CJC-1295 (UK pillar guide): DAC and non-DAC variants, preclinical literature, regulatory status

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CJC-1295 is a 30-residue synthetic analogue of growth-hormone-releasing hormone (GHRH). It is sold by UK research-peptide retailers in two distinct variants. The first is CJC-1295 with DAC, a Drug Affinity Complex modification that allows the peptide to bind covalently to circulating serum albumin and persist in plasma for roughly a week. The second is CJC-1295 without DAC, often labelled “mod GRF (1-29)” or “modified GRF”, which shares the same tetra-substituted 29-residue core but lacks the albumin-binding linker, giving it a serum half-life measured in minutes rather than days. Both sit at research tier in the United Kingdom, with no marketing authorisation as medicines.

What CJC-1295 actually is

CJC-1295 was originally described by Conjuchem (later ConjuChem Biotechnologies) in the mid-2000s. The peptide sequence is built on the first 29 residues of native human GHRH, the same N-terminal fragment that underlies sermorelin. Four amino acid substitutions are made at positions 2, 8, 15 and 27 to resist enzymatic degradation by dipeptidyl peptidase-4 (DPP-4) and trypsin-like proteases. This tetra-substituted backbone, on its own, is the molecule commonly sold as “CJC-1295 without DAC”, or as “mod GRF (1-29)” in older literature.

The DAC modification is what distinguishes the long-acting variant. DAC stands for Drug Affinity Complex. It is a maleimidopropionic acid (MPA) linker conjugated to a lysine residue added to the C-terminus, giving a final 30-residue molecule. The maleimide group on the linker reacts selectively with the free thiol on cysteine-34 of human serum albumin once the peptide enters the bloodstream. This covalent bond means the peptide is no longer freely circulating and is no longer rapidly cleared by the kidneys or degraded by serum proteases. Instead, it travels bound to albumin, the most abundant plasma protein, which has its own half-life of approximately 20 days.

The chemistry is worth understanding because it explains every downstream difference between the two variants. Without DAC, the peptide is a small molecule (around 3.4 kDa) that is filtered and degraded quickly. With DAC, it becomes effectively a large albumin-conjugated complex (around 70 kDa once bound) that the body cannot easily clear. The same active GHRH-receptor binding sequence is present in both, so receptor pharmacology is similar in isolation. Pharmacokinetics is what diverges.

A note on nomenclature, since this is one of the most confused areas in the research-peptide market. “CJC-1295” in primary literature usually refers to the DAC-modified, albumin-binding version, because that is the molecule Conjuchem described and patented. “CJC-1295 without DAC” is a retailer-driven label for the underlying tetra-substituted GRF(1-29) backbone. Some retailers also sell that backbone under the name “mod GRF (1-29)” or simply “modified GRF”. They are the same active sequence. Buyers reading a Certificate of Analysis (CoA) should look for confirmation that DAC is present (visible as a higher molecular weight and a different HPLC retention time) before assuming the long-acting variant.

What the preclinical literature shows

The preclinical and early-clinical literature on CJC-1295 is unusually well-defined for a research peptide, because Conjuchem ran formal phase I and phase II human trials in the mid-2000s. Several of those results were published in mainstream endocrinology journals.

The foundational paper is Teichman SL 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; PMID 16352683). This was a randomised, placebo-controlled, double-blind ascending-dose study in healthy adult men. A single subcutaneous administration produced sustained elevation of GH and IGF-1 over several days, with IGF-1 remaining elevated above baseline for at least 6 days post-administration at the higher doses studied. This is the citation most commonly referenced for the “week-long half-life” claim.

A follow-up by Ionescu and Frohman, “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; PMID 16968794), addressed an important pharmacological question: does prolonged GHRH-receptor stimulation collapse the natural pulsatile pattern of GH secretion into a flat, constantly elevated state? The investigators reported that pulsatility was preserved, with GH secretion amplitude actually increased while pulse frequency stayed within normal range. This finding underpins one of the central research arguments in favour of CJC-1295 DAC: that albumin-bound GHRH agonism produces a more physiological pituitary response than would be expected from a continuously elevated agonist.

