CJC-1295 Research Guide: DAC and No-DAC Variants Explained

Last Updated: April 14, 2026

CJC-1295 is a synthetic growth hormone-releasing hormone (GHRH) analog developed by ConjuChem in the mid-2000s and widely used in preclinical research on the GH/IGF-1 axis. The molecule is built on the truncated GHRH(1-29) sequence — the minimal bioactive fragment of endogenous GHRH — with a series of amino acid substitutions that confer resistance to dipeptidyl peptidase IV (DPP-IV) cleavage, the enzyme responsible for rapidly inactivating native GHRH in circulation. CJC-1295 research encompasses two distinct variants that differ by a single structural feature: the presence or absence of a Drug Affinity Complex (DAC) maleimidopropionic acid linker. The DAC variant covalently binds circulating serum albumin, producing a plasma half-life of roughly 8 days, while the No DAC variant (often called Mod GRF 1-29 or CJC-1295 without DAC) retains the DPP-IV-resistant modifications but lacks the albumin-binding handle, giving it a half-life of approximately 30 minutes. This guide covers the mechanism, pharmacokinetics, reconstitution protocols, and study selection criteria for both variants.

What is CJC-1295 and what makes it distinct from native GHRH?

Native GHRH (1-44) is a hypothalamic peptide that binds the GHRH receptor on pituitary somatotrophs to drive growth hormone synthesis and release. Its bioactive core is GHRH(1-29), but the native peptide is cleaved rapidly at the Ala2-Asp3 bond by DPP-IV, giving it a plasma half-life of only 7-10 minutes. CJC-1295 is built on GHRH(1-29) with four amino acid substitutions: D-Ala at position 2 (DPP-IV resistance), Gln at 8, Ala at 15, and Leu at 27. These changes produce a stabilized GHRH analog with preserved receptor binding and several-fold greater plasma stability than native GHRH. In its No DAC form, CJC-1295 is essentially a cleaner, longer-lasting GHRH. In its DAC form, the addition of a maleimidopropionic acid linker at the C-terminus enables covalent conjugation to circulating serum albumin, dramatically extending half-life. Both variants are well-represented in CJC-1295 research.

How does the DAC modification extend half-life?

The Drug Affinity Complex (DAC) technology pioneered by ConjuChem uses a maleimidopropionic acid (MPA) moiety appended to a lysine residue at the C-terminus of CJC-1295. Maleimide groups react selectively and covalently with free thiol groups, and the most abundant free thiol in circulation is the Cys34 residue of serum albumin. Once injected in a research setting, CJC-1295-DAC rapidly forms a stable thioether bond with albumin, effectively “piggybacking” the GHRH analog onto the long plasma half-life of albumin itself (~19 days in humans, shorter in rodents). Published pharmacokinetic data from Teichman and colleagues (PubMed 16352685) reported a terminal half-life of approximately 8 days for CJC-1295-DAC in healthy volunteers, with sustained elevations in GH pulse amplitude and IGF-1 for up to 14 days following a single dose. This is the foundational clinical pharmacology paper for the DAC variant.

What is CJC-1295 No DAC (Mod GRF 1-29) and how does it differ?

CJC-1295 No DAC — also called Modified GRF (1-29) or Mod GRF 1-29 — is the same stabilized GHRH(1-29) backbone as the DAC variant but without the MPA albumin-binding linker. It retains the four amino acid substitutions (D-Ala2, Gln8, Ala15, Leu27) that confer DPP-IV resistance, giving it a plasma half-life of approximately 30 minutes — substantially longer than native GHRH but dramatically shorter than CJC-1295-DAC. In research protocols, this short half-life is a feature, not a bug: the pulsatile kinetics of No DAC more closely mimic endogenous GHRH release, preserving the natural pulsatility of the GH axis. Preclinical research indicates that pulsatile GH elevation may have distinct downstream effects on the IGF-1 system compared to continuously elevated GHRH tone. The No DAC variant is often the preferred choice for studies investigating pulsatile axis dynamics or short-acting combination protocols with GHRPs like ipamorelin.

How does CJC-1295 activate the GHRH receptor?

