Free shipping over €250 — dispatched the next business day, tracked across the EU, with a lot-matched COA.

en

Comparisons

CJC-1295 With and Without DAC: Albumin Conjugation and Exposure Pattern in Research

One added lysine-maleimide turns a minutes-scale GHRH probe into a days-scale one. What that changes at the receptor, at the bench and on the certificate.

8 minute readWritten for laboratory purchasers and researchers

CJC-1295 with DAC and CJC-1295 without DAC are built on an identical 29-residue GHRH backbone. What separates them is one extra lysine bearing a maleimidopropionyl group, which forms a covalent link to serum albumin. That addition weighs 279.35 g/mol and lifts the molecule from 3367.93 to 3647.28 g/mol, turning a probe that acts over minutes into one that acts over days. Choosing between CJC-1295 no DAC and CJC-1295 DAC therefore means choosing between pulsatile GHRH receptor signalling and continuous receptor occupancy, which are distinct experimental questions.

Each is supplied as lyophilized powder in 2, 5 and 10 mg vials with a lot-matched HPLC certificate: CJC-1295 (No DAC / Mod GRF 1-29) and CJC-1295 with DAC, both within GHRH analogs. Both are research chemicals for in-vitro and preclinical laboratory work only.

Clearing up the naming confusion first

These two names are applied inconsistently across the research-peptide market, and ordering the wrong one is a frequent and costly error. Published research uses "CJC-1295" for the DAC-bearing compound, since the drug affinity complex is what gave the molecule its name. Suppliers, by contrast, often use "CJC-1295" for the version lacking DAC, which is properly called Modified GRF 1-29. That is why we label both versions explicitly, and why any protocol referencing a published CJC-1295 study should establish which molecule that study actually used before matching material to it.

The common backbone and its four substitutions

Both compounds start from GHRH(1-29), the N-terminal fragment that decades of endocrine research have shown carries virtually all the receptor-binding information of the 44-residue hormone. Four residues are exchanged, at positions 2, 8, 15 and 27, each targeting a particular degradation pathway: cleavage by dipeptidyl peptidase-4 at the N-terminus, deamidation of asparagine and oxidation of methionine. The outcome is a peptide that withstands handling and circulation far better than native GHRH(1-29) while acting at the same receptor. Both molecules carry all four changes, and neither differs from the other in receptor identity or in how it engages that receptor.

The chemistry of the DAC

The drug affinity complex is a maleimidopropionyl group carried on an added lysine at position 30. Maleimide undergoes rapid, selective Michael addition with free thiols, and human serum albumin offers one unusually accessible free cysteine at position 34. The product is a covalent peptide-albumin conjugate: a permanent bond, unlike the reversible fatty-acid association used in incretin analogues. Albumin's bulk and long circulating lifetime then protect the peptide from renal filtration and peptidase cleavage, which is why reported persistence shifts from minutes to days.

Two practical consequences follow, and both bite harder at the bench than users tend to expect.

The first is that maleimide reacts with any available thiol, not just albumin's. If the DAC version is reconstituted in buffer containing dithiothreitol, beta-mercaptoethanol, free cysteine or glutathione, the reactive group is consumed before albumin is ever encountered. The peptide is still there and still binds the receptor, but its pharmacokinetics become those of the non-DAC version, a failure that yields a believable result and no warning at all.

The second is hydrolysis. In water, and progressively faster above neutral pH, the maleimide ring opens into a maleamic acid that no longer reacts with thiols. A DAC stock left in mildly alkaline buffer steadily loses its ability to conjugate, again with nothing visible to show for it. Making DAC solutions fresh, holding the pH at or just below neutral and using them without delay is the practical defence.

Pulsatile against continuous: the real experimental distinction

GHRH is naturally secreted in pulses, and the somatotroph response depends on that pattern, not just on cumulative exposure. These two compounds let a laboratory control that variable directly.

The non-DAC form clears quickly, giving a defined exposure window that approximates a single pulse. That suits acute signalling studies, on/off designs in which a long tail would contaminate subsequent arms, and structure-activity comparisons against native GRF 1-29 and sermorelin; our CJC-1295 vs sermorelin article deals with that pairing.

The DAC form maintains receptor occupancy, which represents a different pharmacological state rather than simply more of the same. Continuous agonist exposure at a G-protein-coupled receptor typically triggers desensitisation, internalisation and downstream adaptation, and studying those requires exposure that lasts. It is also the pragmatic option for lengthy rodent protocols where frequent handling would itself become a confounder.

This matters because the two formats can give apparently opposite results on one endpoint while both are valid. A sustained-exposure arm whose response fades over time does not contradict a pulsatile arm with a strong acute response; it is capturing the adaptation that the pulsatile design was built to exclude.

Matching the version to the question

Pick the no-DAC version for acute, pulsatile designs

Cell-based receptor pharmacology, acute signalling time-courses, washout protocols and any comparison with native or shorter GHRH analogues all point to the short-acting molecule. It is also easier to handle, with no thiol-reactive chemistry needing protection.