Subsequent work explored dose-response and IGF-1 kinetics in more detail. The same group published further data on weekly subcutaneous administration in healthy adults showing dose-dependent IGF-1 elevation. Independent preclinical work in animal models examined growth-axis effects, body composition outcomes, and tolerability, including studies referenced in the Sackmann-Sala review of GH secretagogues (Sackmann-Sala et al., Growth Horm IGF Res, 2015).

For the non-DAC variant, the literature is older and rests on the original GRF(1-29) work, since “mod GRF (1-29)” is essentially the tetra-substituted version of the molecule first characterised by Guillemin’s and Rivier’s groups in the late 1970s and early 1980s. The relevant background reading covers Frohman LA and Jansson JO, “Growth Hormone-Releasing Hormone” (Endocr Rev, 1986; PMID 3084848), and the human GRF(1-29) pharmacokinetic studies from that era. Modifications at positions 2, 8, 15 and 27 were shown across multiple groups to extend in vitro stability without disrupting receptor binding.

Useful citations for UK researchers building a literature base on CJC-1295 and its non-DAC counterpart include:

• Teichman SL et al., J Clin Endocrinol Metab, 2006 (PMID 16352683): sustained GH and IGF-1 elevation, single-dose pharmacokinetics
• Ionescu M, Frohman LA, J Clin Endocrinol Metab, 2006 (PMID 16968794): preservation of GH pulsatility under continuous GHRH-receptor stimulation
• Jette L et al., Endocrinology, 2005: DAC technology and albumin binding kinetics, foundational chemistry paper
• Frohman LA, Jansson JO, Endocr Rev, 1986 (PMID 3084848): GHRH biology background
• Sackmann-Sala L et al., Growth Horm IGF Res, 2015: review of GH secretagogue class
• Khorram O et al., J Clin Endocrinol Metab, 1997 (PMID 9329376): GRF effects on aged adults, relevant context for the unmodified parent peptide
• Walker RF, Clin Interv Aging, 2006 (PMID 18046878): broader review of secretagogue strategies including GHRH analogues
• Sigalos JT and Pastuszak AW, Sex Med Rev, 2018 (PMID 28526625): clinical-context review of growth-hormone secretagogues including CJC-1295

These citations are pointers for researchers building their own literature reviews. PMIDs change over time as PubMed records are updated; researchers should always verify the current canonical record.

DAC vs no-DAC: the research framing

The choice between DAC and non-DAC CJC-1295 is the single most consequential decision a researcher makes when designing a protocol that involves this peptide. The two variants behave like different research tools despite sharing a core sequence.

CJC-1295 with DAC produces a sustained, multi-day elevation of GHRH-receptor activity. After a single subcutaneous administration, plasma concentrations rise over the first day, plateau across several days as albumin-bound peptide circulates, then decay over the following week as albumin itself turns over. The downstream effect, in the Teichman dataset, is a stable elevation of IGF-1 above baseline for roughly 6 to 11 days at higher doses. From a research design perspective, this means the variant produces a fundamentally different exposure profile to anything seen with native GHRH or short-acting analogues. It is the version used in studies looking at chronic GH-axis modulation, body-composition outcomes over weeks, and IGF-1 dose-response.

CJC-1295 without DAC behaves entirely differently. The tetra-substituted backbone, without the albumin-binding linker, has a serum half-life measured in minutes (commonly cited as roughly 30 minutes in the research-peptide literature, somewhat longer than the 5 to 10 minutes of unmodified GHRH because of the protease-resistance substitutions, but still short). This means each administration produces a defined pulse of GHRH-receptor activity that decays quickly. Researchers interested in preserving the natural pulsatile pattern of pituitary GH secretion, rather than imposing a continuous stimulus, generally consider the non-DAC variant the more physiological tool. Pulsatility-preservation is the central argument in its favour and is often cited in research protocols that pair the non-DAC variant with a separate ghrelin-receptor agonist (most commonly ipamorelin) to mimic the natural sleep-onset GH pulse pattern.

