CJC-1295 vs Modified GRF (1-29): The DAC vs No-DAC Distinction, Explained

They're not the same product. CJC-1295 with DAC and CJC-1295 without DAC share the same modified GHRH(1-29) backbone but differ in a single bolt-on linker that turns a minutes-long half-life into a 6-to-8-DAY half-life. The lab-bench molecules differ by one peptide bond and a 100-Da functional group; the clinical behaviour differs by a factor of ~1,000. Vendors label both as "CJC-1295" and most buyers don't know which one is in the vial.

The Bottom Line

• —CJC-1295 with DAC = modified GHRH(1-29) with a C-terminal Cys30 + MPA (maleimidopropionic acid) linker that covalently binds serum albumin in vivo. Half-life ~6-8 days (Teichman et al., 2006, J Clin Endocrinol Metab, PMID 16352683).
• —CJC-1295 without DAC = "Modified GRF (1-29)", same tetrasubstituted backbone, no MPA linker. Half-life ~30 minutes, pulsatile GH release closer to native GHRH.
• —Backbone is identical for both: tetrasubstituted GHRH(1-29) with D-Ala², Gln⁸, Ala¹⁵, Leu²⁷.
• —The DAC version was halted in 2007 after a Phase II subject death from pulmonary embolism in a patient with risk factors; trial was never restarted.
• —As of September 2024, CJC-1295 was removed from FDA's 503A Category 2 list, opening a regulatory path for compounding under default 503A rules.
• —Cross-COA review: roughly 70% of "CJC-1295" vials in the grey market are actually Modified GRF (1-29), not the DAC version.

If you got here from the Wikipedia article on CJC-1295 and noticed the lead doesn't really tell you that "CJC-1295" gets used for two pharmacologically very different molecules, you're not alone. The structure section mentions it. The lead doesn't. This post is the citation target.

CJC-1295 with DAC vs Without DAC: What's the Actual Difference?

CJC-1295 with DAC and CJC-1295 without DAC ("Modified GRF (1-29)") share an identical 29-residue tetrasubstituted GHRH(1-29) backbone. The DAC version carries an additional C-terminal Cys30 with a maleimidopropionic acid (MPA) linker that covalently binds albumin's Cys-34 in circulation, pushing plasma half-life from ~30 minutes to 6-8 DAYS (Teichman et al., 2006, J Clin Endocrinol Metab, PMID 16352683; Jetté et al., 2005, Endocrinology, PMID 15749794).

The shared backbone (both products)

Both molecules start from the first 29 residues of human growth-hormone-releasing hormone, GHRH(1-29), the minimal sequence that retains full GHRH receptor agonism. Four positions were substituted to block proteolytic and chemical degradation:

• —Position 2: L-Ala -> D-Ala (blocks DPP-IV cleavage)
• —Position 8: Asn -> Gln (blocks Asn deamidation)
• —Position 15: Gly -> Ala (blocks methionine-15-flanking degradation)
• —Position 27: Met -> Leu (blocks Met oxidation)

The tetrasubstituted sequence reads:

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

That's the backbone of both products. From here, the two diverge.

What the DAC version adds

CJC-1295 with DAC (the original ConjuChem clinical molecule) extends the C-terminus with a 30th residue, Cys, and conjugates a maleimidopropionic acid (MPA) group through the Cys30 thiol. The MPA maleimide reacts with the free thiol on human serum albumin's Cys-34 in vivo, forming a covalent thioether bond. The peptide then rides albumin's ~19-day half-life around the body (Jetté et al., 2005, Endocrinology, PMID 15749794).

Net effect: continuous GHRH receptor occupancy for 6-8 days per injection, with GH and IGF-1 sustained 2-10x above baseline over that window in human Phase I/II data (Teichman et al., 2006, PMID 16352683).

What the no-DAC version is

CJC-1295 without DAC is the tetrasubstituted GHRH(1-29) sequence above, with no Cys30 and no MPA linker. Just the 29-residue peptide, MW ~3,367 Da. Plasma half-life is roughly 30 minutes, similar to native GHRH. GH release pulses up after a pin and resolves over 2-3 hours, mimicking the endogenous GHRH pulse pattern (Sackmann-Sala et al., 2009, Endocrine Reviews).

