61 yr | 30–60 µg/kg | SC | Single + weekly | Multi-dose | GH 2–10×, IGF-1 1.5–3× for 6–11 days |
| Ionescu & Frohman 2006 | Healthy males, 20–40 yr | 60–90 µg/kg | SC | Single dose | Overnight observation | Pulsatile GH preserved. No dose difference (ceiling). |
Research dose summary: 30–60 µg/kg subcutaneous, once weekly. For a 75 kg adult, this translates to approximately 2.25–4.5 mg per weekly injection. The Ionescu study found no additional benefit at 90 µg/kg vs. 60 µg/kg, suggesting a ceiling effect.
Dosing in Self-Experimentation Communities
COMMUNITY-SOURCED INFORMATION
The dosing information below is drawn from community reports, forums, and anecdotal sources — not clinical trials. It reflects what people report using, not what has been validated by research. This is not medical advice.
Community dosing for CJC-1295-DAC is less standardized than for the no-DAC version, partly because the compound is less commonly available and partly because the long half-life makes dosing adjustments slow:
- Common community dose: 2 mg subcutaneous, once or twice weekly
- Some protocols: 1 mg twice weekly (spreading the dose for more even levels)
- Cycle length: 8–12 weeks. Some users report longer cycles given the weekly dosing convenience.
- Combination stacks: Less commonly combined with ipamorelin than the no-DAC version (because the sustained DAC profile is already "always on"—adding a daily GHS-R1a agonist produces continuous dual-pathway stimulation rather than timed pulses)
- Key community concern: The irreversibility. Experienced community members note that adverse effects from CJC-1295-DAC persist for days, making dose titration difficult and "starting low" particularly important.
No published clinical data validates any community dosing protocol for CJC-1295-DAC. The published research doses (30–60 µg/kg weekly) translate to approximately 2.25–4.5 mg weekly for a 75 kg adult, which is broadly consistent with community protocols.
Combination Stacks
COMMUNITY-SOURCED INFORMATION
The dosing information below is drawn from community reports, forums, and anecdotal sources — not clinical trials. It reflects what people report using, not what has been validated by research. This is not medical advice.
Research into CJC-1295 with DAC combination protocols is limited. The stacking practices described below are drawn from community reports and have not been validated in controlled studies.
If you are considering combining CJC-1295 with DAC with other compounds, consult a qualified healthcare provider. Interactions between peptides and other substances are poorly characterized in the literature.
Frequently Asked Questions
: Is CJC-1295 with DAC the same compound as CJC-1295 (no DAC)?
A: No. They share the same base peptide (tetrasubstituted GRF(1-29)) but differ fundamentally. The DAC modification adds a chemical linker that permanently binds the peptide to albumin in your blood, extending the half-life from ~30 minutes to ~6–8 days. They produce different GH profiles (sustained vs. pulsatile), require different dosing schedules (weekly vs. daily), and have different safety considerations (irreversible vs. rapidly cleared). Data from one does not apply to the other.
: Why does CJC-1295 with DAC work for a week per injection?
A: The DAC (Drug Affinity Complex) is a chemical linker that forms a permanent bond with albumin—the most abundant protein in your blood. Once attached, the peptide circulates with albumin for nearly a week, continuously stimulating the GHRH receptor on your pituitary gland. The half-life of 5.8–8.1 days is determined by how long the albumin-peptide complex stays biologically active.
: What happened in the HIV trial?
A: ConjuChem conducted a Phase II trial (NCT00267527) in approximately 192 HIV patients with visceral obesity. A patient in Argentina died approximately three hours after receiving their eleventh weekly injection. The attending physician attributed the death to pre-existing asymptomatic coronary artery disease, not to the drug. The trial was terminated and never published. The data—including any other safety signals from 192 patients—remain proprietary and unpublished.
: Does the trial death mean CJC-1295 with DAC is dangerous?
A: Not necessarily—but the question cannot be answered definitively because the trial data were never published. Temporal proximity to an injection does not prove causation. Pre-existing coronary artery disease is a common cause of acute MI. However, the trial was terminated (not merely paused), the data were sealed, and the company went bankrupt. Without published safety data from 192 patients, the community cannot independently assess the cardiovascular safety profile.
: Is pulsatile GH release preserved with the DAC version?
A: Ionescu 2006 found that GH pulsatility was preserved during overnight sampling after a single dose. This is reassuring but limited—it was a small study with short follow-up. The "pulsatile" pattern was superimposed on dramatically elevated baseline levels (trough GH +7.5-fold). Whether pulsatility is preserved during chronic weekly dosing over months is unknown.
: Why did ConjuChem go bankrupt?
A: ConjuChem's financial difficulties preceded the trial death but were compounded by it. The company had multiple pipeline programs but limited revenue. The HIV trial termination removed their most advanced clinical asset. By 2010, the company filed for bankruptcy. Patrick Soon-Shiong acquired the assets in 2010–2011 but did not resume CJC-1295 development.
: Can I reverse the effects if I have a bad reaction?
A: No. The DAC linker forms an irreversible covalent bond with albumin. Once injected, the compound cannot be removed, neutralized, or dialyzed out. If adverse effects occur, they persist for the duration of the complex's half-life (5.8–8.1 days). This is the most important safety consideration unique to this compound and the fundamental trade-off for the weekly dosing convenience.