In practical terms, research uses tend to split as follows. CJC-1295 with DAC appears in protocols where investigators want sustained exposure with minimal administration frequency: weekly subcutaneous dosing schedules in animal-model research, long-running body-composition or IGF-1 studies, and any protocol where consistent exposure is more important than physiological pulsatility. CJC-1295 without DAC appears in protocols where investigators want a defined, short-duration GHRH pulse, typically combined with a ghrelin-receptor agonist for amplification, often administered around the natural overnight GH-secretion window.

It is worth flagging that pulsatility preservation is itself a contested concept. The Ionescu and Frohman 2006 paper argues, on the DAC variant data, that the pituitary continues to generate pulses even under continuous GHRH-receptor stimulation. If that is correct, the “non-DAC preserves pulsatility, DAC abolishes it” framing is too simple. The available evidence suggests pulses persist under both modes of stimulation, but the underlying baseline tone is higher with DAC. Researchers should treat the pulsatility argument as a working hypothesis backed by limited evidence rather than a settled question.

What the literature does NOT show

The preclinical and early-clinical literature has clear limits. UK researchers should be aware of what is not in the public record on CJC-1295.

There is no phase III clinical trial data. Conjuchem ran phase I and phase II programmes in the mid-2000s, primarily aimed at lipodystrophy in HIV patients and at the general GH-deficiency space. None of those programmes reached phase III. Conjuchem was acquired and the drug-development pipeline was wound down. As a result, there is no large-scale efficacy or safety dataset of the sort that supports a marketing authorisation.

There is no head-to-head trial comparing the DAC and non-DAC variants in humans on body-composition, recovery, or any other functional endpoint. The two are used differently in research protocols, but the protocol-level reasoning is built on pharmacokinetic logic rather than on direct comparative evidence.

There is no published data on long-term human safety beyond the original phase I and II trials. Anything in the multi-year exposure window for either variant is outside the published record.

There is no UK marketing authorisation for either variant for any indication. The Medicines and Healthcare products Regulatory Agency (MHRA) has not assessed CJC-1295 for human therapeutic use.

There is no resolution of the optimum-variant question. Some research arguments favour DAC for sustained exposure. Others favour non-DAC for pulsatility. Neither has been validated in head-to-head clinical work.

There is no consensus on optimum dose, schedule, or duration in either variant. Retailer pages sometimes publish suggested research protocols. Those are not derived from clinical trials. Peer-reviewed literature is generally silent on dose recommendations outside the original Teichman dose-escalation work.

We do not publish dosing, mg/kg tables, schedules, or human-use protocols on this site. The encyclopedia framing is editorial commentary on what the literature shows, not a clinical or research instruction manual.

UK regulatory status

CJC-1295 in either variant has no marketing authorisation from the MHRA. It is not a licensed medicine in the UK. It is not available on prescription in the National Health Service. It does not appear in the British National Formulary.

UK retailers sell CJC-1295 under “research use only” framing. The “not for human or animal consumption” label on retailer pages is the legal positioning that allows the product to be supplied without a Marketing Authorisation. The MHRA’s enforcement focus has historically been on retailers that cross the line into making therapeutic claims, or that supply the peptide in a form (such as pre-filled pens) that implies human administration.

WADA, the World Anti-Doping Agency, lists CJC-1295 and its analogues under S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) of the Prohibited List. It is banned in and out of competition for athletes covered by the WADA code. UK Anti-Doping (UKAD) operates the same list. Any researcher who is also a competing athlete should consult the current UKAD Prohibited List before any protocol involving CJC-1295 or related GHRH analogues.

Customs and import treatment is worth flagging. The Border Force has discretion to seize shipments of unlicensed medicines into the UK. Retailers based outside the UK have been intercepted in the past. The UK-warehouse retailers listed below ship domestically, which sidesteps the import question.

The legal position can be summarised as follows: research-tier sale by UK retailers under research-use-only framing is currently tolerated by MHRA. Human use of the peptide is unsupported by any marketing authorisation, unsupervised by any prescriber, and outside the licensed-medicine regulatory framework.