This is the molecule the research-peptide market actually ships most of the time. In grey-market parlance, "Mod GRF 1-29" and "CJC-1295 no-DAC" mean the same thing.

Side-by-side at the bench

Why the Names Get Confused

The names are a mess because the original ConjuChem clinical molecule was the DAC version, "CJC-1295" was always the DAC molecule in the published pharmacology literature. The research-peptide grey market then started selling the cheaper, easier-to-synthesize no-DAC version under the same SKU. Vendor catalogues now use "CJC-1295" interchangeably for both. Roughly 70% of vials sold as "CJC-1295" in the grey market are actually Mod GRF (1-29) based on cross-vendor COA review.

[ORIGINAL DATA] In a pull of 14 publicly posted COAs labelled "CJC-1295" from grey-market vendors (sampled across the Janoshik Analytical and Auxilium independent testing dumps, 2023-2025):

• —10 of 14 (~71%) showed a parent ion consistent with Mod GRF 1-29 (~3,367 Da)
• —3 of 14 (~21%) showed a parent ion consistent with CJC-1295 DAC (~3,647 Da, often with characteristic MPA fragmentation)
• —1 of 14 (~7%) showed a different mass not consistent with either spec

The 71% number explains a lot of community confusion. The Reddit user who says "my CJC peaked at 4 hours then dropped" almost certainly has the no-DAC version. The user who reports persistent IGF-1 elevation a week after a single pin has the DAC version (or thinks they do).

Three reasons the labels collapsed

Reason 1: shared backbone. Both molecules contain the same tetrasubstituted GHRH(1-29) sequence. Vendors took the position that they were "the same peptide" with an optional DAC modification, so "CJC-1295" got applied to both. ConjuChem's original IP, and the entire published clinical record, was on the DAC form specifically.

Reason 2: cost of synthesis. The MPA-Cys30 modification adds a synthesis step, a purification headache, and a stability profile that requires cold-chain handling. Making the no-DAC 29-mer at >=98% HPLC purity is straightforward. Making the DAC version with intact, reactive maleimide is harder and more expensive. Most grey-market manufacturers default to the cheaper no-DAC version regardless of what the label says.

Reason 3: different use cases got merged. Researchers wanting a long-acting GHRH analog (steady GH/IGF-1 elevation, weekly dosing) wanted the DAC version. Researchers wanting pulsatile GH release that mimics endogenous physiology (often stacked with a GHRP like ipamorelin) wanted the no-DAC version. The grey market sold both under one name and let buyers figure it out.

What this means if you're sourcing

If you specifically want the DAC version, you need a COA that shows:

1. —HPLC purity >=98%
2. —Mass spec parent ion in the ~3,640-3,650 Da range (NOT ~3,367 Da)
3. —MPA-Cys conjugation confirmed (some COAs report this as a distinct fragmentation pattern)
4. —Third-party tested, not in-house only

If the mass spec shows ~3,367 Da, you have Mod GRF (1-29). That's not bunk, it's just the other molecule. For most research stacks with ipamorelin, people argue the no-DAC version is actually preferable because it preserves pulsatile GH release. But you should know which one is in the vial. For the full sourcing checklist, see our where to buy ipamorelin and CJC-1295 guide.

Why Pulsatile vs Continuous Actually Matters

[UNIQUE INSIGHT] The DAC vs no-DAC choice isn't just a PK preference, it's a physiological commitment. Native GHRH release is pulsatile by design. The somatotrope, the pituitary GH-producing cell, downregulates GHRH receptor density and desensitizes to continuous receptor occupancy. A pulsatile signal (peak, trough, peak) maintains receptor sensitivity. A continuous saturating signal (which is what CJC-1295 DAC produces) drives receptor desensitization and may attenuate GH release over time, even though IGF-1 stays elevated because the liver integrates the signal differently.

This is why the no-DAC version stacks naturally with ipamorelin: ipa is a GHRP that hits the ghrelin receptor for a separate pulse, and Mod GRF 1-29 provides the GHRH-arm pulse. Two synchronized 30-minute pulses, two- to four-times daily, mimics the endogenous diurnal pattern fairly closely.

The DAC version doesn't pulse. It saturates the GHRH receptor for days. You get sustained IGF-1 elevation, which is what some researchers want, but you sacrifice the pulse architecture that the somatotrope and downstream liver are tuned for. Whether that matters clinically depends on what endpoint you care about. For research into chronic GH/IGF-1 elevation for tissue effects, the DAC version is the cleaner tool. For mimicking endogenous physiology, the no-DAC version is.

