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CJC-1295 DAC vs No DAC: The Naming Gets It Backwards

Research Guides SEP 2, 2026 10 MIN READ

Most content comparing “CJC-1295 DAC vs no DAC” gets the naming backwards before it gets to the chemistry. So the single most useful thing this post can do is fix the label before anything else.

In the published scientific literature, CJC-1295 IS the DAC-conjugated compound. “CJC-1295” and “CJC-1295 with DAC” are the same molecule. When a research paper says CJC-1295, it means the version carrying the Drug Affinity Complex. That is not a stylistic choice; it is what the name was coined to describe.

“CJC-1295 without DAC” is a research-chemical-market coinage. It is the name that grew up around the compound the literature calls Modified GRF(1-29). The market took the recognizable brand-style name, stripped off the part it did not have, and sold the result as “CJC-1295 no DAC.” Chemically the two things are related but distinct, and the naming convention has been quietly inverting reader expectations ever since.

Get that inversion straight and everything downstream makes sense: the half-life gap, the pulsatile-versus-sustained distinction, and the reason the no-DAC version, not the DAC version, became the standard partner for ipamorelin in research pairings.

Everything below describes published pharmacology. All compounds referenced are supplied for laboratory and research use only and are not for human consumption. Nothing here is dosing guidance, administration guidance, or safety guidance.

The short version

CJC-1295 (with DAC) CJC-1295 without DAC
Literature name CJC-1295 Modified GRF(1-29), also written mod GRF(1-29)
What the name means in papers The DAC-conjugated compound The market name for mod GRF(1-29)
Backbone Modified GRF(1-29) sequence Modified GRF(1-29) sequence
Added group Drug Affinity Complex at the C-terminus None
Albumin interaction Covalent bond to serum albumin None
Reported half-life in humans Approximately 5.8 to 8.1 days (Teichman et al., JCEM 2006) Approximately 30 minutes
Growth hormone signal shape Sustained elevation Preserved pulsatility
Common research partner Studied on its own for sustained-exposure designs Ipamorelin, in pulsatile-signal designs

Where the name came from

Native human growth hormone releasing hormone (GHRH) is a 44-amino-acid hypothalamic peptide, and its biological activity lives almost entirely in the first 29 residues. That 29-residue fragment, GRF(1-29), is the shared starting point for this whole family, including sermorelin, which is the unmodified fragment. The sermorelin vs ipamorelin comparison covers the unmodified end of the family in detail.

CJC-1295 was developed by ConjuChem as a way to make a GHRH analog last far longer in circulation than the raw fragment. The design had two parts. First, the backbone was stabilized with four amino acid substitutions to resist enzymatic breakdown. Second, a Drug Affinity Complex was attached so the stabilized peptide could bond to serum albumin and ride the bloodstream for days instead of minutes.

The DAC is the whole point of the name. CJC-1295 was the albumin-binding molecule. When vendors later began selling the stabilized backbone on its own, without the albumin-binding group, they needed a name buyers would recognize, so they called it “CJC-1295 without DAC.” The backbone alone already had a literature name: Modified GRF(1-29). That is why you will see the same vial described two completely different ways depending on whether the source is a chemistry database or a product page.

What the DAC actually is

DAC stands for Drug Affinity Complex. Structurally it is a maleimidopropionyl-lysine group added at the C-terminus of the peptide. Its job is to react with a specific cysteine residue on serum albumin, the most abundant protein in blood plasma.

The word “complex” undersells what happens. This is not reversible affinity binding, where a molecule drifts on and off its target. The maleimide group forms a covalent bond with albumin. Once attached, the peptide is chemically joined to a long-lived carrier protein, and it is protected from the enzymes and filtration that would otherwise clear a small peptide within minutes.

The pharmacokinetic result is dramatic. The foundational human characterization (Teichman and colleagues, published in the Journal of Clinical Endocrinology and Metabolism in 2006) reported a terminal half-life on the order of 5.8 to 8.1 days. A GHRH fragment that would normally survive minutes in plasma, once covalently tethered to albumin, persists for the better part of a week. That single engineering decision is the entire difference between the two compounds this post compares.