Where UK researchers source CJC-1295

UK and UK-shipping research peptide retailers stock both the DAC and non-DAC variants. The market is small enough that most serious operators carry both. Below is a non-exhaustive list of the most commonly cited UK suppliers, with notes on the typical CoA tier and variant coverage. We are an editorial comparison site. Click-throughs fire affiliate codes where one is in place; the retailer price is unchanged.

my-peptides is a UK-warehoused supplier with established research-grade range. Both CJC-1295 DAC and non-DAC are usually stocked. HPLC purity claims at 99%+ with CoA supplied with order. Next-day UK delivery is the operational draw.

Pure Peptides UK is a long-established UK supplier with overlapping range. Both variants stocked. HPLC purity 99%+, CoA on request. Card and bank transfer payment.

Direct Sarms carries CJC-1295 in both DAC and non-DAC form alongside SARMs. HPLC verified, CoA on request. Card and crypto payment, useful where card processors have rejected research-peptide merchants.

Aquila Peptides is a smaller UK-EU operator with niche peptides and both CJC-1295 variants typically in stock. HPLC verified. Card and crypto payment.

Pinnacle Peptides and Nooku are also UK-shipping options that carry the standard GHRH-analogue range, though stock-keeping on the DAC variant specifically should be verified before ordering.

The CoA question matters more for CJC-1295 than for most peptides because DAC verification is a non-trivial analytical question. The DAC-modified molecule has a distinct molecular weight and HPLC retention profile compared to the unmodified GRF(1-29) backbone. A CoA that confirms only “CJC-1295” without specifying the DAC modification status leaves room for ambiguity. UK researchers buying the long-acting variant should look for explicit DAC confirmation on the CoA, ideally including a mass spectrometry result that resolves the molecular weight to within the expected range. This is the single most common quality-control issue in the CJC-1295 retail market.

Storage and reconstitution are also material. Both variants are typically supplied as lyophilised powder in 2 mg or 5 mg vials. Once reconstituted with bacteriostatic water, the DAC variant retains stability for considerably longer than the non-DAC backbone, but both should be refrigerated and used within standard research-peptide storage windows. The cold-chain question is the same as for other lyophilised GHRH analogues.

Common stacks and where CJC-1295 sits

CJC-1295 appears in two named UK research-peptide stacks more often than any others.

The first is the “GH Stack”, which pairs CJC-1295 (usually the DAC variant) with ipamorelin. The pairing rationale is mechanistic: CJC-1295 is a GHRH-receptor agonist, ipamorelin is a ghrelin-receptor agonist, and the two receptor families converge on the same pituitary somatotroph cell. Co-administration in animal models produces a larger GH response than either alone, because the synergistic receptor-cross-talk amplifies somatotroph output. This is the textbook GH-secretagogue pairing and is the basis of multiple decades of growth-axis research.

The second is the “Hulk Stack”, a retailer-branded bundle that varies between suppliers but most commonly contains CJC-1295 (often non-DAC), ipamorelin, and one or more of BPC-157 or TB-500. The Hulk-stack framing is built around recovery and tissue-repair positioning rather than pure GH-axis modulation. The CJC-1295 and ipamorelin components handle the GH-axis side; the BPC-157 and TB-500 components are positioned around the tissue-recovery angle.

Full editorial coverage of UK research-peptide stack composition is on the stacks directory. The ipamorelin pillar covers the ghrelin-receptor side of the pairing in more depth.

FAQ

What is the difference between CJC-1295 with DAC and CJC-1295 without DAC?

The DAC modification is a maleimidopropionic acid linker that allows the peptide to bind covalently to serum albumin once injected. This extends serum half-life from roughly 30 minutes (without DAC) to approximately one week (with DAC). The underlying GHRH-active sequence is the same; the difference is entirely pharmacokinetic. The DAC variant produces sustained GHRH-receptor activity over multiple days. The non-DAC variant produces short pulses that resemble the natural GHRH release pattern more closely.

Is CJC-1295 the same molecule as Tesamorelin?

No. Tesamorelin is a separate GHRH analogue with a trans-3-hexenoic acid modification at the N-terminus. It has a marketing authorisation in the United States as Egrifta for HIV-associated lipodystrophy and is licensed there as a prescription medicine, though not in the United Kingdom. Tesamorelin and CJC-1295 are both GHRH-receptor agonists but they sit at different regulatory tiers (Tesamorelin is a US-licensed medicine, CJC-1295 is unlicensed everywhere) and have very different pharmacokinetic profiles. See the tesamorelin pillar for more.