The GHRH receptor (GHRH-R) is a class B G-protein-coupled receptor expressed primarily on somatotroph cells of the anterior pituitary. When GHRH or an analog like CJC-1295 binds, the receptor couples to Gs, activates adenylyl cyclase, and elevates intracellular cAMP. This drives both the transcription of GH mRNA (upregulating GH synthesis) and the release of stored GH from secretory granules. Because CJC-1295 binds the same receptor as native GHRH with comparable affinity, published studies suggest it produces GH release through an identical signaling cascade — the differences between variants are pharmacokinetic, not pharmacodynamic. In combination research with a GHRP like ipamorelin (which acts on GHSR-1a), the two receptor pathways converge on increased GH secretion with additive-to-synergistic effects, well-characterized in the Bowers lab literature on GHRH/GHRP synergy.

What does the Teichman 2006 paper show for CJC-1295 research?

The Teichman and colleagues study (PubMed 16352685, published in J Clin Endocrinol Metab, 2006) characterized the pharmacokinetics and pharmacodynamics of CJC-1295-DAC in a randomized, double-blind, placebo-controlled study of healthy adults. Single subcutaneous doses of CJC-1295-DAC produced dose-dependent increases in mean GH concentrations (2-10 fold over baseline for 6+ days) and IGF-1 concentrations (1.5-3 fold over baseline for 9-11 days). The terminal half-life was approximately 5.8-8.1 days depending on dose. Importantly, GH pulse amplitude was preserved during sustained GHRH elevation, suggesting that CJC-1295-DAC amplifies endogenous pulsatile secretion rather than flattening it. For CJC-1295 research, Teichman 2006 remains the primary reference demonstrating that DAC-modified GHRH analogs can produce multi-day GH/IGF-1 elevation in a pharmacologically meaningful way.

When should researchers choose DAC vs No DAC?

The choice between CJC-1295 DAC and No DAC depends on the research question. Studies investigating sustained GH/IGF-1 axis elevation, chronic dosing convenience, or steady-state pharmacology typically use the DAC variant for its 8-day half-life — it enables once- or twice-weekly research protocols with sustained IGF-1 elevation. Studies investigating pulsatile axis dynamics, GHRP synergy (e.g., with ipamorelin), or short-duration receptor activation typically use the No DAC variant for its 30-minute half-life, which preserves natural pulsatility when combined with short-acting GHRPs. In combination research with a GHRP, No DAC is often preferred because sustained albumin-bound GHRH tone from DAC may partially desensitize the synergistic response over time. See our detailed CJC-1295 DAC vs No DAC comparison for a full decision framework.

What are the reconstitution protocols for each variant?

For laboratory research, CJC-1295 lyophilized powder is reconstituted with bacteriostatic water (0.9% benzyl alcohol) or sterile water for injection. For a 5 mg vial of CJC-1295 With DAC, a typical research reconstitution uses 2.5 mL of diluent, yielding a stock concentration of 2 mg/mL. For a 10 mg vial of CJC-1295 No DAC, a typical reconstitution uses 2 mL of diluent, yielding 5 mg/mL. Both variants should be stored lyophilized at -20°C or below in a desiccated, light-protected container; lyophilized material is generally stable for 24+ months under these conditions. Reconstituted CJC-1295 solutions should be refrigerated at 2-8°C. The DAC variant, once reconstituted, is generally stable for 30 days at refrigerated temperatures; the No DAC variant is typically used within 14-21 days of reconstitution for research stability, as the unmodified C-terminus is somewhat less stable in solution than the DAC-modified form.

What does the preclinical literature show about sustained GHRH elevation?

One of the central research questions around CJC-1295-DAC is whether sustained elevation of GHRH tone over days-to-weeks produces GH/IGF-1 responses qualitatively different from pulsatile GHRH stimulation. Published studies suggest that even under sustained DAC-bound GHRH elevation, the pituitary maintains pulsatile GH secretion — the amplitude and frequency of GH pulses are amplified, but the axis does not flatline into continuous GH release. This is an important finding for CJC-1295 research because it indicates the somatotroph retains its intrinsic pulsatility even under elevated stimulatory tone. Preclinical research indicates that IGF-1, being produced hepatically over hours-to-days in response to integrated GH exposure, rises in a sustained fashion with DAC variant administration, reaching a new plateau within 4-7 days of dosing. These kinetics are central to understanding when DAC is preferable to No DAC in research design: studies concerned with integrated exposure favor DAC, while studies concerned with peak-to-trough dynamics favor No DAC.