: How does CJC-1295 with DAC compare to MK-677?
A: Both produce sustained GH elevation, but through different receptors (GHRHR vs. GHS-R1a). MK-677 is oral with a 24-hour effect; CJC-1295-DAC is injectable with a week-long effect. MK-677 stimulates appetite (ghrelin receptor); CJC-1295-DAC does not. MK-677 has 11 published human trials; CJC-1295-DAC has 2 published and 1 terminated. MK-677 can be stopped with effects clearing in ~24 hours; CJC-1295-DAC effects persist for nearly a week after injection.
: Is CJC-1295 with DAC legal?
A: Its regulatory status is in flux. It was placed on the FDA's Category 2 list (2023–2024) and removed in September 2024. HHS announced intent to lift peptide bans in February 2026. It is not FDA-approved, not a controlled substance, not a dietary supplement, and is WADA-prohibited. Available through specialty peptide vendors.
: Why are there no new studies after 2006?
A: Because the company that owned the compound went bankrupt. CJC-1295-DAC is a proprietary formulation—the DAC conjugation technology was ConjuChem's intellectual property. When the company ceased to exist and the assets were acquired without further development, the clinical program died. No academic group has independently pursued human trials with this specific conjugate.
: Should I use the DAC or no-DAC version?
A: They have different pharmacological profiles suited to different goals. The DAC version offers weekly dosing convenience and sustained GH elevation but with irreversible exposure. The no-DAC version produces pulsatile GH release closer to natural physiology but requires daily injections. The DAC version has human clinical data; the no-DAC version does not. Neither has been compared head-to-head. The choice depends on individual risk tolerance, dosing preferences, and whether you prioritize convenience (DAC) or physiological fidelity (no DAC).
: What would it take to restart clinical development of CJC-1295 with DAC?
A: A pharmaceutical sponsor willing to fund new IND-enabling studies, address the FDA's concerns from the terminated HIV trial, and conduct fresh Phase II trials with proper safety monitoring. Given the availability of newer long-acting GH approaches (e.g., long-acting somatropin, LUM-201), the commercial incentive is limited. The compound is effectively orphaned.
Summary of Key Findings
CJC-1295 with DAC represents both the promise and the fragility of pharmaceutical development. The science is genuinely clever—a covalent albumin-binding strategy that transforms a 30-minute peptide into a week-long growth hormone stimulant. The human data confirms the concept works: GH increases 2–10-fold, IGF-1 increases 1.5–3-fold, and pulsatile GH secretion is preserved despite continuous stimulation.
And then the story stops. A patient death in a Phase II trial—attributed to pre-existing coronary artery disease, not to the drug—terminated the largest clinical study. The data were never published. The company went bankrupt. The assets were acquired and shelved. No new human data has been published in twenty years.
What remains is a compound with genuine Phase I/II data, an elegant pharmacological mechanism, and complete pharmaceutical abandonment. The community uses it based on two published papers from 2006. The safety profile beyond those papers is unknown—the sealed trial data that might answer the most important safety questions may never be released.
Verdict Recapitulation
CJC-1295 with DAC earns Reasonable Bet because the published human data is genuine and the pharmacological mechanism is well-characterized. But the "Bet" qualifier is heavy. The irreversible albumin binding means adverse effects persist for days. The largest trial was terminated after a patient death and never published. The developer went bankrupt. No new data in twenty years. Users should understand that they are working from a thin evidence base and that the convenience of weekly dosing comes with the irreversibility of weekly commitment.
For readers considering CJC-1295 with DAC, the evidence above represents the current state of knowledge. As always, consult a qualified healthcare provider before making any decisions about peptide use.
Where to Source CJC-1295 with DAC
Further Reading and Resources
If you want to go deeper on CJC-1295 with DAC, the evidence landscape for growth hormone secretagogues peptides, or the methodology behind how we evaluate this research, these are the places worth your time.
ON PEPTIDINGS
- Growth Hormone Secretagogues Research Hub — Overview of all compounds in this cluster
- Reconstitution Guide — How to properly prepare injectable peptides
- Storage and Handling Guide — Proper storage to maintain peptide stability
- About Peptidings — Our editorial methodology and evidence framework
EXTERNAL RESOURCES
- PubMed: CJC-1295 with DAC — All indexed publications
- ClinicalTrials.gov — Active and completed trials
Selected References and Key Studies
- Teichman SL, Neale A, Lawrence B, et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. 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
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DISCLAIMER
CJC-1295 with DAC is not approved by the FDA for any indication in the United States. The information presented in this article is for educational and research purposes only. Nothing in this article constitutes medical advice, and no material here is intended to diagnose, treat, cure, or prevent any disease or health condition.
Consult a qualified healthcare provider before making any decisions about peptide use. Report adverse events to the FDA via MedWatch.
For the full Peptidings editorial methodology and evidence framework, visit our About page and Evidence Framework pages.
Article last reviewed: April 06, 2026. Next scheduled review: October 03, 2026.
About the Author
Lawrence Winnerman
Founder of Peptidings.com. Former big tech product manager. Independent peptide researcher focused on translating clinical evidence into accessible science.