What Modified GRF(1-29) actually is

Modified GRF(1-29) is the same 29-residue GHRH fragment as sermorelin, carrying four amino acid substitutions relative to native GRF(1-29):

Position Substitution Purpose
2 D-Ala Blocks the dipeptidyl peptidase-4 (DPP-4) cleavage site, the main stability gain
8 Gln Addresses an asparagine deamidation liability
15 Ala Addresses a stability liability in the backbone
27 Leu Replaces a methionine prone to oxidation

The substitution at position 2 is the one that matters most. Native GRF(1-29) carries a DPP-4 cleavage site right at its N-terminus, and DPP-4 is the enzyme responsible for the fragment’s rapid clearance. Swapping in a D-alanine at position 2 blocks that cleavage. That is the headline stability gain. The other three substitutions clean up secondary chemical liabilities (deamidation at position 8, an oxidation-prone methionine at position 27, and a backbone stability issue at position 15), so the molecule holds up in storage and in solution.

The result is a GHRH analog that resists the enzyme that clears the unmodified fragment, but carries no albumin-binding group. Its reported half-life sits around 30 minutes. That is far longer than raw GRF(1-29), and far shorter than the DAC version. It occupies the useful middle: stable enough to act as a practical research tool, short enough to leave the natural rhythm of growth hormone signaling intact.

Pulsatile vs sustained: why the half-life gap changes the experiment

This is the part that actually matters for research design, and it is where “which one is better” stops being a meaningful question. The two compounds do not produce a stronger and a weaker version of the same signal. They produce two different signal shapes.

Growth hormone is released from the pituitary in pulses. The endogenous system fires bursts of GH separated by low-signal troughs, and a great deal of downstream biology is thought to depend on that pulsatile pattern rather than on total exposure alone. The troughs are not idle time; they are part of the signal.

A GHRH analog with a roughly 30-minute half-life, like Modified GRF(1-29), rises and clears fast enough that it can reinforce a pulse without erasing the trough that follows. Research designs interested in preserving the natural pulsatile pattern reach for the no-DAC version specifically because it does not flatten the rhythm.

The DAC version does the opposite. With a half-life measured in days, it holds the GHRH signal elevated continuously. The pituitary sits under sustained stimulation rather than intermittent bursts. That is a fundamentally different experimental condition, useful when the research question is about sustained-exposure effects rather than about the pulse pattern. Neither is a defect. They are two tools for two different questions.

So the honest framing of “CJC-1295 DAC vs no DAC” is not better versus worse. It is sustained signal versus pulsatile signal, chosen to match what a given study is trying to observe.

Why the no-DAC version became the standard ipamorelin partner

Search volume for “cjc-1295 ipamorelin” runs many times higher than for either compound alone, which tells you the pairing is what people are actually researching. And when researchers pair a GHRH analog with ipamorelin, it is almost always the no-DAC version, Modified GRF(1-29), that shows up in the combination.

There are two reasons, and both trace back to the pulsatile-versus-sustained distinction.

First, ipamorelin is itself a fast-acting, pulse-shaped input. It is a selective ghrelin receptor agonist that drives a burst of GH release and clears on a timescale of a couple of hours. Pairing it with a fast GHRH analog keeps both halves of the combination working on the same rhythm. Both inputs rise together, both clear, and the pulse structure is preserved. Bolt ipamorelin onto a compound with a multi-day half-life and you mismatch the timescales: one input is a burst, the other is a plateau.

Second, the two compounds act through different receptors, which is the whole reason combining them is interesting. Ipamorelin binds the growth hormone secretagogue receptor (GHS-R1a), the ghrelin receptor. A GHRH analog binds the GHRH receptor. Combination studies of a GHRH analog with a ghrelin receptor agonist consistently report a larger growth hormone response than either class produced alone in the same model, and the mechanism behind that outsized combined response has never been fully resolved in the literature. That non-redundancy is exactly why the pairing exists as a studied configuration rather than a marketing bundle.

Put those together and the standard research pairing is a fast GHRH analog plus a fast ghrelin mimetic, timescales matched, receptors distinct. That is why CJC-1295 no DAC with ipamorelin exists as a single pack rather than as two unrelated line items, and why CJC-1295 no DAC on its own is the GHRH-side compound most often requested for these designs.