Is CJC-1295 the same molecule as Sermorelin?

No, but they are structurally related. Sermorelin is the unmodified first 29 residues of native human GHRH, with no protease-resistance substitutions and no DAC. CJC-1295 builds on the same 29-residue scaffold but adds four amino-acid substitutions and (optionally) the DAC linker. Sermorelin has a serum half-life of roughly 10 to 20 minutes; CJC-1295 without DAC runs about 30 minutes; CJC-1295 with DAC runs about a week. See the CJC-1295 vs Sermorelin comparison for more.

Why is CJC-1295 sold as a research peptide rather than a medicine?

Because no regulatory authority, including the MHRA, has granted it a marketing authorisation. Conjuchem developed the molecule through phase I and phase II clinical trials in the mid-2000s but did not reach phase III before the development programme was discontinued. With no licensed indication and no licensed manufacturer, the only route to market is the research-peptide channel, which operates under “research use only, not for human or animal consumption” framing.

What is “mod GRF (1-29)” and how is it different from CJC-1295?

“Modified GRF (1-29)” is the original research nomenclature for the tetra-substituted 29-residue backbone. It is the same molecule that retailers now commonly label “CJC-1295 without DAC”. The labels are interchangeable in practice. UK researchers should be aware that some retailers use one term, some use the other, and CoAs should be checked carefully if there is any doubt about which variant has been supplied.

Is CJC-1295 banned by WADA?

Yes. CJC-1295 and related GHRH analogues are listed under S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) of the WADA Prohibited List. The listing covers both DAC and non-DAC variants, and applies in and out of competition. Competing athletes covered by the WADA code, or UKAD-tested in the UK, should treat any protocol involving CJC-1295 as anti-doping-relevant.

Outstanding research questions

Several open questions remain in the CJC-1295 literature that UK research-tier readers should be aware of.

The optimum-variant question is unresolved. There is no published head-to-head trial comparing DAC and non-DAC variants on any functional endpoint in humans. Researchers choosing between the two are reasoning from pharmacokinetic principles rather than from comparative outcome data.

Long-term human safety is not characterised. The published phase I and II data extends to a small number of administrations over short windows. Multi-month and multi-year exposure data does not exist in the public record. The implications of sustained, supra-physiological IGF-1 elevation across years of repeated administration are not known.

The pulsatility preservation argument is partially evidence-based but contested. Ionescu and Frohman’s 2006 work suggests pituitary pulsatility persists under continuous GHRH-receptor stimulation. The widely repeated “non-DAC preserves pulsatility, DAC abolishes it” framing is more pharmacological intuition than published finding. Better head-to-head data would resolve this.

Cross-platform CoA verification standards are not consistent. Different retailers report HPLC purity in different ways, with different levels of mass-spectrometry confirmation, and with varying explicitness about DAC modification status. A standardised UK-retailer CoA framework would help, though no industry body currently operates one.

Interaction with prescription medicines is not characterised. CJC-1295 has not been studied alongside common UK prescriptions. Implications for hepatic enzyme activity, glycaemic control, or interaction with prescription growth-hormone therapy are not in the public record.

For UK researchers building protocols around CJC-1295, the practical baseline is: read the original Teichman and Ionescu/Frohman papers in full; verify CoA quality on every order with explicit attention to DAC modification status; use only UK-warehoused retailers to sidestep customs risk; and treat the peptide as a research-tier compound with no regulatory backing for human use.

This is an editorial pillar published for UK research-tier readers. PeptideClear is a comparison and information service. We do not sell, dispense, or prescribe. We do not publish dosing protocols, mg/kg tables, or human-use instructions. Research use only. Not for human or animal consumption.

Cross-reference: Sermorelin encyclopedia · Tesamorelin encyclopedia · Ipamorelin encyclopedia · UK research peptide retailers compared · Named UK peptide stacks · CJC-1295 vs Sermorelin · Research use only meaning · HPLC purity meaning · WADA prohibited list peptides.