Pick the DAC version for sustained-occupancy designs

Desensitisation, receptor downregulation, downstream IGF-1 adaptation and multi-week animal studies all favour the conjugated form. The price is more demanding handling and a narrower range of compatible buffers.

Either version can be paired with a secretagogue

GHRH analogues and ghrelin-receptor secretagogues target separate receptors, which is why they are so frequently studied in combination. We supply co-formulated CJC-1295 with ipamorelin and CJC-1295 DAC with ipamorelin vials for such designs, plus ipamorelin on its own for single-component arms where attribution matters. Our survey of the secretagogue landscape charts the family.

Differences in handling, reconstitution and storage

The non-DAC version follows ordinary peptide practice: keep the sealed lyophilized vial frozen, let it reach room temperature before piercing the stopper so moisture cannot condense on cold powder, run the diluent down the vial wall, dissolve without shaking and aliquot so the stock is not frozen and thawed repeatedly. See our reconstitution guide and storage guide.

For the DAC version, add three rules. Use no diluent or buffer containing free thiols, since they destroy the maleimide. Hold the pH at or slightly below neutral and avoid prolonged storage in solution, because maleimide hydrolysis is base-catalysed and irreversible. Make working solutions shortly before use rather than storing them, and stick to single-use aliquots even more strictly than usual, since every thaw prolongs the aqueous exposure that drives hydrolysis.

Concentration is a lab calculation, not a usage recommendation: 5 mg reconstituted in 2 mL of diluent gives 2.5 mg/mL, that is 2,500 mcg/mL, so 0.1 mL holds 250 mcg. Since the two molecules differ in mass by 279.35 g/mol, roughly 8 percent, identical mass concentrations are not identical molarities, and any side-by-side receptor pharmacology comparison should be set up on a molar basis.

Purity, identity and certificate checks

Ask for the lot-matched certificate for every vial and verify HPLC purity with the chromatogram visible, a mass spectrometry value matching the expected figure (3367.93 g/mol without DAC, 3647.28 g/mol with it) and a lot number that matches the vial. The mass check decides the matter here, because both products share a CAS number and differ by a single modification; a certificate showing a mass consistent with the plain backbone on a vial labelled DAC is a contradiction to settle before use. For the DAC version, ask specifically whether the certificate reflects intact maleimide, since hydrolysed material has the same sequence, a mass 18 Da higher, and none of the conjugating behaviour that makes the product what it is. Our COA guide sets out what a complete document includes.

Regulatory framing

Both compounds are sold as research chemicals for laboratory use only. Neither holds a marketing authorisation as a medicine in the EU or the United States, and the published record for both remains preclinical and investigational. For wider context on this family of research tools, see our growth and performance research overview.

Questions

What does the DAC in CJC-1295 stand for?

Drug affinity complex: a maleimidopropionyl group carried on an extra lysine at position 30. The maleimide reacts with the lone free cysteine at position 34 of serum albumin, creating a covalent peptide-albumin conjugate that protects the peptide from renal clearance and from peptidases.

Is it the same molecule with and without DAC?

They use the same tetrasubstituted GHRH(1-29) backbone and the same receptor, but they are chemically different compounds. The DAC version adds a lysine and linker weighing 279.35 g/mol, raising the mass from 3367.93 to 3647.28 g/mol. Both share a CAS number, so the mass on the certificate is the dependable identifier.

Why are the names so easily confused?

Published papers use CJC-1295 for the DAC-bearing molecule, after which it was named, while vendors often apply the same name to the version without DAC, correctly called Modified GRF 1-29. Any protocol built on a published study should verify which of the two that study used.

Can the DAC version be reconstituted in DTT-containing buffer?

No. Maleimide reacts with any free thiol it can reach, so dithiothreitol, beta-mercaptoethanol, free cysteine or glutathione will use up the reactive group before it encounters albumin. The peptide still binds the receptor but loses the extended exposure that defines it, and the solution looks perfectly normal.

Does the maleimide group break down in solution?

It does. Maleimide hydrolyses into a maleamic acid that no longer reacts with thiols, and because the reaction is base-catalysed it speeds up above neutral pH. The hydrolysed form keeps the same sequence and weighs 18 Da more. Prepare solutions fresh, keep the pH at or just below neutral and use them quickly.

Which version suits receptor desensitisation studies?

The DAC version. Desensitisation, internalisation and downstream adaptation all need sustained receptor occupancy, which covalent albumin conjugation provides. The non-DAC version is cleared within minutes and is built for the opposite purpose: acute, pulsatile signalling.

Can the two versions give contradictory results on one endpoint?

They can appear to, without either being incorrect. A sustained-exposure arm whose response weakens over time is measuring receptor adaptation, precisely what a pulsatile design sets out to avoid. Reading the two together means treating exposure pattern as a variable rather than an annoyance.