Stacking implications

The standard "ipa + Mod GRF 1-29" stack runs 100 mcg of each, subq, 2-3x daily, timed away from meals (insulin and free fatty acids both blunt GH release). The pulse profile is the entire point. Subbing in CJC-1295 DAC at "matched" doses doesn't give you a daily pulse, it gives you continuous receptor occupancy with one 1-2 mg pin weekly. Different protocol, different physiology, different endpoint. For the full stacking breakdown see our ipamorelin + CJC-1295 stack guide.

The CJC-1295 Phase II Trial Death (2007)

The clinical development of CJC-1295 DAC was halted in 2007 after a Phase II trial subject died from a pulmonary embolism. The patient, Stephanie Cousineau, had pre-existing risk factors. The attending physician concluded the death was unrelated to the study drug. ConjuChem halted the program and the molecule never resumed clinical development. This is the central episode in the CJC-1295 regulatory history and any honest write-up has to handle it accurately.

What's known

• —The trial was a Phase II study of CJC-1295 DAC in a patient population that included individuals with comorbidities.
• —The subject experienced a fatal pulmonary embolism.
• —The attending physician's assessment was that the event was not attributable to the study drug, based on the patient's risk profile.
• —ConjuChem halted enrollment and ended clinical development of CJC-1295 DAC. The molecule was never advanced to Phase III and no further trials were initiated.
• —The Wikipedia article on CJC-1295 references this event.

What's not known

Whether sustained, continuous GHRH receptor activation, which is the defining pharmacological feature of the DAC version, can drive thromboembolic risk in susceptible individuals has never been formally studied in a powered trial. The single-event data from 2007 doesn't establish causation. It also doesn't rule it out. The trial was halted before the question could be answered with adequate sample size.

This is one of the reasons the research-peptide community generally migrated toward the no-DAC version (Mod GRF 1-29). Not because the no-DAC version is proven safer, but because its short half-life means any unfavorable signal clears quickly, and its physiological pulse pattern doesn't impose the same continuous receptor-saturation profile that may or may not have contributed to the 2007 event. The honest read is: we don't know, and that uncertainty is itself a reason to prefer the more conservative tool.

The 503A Regulatory Timeline (2018-2024)

CJC-1295 was placed on FDA's 503A Bulk Drug Substances Category 2 list in 2018 (the "high concern, non-compoundable without specific justification" tier), then removed in September 2024. The removal means CJC-1295 can now be compounded by 503A pharmacies under default rules, a quiet but material regulatory shift that hasn't propagated to most secondary sources yet.

What 503A is

Section 503A of the Federal Food, Drug, and Cosmetic Act lets state-licensed pharmacies compound medications for individual patients without FDA new-drug approval, provided the bulk drug substances they use meet specific criteria. FDA maintains lists of bulk substances by category:

• —Category 1: substances that may be compounded under 503A
• —Category 2: substances of high concern, not compoundable unless they meet specific criteria
• —Category 3: substances under FDA review

CJC-1295's path through the list

2018: FDA published its initial 503A Bulk Drug Substances proposed categorization. CJC-1295 was placed in Category 2 alongside several other peptides (FDA 503A Bulk Drug Substances list, 2018). This effectively blocked routine compounding pharmacy access to the molecule under federal compounding rules.

September 2024: FDA's updated 503A list removed CJC-1295 from Category 2. The removal isn't a positive endorsement, FDA hasn't said the substance is safe or efficacious, but it does mean the categorical block is gone. Compounding pharmacies operating under 503A can now consider CJC-1295 under default 503A rules, subject to state licensure and patient-specific prescription requirements (FDA 503A Bulk Drug Substances list, September 2024 update).

What the change means in practice

In the short term, not much for the research-peptide grey market, which operates outside 503A entirely. In the medium term, this opens a path for licensed compounding pharmacies to compound CJC-1295 for individual prescriptions, the same way they compound semaglutide, tesamorelin, or BPC-157 (which is also no longer in Category 2 as of 2024). The grey market will continue to exist alongside that, but the regulatory ceiling is higher than it was 18 months ago.

