CJC-1295 (No DAC): What the Research Shows

Educational Notice

This article is written for researchers, clinicians, and informed adults seeking to understand the scientific literature on CJC-1295 (without DAC). It is not medical advice, a treatment recommendation, or an endorsement of any specific use. CJC-1295 (no DAC) is not approved by the FDA for any indication and is prohibited in competitive sport under WADA regulations. Consult a qualified healthcare professional before making any health or treatment decisions.

CJC-1295 without DAC—also called Modified GRF(1-29) or Mod GRF—is a synthetic 29-amino acid analog of human growth hormone-releasing hormone (GHRH) engineered to resist the plasma enzyme dipeptidyl peptidase IV (DPP-IV) that rapidly degrades endogenous GHRH. The result is a compound with a half-life of approximately 30 minutes: long enough to produce a meaningful GH pulse at the pituitary, short enough to maintain the pulsatile GH secretion pattern that natural physiology employs. It is not the longest-acting GHRH analog, it is not the one with the most human trial data, and it is not the only option in its class. What it is, in the context of community protocols, is the GHRH agonist that best preserves the physiological GH pulse architecture while providing a sufficiently extended active window to be practically useful.

Understanding CJC-1295 without DAC requires first confronting a naming problem that has confused this space for years. “CJC-1295” refers, depending on the supplier, to either the no-DAC form (this article) or to a completely different compound—CJC-1295 with DAC—that uses a Drug Affinity Complex to bind albumin and produce continuous GH elevation for up to 14 days from a single injection. Same name prefix. Same receptor target. Half-lives that differ by a factor of approximately 300. The distinction is pharmacologically fundamental and this article addresses it directly before covering anything else.

The pharmacological case for CJC-1295 (no DAC) as a combination partner with ipamorelin is the strongest in the GH Secretagogues cluster. CJC-1295 (no DAC) acts via the GHRH receptor (GHRHR) using a cAMP/PKA intracellular pathway. Ipamorelin acts via GHS-R1a using an IP3/calcium pathway. The two pathways are independent and both converge on pituitary GH exocytosis. Co-administering both compounds activates two complementary signals simultaneously, producing a GH pulse that is greater than either compound alone. The kinetics match—both have half-lives in the 30-minute range, producing synchronized pulses. This is the pharmacological rationale that the community has been acting on for over a decade, and it is sound. It is not proven in a human RCT. Sound pharmacological rationale and clinical proof are different standards.

The research moves fast. We read all of it so you don’t have to.

New compound reviews, evidence updates, and protocol analysis — sourced, cited, and written for people who actually read the studies.

Subscribe to Peptidings Weekly

Quick Facts

Type Synthetic GHRH analog; 29-amino acid fragment of human GHRH with stabilizing modifications
Also known as Modified GRF(1-29); Mod GRF 1-29; CJC-1295 no DAC; sermorelin analog
Molecular weight ~3367 Da
Target receptor GHRHR (growth hormone-releasing hormone receptor)
Mechanism GHRHR agonist → pulsatile pituitary GH release; DPP-IV resistant modifications extend active half-life
Plasma half-life ~30 minutes (subcutaneous injection)
GH profile Pulsatile — discrete GH pulses, closely mimicking natural GHRH physiology
Route of administration Subcutaneous injection (research use)
Developer ConjuChem Biotechnologies (Canada); later modified by research community
FDA status Category 3 — not approved for any indication
WADA status Prohibited — S2 (Peptide Hormones, Growth Factors, and Related Substances)
Evidence tier Preclinical / Limited Phase I — class pharmacology well-established; compound-specific human data limited
Critical distinction Not equivalent to CJC-1295 with DAC — half-lives differ by a factor of ~300; completely different physiological GH profiles

What Is CJC-1295 (No DAC)?

CJC-1295 without DAC is a 29-amino acid peptide corresponding to the biologically active N-terminal fragment of human GHRH, modified at four positions to resist DPP-IV cleavage: Ala8, Gln15, Ala19, and Ala26 substitutions replace the amino acids that DPP-IV preferentially cleaves in the native sequence. These substitutions extend the compound’s functional half-life from the less-than-10-minute window of endogenous GHRH to approximately 30 minutes—sufficient to produce a GH pulse of meaningful magnitude at the pituitary without creating the extended continuous stimulation that would result from albumin binding.

Plain English

The body normally destroys GHRH in under 10 minutes. CJC-1295 (no DAC) swaps in four modified amino acids at the exact spots where the destroying enzyme cuts, extending its working life to about 30 minutes—long enough to trigger a real GH pulse, short enough to clear before the next one.