How does CJC-1295 interact with somatostatin tone?

The GHRH receptor signals through Gs/cAMP to promote GH release, but this signal is modulated at the pituitary level by somatostatin (SST), which acts through Gi/cAMP suppression on the same somatotroph cells. CJC-1295, as a pure GHRH analog, does not directly alter somatostatin tone — it simply provides stronger GHRH-side signaling. This is a key mechanistic distinction from GHRPs like ipamorelin, which reduce somatostatin tone at both the hypothalamus and pituitary. When CJC-1295 is used alone in research protocols, GH release is constrained by endogenous somatostatin pulses, giving the characteristic peak-and-trough pattern seen in many studies. When CJC-1295 is combined with a GHRP, the GHRP lifts the somatostatin brake while CJC-1295 presses the GHRH accelerator, producing the synergistic GH output that defines the combination literature. This interaction is why variant selection (DAC vs No DAC) interacts with combination partner choice in CJC-1295 research.

How does CJC-1295 compare to tesamorelin and sermorelin?

CJC-1295, tesamorelin, and sermorelin are all GHRH-based research compounds, but they differ in modifications and pharmacokinetics. Sermorelin is essentially unmodified GHRH(1-29) with a half-life of approximately 10-20 minutes — it is the shortest-acting of the three. Tesamorelin carries an N-terminal trans-3-hexenoyl modification that provides DPP-IV resistance and improved stability, with a half-life measured in hours. CJC-1295 No DAC has four internal amino acid substitutions producing similar DPP-IV resistance to tesamorelin with a ~30 minute half-life. CJC-1295 DAC extends this dramatically via albumin binding to ~8 days. In research selection, sermorelin offers minimal modification (closest to native GHRH), tesamorelin offers intermediate stability (and is the only GHRH analog with FDA approval for a specific indication), and CJC-1295 offers the most extended pharmacokinetic profile in the DAC form. See our longevity peptides guide for a broader comparison.

How is CJC-1295 purity verified for laboratory research?

Research-grade CJC-1295 (both variants) is produced by solid-phase peptide synthesis and characterized using RP-HPLC for purity assessment and mass spectrometry for identity confirmation. The DAC variant presents additional analytical considerations because of the maleimidopropionic acid (MPA) moiety at the C-terminus: mass spectrometry must confirm the expected mass of the full DAC-conjugated peptide, and purity profiling should detect any non-DAC-modified deletion sequences. High-quality research material for both variants is typically specified at greater than 98% purity by HPLC area percent. A Certificate of Analysis from a third-party analytical laboratory should document peptide content, water content, acetate content, and endotoxin levels where applicable. For CJC-1295 research reproducibility — particularly in studies comparing DAC and No DAC kinetics — working from well-characterized material is important because incomplete MPA conjugation or variable DAC content across lots could confound pharmacokinetic measurements.

How does CJC-1295 fit into longevity peptide research?

The GH/IGF-1 axis declines with age — a phenomenon termed somatopause — characterized by reduced GH pulse amplitude, reduced IGF-1, and associated shifts in body composition, bone density, and metabolic markers. CJC-1295 research in this context addresses two questions: can sustained GHRH elevation (DAC variant) restore axis function in aged preclinical models, and does pulsatile GHRH stimulation (No DAC variant, often combined with a GHRP) better approximate the youthful secretory pattern than sustained elevation? Published studies suggest both approaches can restore GH output in aged models, but may produce qualitatively different tissue effects downstream. The DAC variant’s once- or twice-weekly research dosing convenience makes it attractive for chronic longevity studies, while the No DAC variant’s pulsatile profile aligns with researchers who prioritize physiological mimicry over pharmacological convenience. For the broader research context on GH-axis peptides in aging research, see our longevity peptides guide.

What future CJC-1295 research directions are emerging?