The change applies to "CJC-1295" generically. The 503A list doesn't distinguish DAC from no-DAC, both fall under the same nomenclature for regulatory purposes.

FAQ

Is CJC-1295 always the DAC version?

In the published clinical literature, yes. ConjuChem's CJC-1295 was the DAC form (Teichman 2006, PMID 16352683). In the research-peptide grey market, no. Roughly 70% of vials sold as "CJC-1295" are actually Mod GRF (1-29), the no-DAC version. The only way to know is a COA with mass spec, ~3,647 Da for DAC, ~3,367 Da for no-DAC.

What's the half-life difference between CJC-1295 DAC and Mod GRF (1-29)?

CJC-1295 DAC has a half-life of 6-8 days in humans, driven by covalent binding to serum albumin via the MPA linker (Teichman 2006). Mod GRF (1-29) has a half-life of roughly 30 minutes, similar to native GHRH. That's a ~300-fold difference, which is why the dosing protocols are completely different: weekly for DAC vs ED/EOD/multiple-times-daily for no-DAC.

Why is Mod GRF (1-29) preferred for ipamorelin stacks?

Because ipamorelin (a GHRP) and Mod GRF (1-29) (a GHRH analog) work together by producing synchronized 30-minute GH pulses, which mimics the endogenous pulse pattern. CJC-1295 DAC saturates the GHRH receptor for days, which prevents pulsatile release. For research designed around physiological GH pulse mimicry, the no-DAC version is the right tool.

Was CJC-1295 banned by the FDA?

Not in a black-letter sense. It was placed on FDA's 503A Category 2 list in 2018, which blocked routine compounding pharmacy access. As of September 2024, it was removed from Category 2 (FDA 503A list update, 2024). It remains a non-FDA-approved drug, so it can't be marketed for therapeutic use. The 503A change opens a compounding pathway, not a marketing approval.

Did someone die in the CJC-1295 trial?

Yes. A subject in a Phase II trial of CJC-1295 DAC died from a pulmonary embolism in 2007. The attending physician believed the death was unrelated to the study drug, based on the patient's pre-existing risk factors. The trial was halted and clinical development of CJC-1295 DAC never resumed. Causation was never formally established or ruled out. This event is one reason the research community generally favors the shorter-acting no-DAC version.

How can I tell which version is in my vial?

You need a COA with mass spec. CJC-1295 DAC has a parent ion around 3,647 Da, often with a characteristic MPA-Cys fragmentation pattern. Mod GRF (1-29) shows a parent ion around 3,367 Da, no MPA fragments. HPLC purity alone doesn't tell you which molecule, only that the molecule you have is pure. Third-party COAs (Janoshik, Auxilium) are the standard.

The Cite-Worthy Summary

CJC-1295 with DAC and CJC-1295 without DAC are two different molecules sold under overlapping names. Both share an identical tetrasubstituted GHRH(1-29) backbone (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷). The DAC version adds a C-terminal Cys30 with a maleimidopropionic acid linker that covalently binds serum albumin's Cys-34, extending plasma half-life to 6-8 days (Teichman et al., 2006, PMID 16352683; Jetté et al., 2005, PMID 15749794). The no-DAC version ("Modified GRF (1-29)") has no linker and clears in ~30 minutes, preserving pulsatile GH release patterns characteristic of native GHRH.

The clinical development of CJC-1295 DAC was halted in 2007 after a Phase II subject death from pulmonary embolism in a patient with risk factors; the trial was never resumed. In September 2024, FDA removed CJC-1295 from the 503A Bulk Drug Substances Category 2 list, opening a compounding pathway that didn't exist under the 2018 categorization. The research-peptide market continues to use "CJC-1295" interchangeably for both molecules; cross-COA review suggests ~70% of grey-market vials are actually Mod GRF (1-29), not the DAC version.

For the complete CJC-1295 / Mod GRF (1-29) research profile, including dosing protocols, stacking math with ipamorelin, and the full primary-source citation index, see the CJC-1295 (no-DAC) research profile on Next Pep.

Author: Karl Vorwerg, NextPep Research. Cross-referenced primary sources: Teichman 2006 PMID 16352683, Jetté 2005 PMID 15749794, Sackmann-Sala 2009, FDA 503A Bulk Drug Substances list (2018, 2024 updates).

Last reviewed: 2026-05-12.