The compound acts as a full agonist at the GHRHR expressed on pituitary somatotroph cells. GHRHR activation stimulates Gs protein coupling, adenylyl cyclase, cAMP accumulation, and PKA activation, which phosphorylates targets driving GH exocytosis from secretory granules. This is the same signaling pathway used by endogenous GHRH, by sermorelin, and by tesamorelin. CJC-1295 (no DAC) differs from these primarily in its structural modifications for DPP-IV resistance and in its half-life, not in its fundamental receptor pharmacology.

Plain English

Once CJC-1295 (no DAC) binds its receptor on pituitary cells, it triggers a chain reaction—protein switch → enzyme activation → calcium influx—that forces stored growth hormone out of the cell. Same pathway your body’s own GHRH uses.

The 29-amino acid sequence is the same length as sermorelin. The full 44-amino acid GHRH sequence is not required for GHRHR binding and activation—the N-terminal 29 residues carry all the information needed for full agonist activity at the receptor. The additional modifications for DPP-IV resistance give CJC-1295 (no DAC) a modestly longer half-life than sermorelin (~30 minutes vs. ~10–20 minutes), translating to a somewhat more sustained GH pulse per injection.

The Critical Distinction: CJC-1295 with DAC vs. without DAC

This section exists because the naming confusion between CJC-1295 with DAC and CJC-1295 without DAC is not a minor terminology issue. It is a pharmacologically consequential confusion that leads users to believe they are running equivalent protocols when they are not. The two compounds share a receptor target and a name prefix. Everything else that matters pharmacologically is different.

Property CJC-1295 Without DAC (Mod GRF) CJC-1295 With DAC
Also called Modified GRF(1-29); Mod GRF DAC:GRF; often just “CJC-1295”
Modification D-amino acids + Ala8, Gln15, Ala19, Ala26 substitutions for DPP-IV resistance Same peptide core + maleimidopropionic acid (DAC) for albumin binding
Half-life ~30 minutes ~6–8 days (terminal); active ~14 days
GH profile Discrete physiological pulses Continuous sustained elevation
Injection frequency 1–3× per day (per protocol) Once weekly or less
Combination with ipamorelin Strong rationale — matching pulsatile kinetics, complementary receptor pathways Weaker rationale — kinetic mismatch; pulsatile + continuous baseline
Axis physiology preservation High — pulses followed by troughs preserve natural pulsatility rhythm Lower — continuous stimulation overrides natural pulsatility
Human evidence Limited Phase I class data Phase I/II (Teichman 2006 RCT)
Naming confusion risk Often incorrectly labeled as “CJC-1295 with DAC” by suppliers Often sold as just “CJC-1295,” obscuring DAC modification

Supply Chain Warning

Many research chemical suppliers label CJC-1295 with DAC simply as “CJC-1295” and CJC-1295 without DAC as “Mod GRF” or “Modified GRF(1-29).” Some list both under the same name with different vial sizes. Before using any product in this space, verify which compound you have by checking the documented half-life: ~30 minutes = no DAC; ~14 days = with DAC. If a supplier cannot tell you which form they carry, do not purchase.

The combination rationale with ipamorelin—the most commonly cited reason for using CJC-1295 (no DAC) in community protocols—depends specifically on the no-DAC form. The rationale is: both compounds produce discrete GH pulses via complementary receptor pathways, and the GH response to dual-pathway stimulation exceeds either compound alone. This logic requires both compounds to be operating in the same pulsatile mode. CJC-1295 with DAC operates in sustained-elevation mode. The dual-pathway synergy rationale does not cleanly transfer to a combination of ipamorelin (pulsatile, ~2 hr) with CJC-1295 with DAC (sustained, ~14 days). A dedicated article covering CJC-1295 with DAC is at peptidings.com/peptides/cjc-1295-dac/.

Origins and Development

ConjuChem Biotechnologies, a Canadian biopharmaceutical company, developed the CJC peptide series as part of a broader program using their Drug Affinity Complex (DAC) technology to extend peptide half-lives. CJC-1295 without DAC emerged from the same program as the DAC form—it represents the base peptide (Modified GRF 1-29 with DPP-IV-resistant substitutions) before the DAC moiety is attached. In ConjuChem’s development timeline, the no-DAC form was a characterization step rather than the ultimate clinical candidate; the DAC form was the compound ConjuChem advanced into clinical trials.

The research community, working with pharmacological literature on GHRH analogs and the published GHRH + GHRP synergy data, adopted the no-DAC form for protocols emphasizing pulsatile GH stimulation. The compound became widely available through research chemical suppliers under the name Modified GRF(1-29) or Mod GRF, and less accurately under the name CJC-1295, creating the naming ambiguity that persists today.