What each version is examined for

Neither compound has an approved human indication in the form sold as a research chemical, and nothing below is a claim about outcomes.

CJC-1295 without DAC (Modified GRF(1-29)) appears in published research examining:

CJC-1295 with DAC appears in published research examining:

For a look at how the GHRH family diverges once you compare stabilized analogs against each other, the companion piece is tesamorelin vs sermorelin.

Practical differences when sourcing either version

For a lab or a reseller, the naming inversion has real consequences at the point of purchase, and a few other details are worth knowing.

Confirm what you are actually buying. Because “CJC-1295 no DAC” and “Modified GRF(1-29)” name the same thing, and “CJC-1295” alone can mean either the DAC version or be used loosely, the label on the vial is not always enough. The certificate of analysis, with the stated sequence and mass, is the document that tells you which molecule is in the pack. The two compounds have different molecular weights because one carries the DAC group and one does not.

Longer peptides carry a more demanding purity spec. Both versions are built on a 29-residue backbone, which has more synthesis steps and more opportunity for deletion sequences than a short peptide. The DAC version adds a conjugation step on top of that. This is exactly the situation where the purity number on the COA earns its keep.

Both are supplied as lyophilized powder in 10-vial packs. Storage is standard cold chain for lyophilized peptides. Solvent and handling parameters are documented in the published peptide chemistry literature and are the researcher’s call, not ours to specify.

Check the COA before you check the price. You can browse the COA library without an account. Every batch is supplied to a ≥99% purity specification. Send us a COA from any independent test and we’ll issue $300 store credit regardless of what it shows.

Common questions

Is CJC-1295 the same as CJC-1295 with DAC?

Yes. In the scientific literature, CJC-1295 refers to the DAC-conjugated compound. “CJC-1295” and “CJC-1295 with DAC” name the same molecule. The confusion comes from the market, where “CJC-1295 without DAC” was coined for a related but different compound, Modified GRF(1-29). If a source says CJC-1295 with no qualifier, it is most likely referring to the DAC version.

What is CJC-1295 without DAC, then?

It is the research-chemical-market name for Modified GRF(1-29): the same 29-residue GHRH fragment as sermorelin carrying four amino acid substitutions that improve resistance to enzymatic cleavage. It has no Drug Affinity Complex, no albumin binding, and a reported half-life of about 30 minutes rather than several days.

What does the DAC do to the half-life?

The Drug Affinity Complex is a maleimidopropionyl-lysine group that forms a covalent bond with serum albumin. That covalent tether protects the peptide from the enzymes and filtration that clear small peptides quickly. The reported human half-life goes from roughly 30 minutes for the no-DAC version to approximately 5.8 to 8.1 days for the DAC version (Teichman et al., JCEM 2006).

Why is CJC-1295 without DAC the version paired with ipamorelin?

Timescale matching and receptor separation. Ipamorelin is a fast, pulse-shaped ghrelin receptor agonist. Pairing it with a fast GHRH analog keeps both inputs on the same rhythm and preserves the pulsatile growth hormone pattern that much of the downstream biology is thought to depend on. The DAC version, with its multi-day half-life, produces a sustained plateau instead, which mismatches ipamorelin’s burst timescale. The two compounds also act through different receptors, which is why the combination is studied at all.

Does the DAC version produce a stronger effect than the no-DAC version?

That framing does not really hold. They produce different signal shapes rather than a stronger and a weaker version of one signal. The no-DAC version preserves pulsatile GH release; the DAC version drives sustained elevation. Which is more appropriate depends entirely on the research question being asked.

Where to source these compounds

We manufacture both the no-DAC compound and the ipamorelin pairing and ship direct, in 10-vial packs, with no retail packaging in between. That is why the vials arrive unlabeled and why the per-vial cost is what it is.

For the unmodified end of the GHRH family and why ipamorelin belongs to a separate receptor class, see sermorelin vs ipamorelin. For a comparison of stabilized GHRH analogs against each other, see tesamorelin vs sermorelin.

All products are supplied for laboratory and research use only. Not for human consumption, ingestion, injection, or therapeutic use.

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