Two decades after the DAC platform was developed, CJC-1295 research continues to expand in several directions. Combination pharmacology studies — particularly with selective GHRPs such as ipamorelin — remain a productive area for characterizing synergistic GH release kinetics and downstream IGF-1 responses. Pharmacokinetic optimization research examines whether even longer-acting GHRH analogs (via different albumin-binding chemistries or Fc-fusion approaches) can further extend dosing intervals without sacrificing pulsatility. Mechanistic studies using CJC-1295 No DAC as a probe for pulsatile versus continuous GHRH signaling help dissect which downstream effects depend on pulse pattern versus integrated exposure. Researchers should also be aware that CJC-1295 (without DAC) is well-characterized enough to serve as a benchmark GHRH analog in comparative studies of newer peptides. Primary literature and recent review articles remain the best source for current CJC-1295 research developments.

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Frequently Asked Questions

What is CJC-1295 research focused on?

CJC-1295 research investigates the pharmacology of stabilized GHRH analogs, including receptor activation kinetics, GH/IGF-1 axis modulation, pulsatile versus sustained GHRH signaling, and combination effects with GHRPs such as ipamorelin. The DAC and No DAC variants enable distinct research questions around long-acting versus pulsatile GHRH exposure.

What is the difference between CJC-1295 With DAC and CJC-1295 No DAC?

Both variants share the same DPP-IV-resistant GHRH(1-29) backbone. The DAC variant adds a maleimidopropionic acid linker that covalently binds serum albumin, extending half-life to approximately 8 days. The No DAC variant lacks this linker, resulting in a half-life of approximately 30 minutes and pulsatile kinetics. See our DAC vs No DAC guide for a full comparison.

What is Mod GRF 1-29 and is it the same as CJC-1295 No DAC?

Yes — Modified GRF (1-29), or Mod GRF 1-29, is the same molecule as CJC-1295 No DAC. Both names refer to the DPP-IV-resistant GHRH(1-29) analog without the albumin-binding DAC modification. The “CJC-1295 No DAC” naming became common through research vendors; the “Mod GRF 1-29” naming is older and more chemically descriptive.

Why is CJC-1295 often paired with ipamorelin in research protocols?

CJC-1295 (a GHRH analog) and ipamorelin (a GHRP) act on different receptors — GHRH-R and GHSR-1a respectively — and produce synergistic GH release when co-administered in preclinical models. The GHRH pathway amplifies GH synthesis and pulse amplitude while the GHRP pathway triggers release and suppresses somatostatin tone. Published studies suggest this dual activation yields greater GH area-under-the-curve than either pathway alone.

How long does CJC-1295 With DAC remain active after a single dose?

According to the Teichman 2006 pharmacokinetic study, a single dose of CJC-1295-DAC produces elevated GH concentrations for approximately 6-8 days and elevated IGF-1 concentrations for 9-14 days, depending on dose. The terminal half-life is approximately 5.8-8.1 days due to covalent albumin binding.

What is the half-life of CJC-1295 No DAC?

CJC-1295 No DAC has a plasma half-life of approximately 30 minutes in preclinical models — considerably longer than native GHRH (7-10 minutes) due to DPP-IV resistance, but far shorter than the DAC variant. This short half-life supports pulsatile research protocols and combination studies with short-acting GHRPs.

How are CJC-1295 variants reconstituted for research?

Both variants are reconstituted with bacteriostatic water or sterile water for injection under aseptic technique. A 5 mg DAC vial is typically reconstituted with 2.5 mL diluent (2 mg/mL); a 10 mg No DAC vial is typically reconstituted with 2 mL diluent (5 mg/mL). Lyophilized material is stored at -20°C; reconstituted solutions are refrigerated at 2-8°C and used within 14-30 days.

Is CJC-1295 approved for human use?

No. Neither CJC-1295 With DAC nor CJC-1295 No DAC has received marketing approval from the FDA, EMA, or any other major regulatory agency. Both variants remain investigational compounds supplied exclusively for laboratory and research purposes. Peptideware products are not for human or animal consumption.

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Research Disclaimer: All products are intended for laboratory and research purposes only. Not for human or animal consumption. These statements have not been evaluated by the FDA. Information presented is drawn from published preclinical literature and is provided for educational purposes to qualified researchers.