The GHRH receptor pharmacology underlying CJC-1295 (no DAC)’s mechanism was established before the compound itself—decades of research on endogenous GHRH and on earlier GHRH analogs like sermorelin characterized the receptor signaling pathway in detail. The compound’s pharmacological behavior is predictable from first principles given the well-characterized GHRHR biology.

Mechanism of Action

Pituitary GHRHR Activation

CJC-1295 (no DAC) binds the GHRHR on pituitary somatotroph cells. GHRHR is a class B GPCR (G protein-coupled receptor) that couples to Gs protein upon ligand binding. Gs activates adenylyl cyclase, increasing intracellular cAMP. Elevated cAMP activates protein kinase A (PKA), which phosphorylates multiple downstream targets including voltage-gated calcium channels. Calcium influx, combined with direct PKA-mediated effects on the secretory machinery, drives exocytosis of GH-containing secretory granules. The result is a discrete GH pulse entering systemic circulation within minutes of injection.

Plain English

CJC-1295 (no DAC) lands on pituitary cells and flips a molecular switch that opens calcium gates, causing those cells to release a burst of growth hormone into the bloodstream within minutes.

The Somatostatin Brake

A critical feature of GHRHR-mediated GH release is that somatostatin feedback remains fully operative. Somatostatin, released by hypothalamic neurons, is the primary inhibitory regulator of GH secretion. As the GH pulse from CJC-1295 (no DAC) elevates circulating GH and subsequently IGF-1, hypothalamic somatostatin release increases, suppressing further GH secretion. This means the compound cannot produce pathologically high GH levels—the pituitary’s own regulatory architecture imposes a ceiling. This is the mechanistic basis for the clinical preference for GHRHR agonists over direct GH injection in populations where GH excess risk is a concern.

Plain English

Your brain has a built-in safety brake: as GH rises, another hormone (somatostatin) kicks in to shut down further release. This means CJC-1295 (no DAC) cannot push GH to dangerous levels—the pituitary has a ceiling.

Synergy with GHS-R1a Agonists

The intracellular signaling cascade at GHRHR (Gs → cAMP → PKA) is distinct from the cascade at GHS-R1a (Gq → PLC → IP3 → Ca²⁺). Both pathways converge on the same effector—GH exocytosis from somatotroph granules—but through independent intracellular routes. This independence means co-administering a GHRHR agonist (CJC-1295 no DAC) with a GHS-R1a agonist (ipamorelin) activates two complementary amplification cascades simultaneously. The pharmacological literature consistently shows that GHRH + GHRP co-administration produces larger GH responses than either alone. This is the mechanistic foundation for the most commonly used community protocol in the GH Secretagogues cluster.

Plain English

CJC-1295 (no DAC) and ipamorelin trigger growth hormone release through two completely independent signaling routes inside the same pituitary cell—so combining them produces a bigger GH pulse than either one alone.

Why the No-DAC Form Specifically?

The synergy rationale requires complementary kinetics. CJC-1295 (no DAC) has a half-life of ~30 minutes and produces a GH pulse in the same timeframe as ipamorelin (~2 hours). When co-injected, both compounds are active simultaneously and produce synchronized dual-pathway GH pulses. CJC-1295 with DAC’s 14-day continuous GH elevation does not provide this synchronized pulsatile match. The pharmacological argument for the no-DAC form in this combination is the matching kinetics—not simply the GHRHR receptor target.

Hypothalamic Effects

GHRHR is expressed not only in the pituitary but also in the hypothalamus. GHRH analog binding at hypothalamic receptors may modulate local signaling, including effects on somatostatin neuron activity. Whether CJC-1295 (no DAC)’s 30-minute half-life is sufficient to produce meaningful hypothalamic effects beyond the pituitary is not definitively characterized. The primary mechanism of action is pituitary GHRHR activation.

Key Research Areas and Studies

CJC-1295 (no DAC)’s human evidence base is thin as a compound-specific data set. The GHRHR pathway it activates is extensively characterized—this is well-established pharmacology with decades of mechanistic research and clinical data from endogenous GHRH and GHRH analogs including sermorelin. Compound-specific Phase I human pharmacokinetic and pharmacodynamic data for CJC-1295 (no DAC) itself was not published in the peer-reviewed record. The most directly applicable published human data is from the CJC-1295 with DAC Phase I/II program (Teichman 2006) and from sermorelin clinical trials.

GHRH Class Evidence

The mechanistic framework for CJC-1295 (no DAC) is established through decades of GHRH receptor pharmacology research. Frohman and Jansson (1986) characterized the GHRHR signaling pathway in detail. Corpas et al. (1992) and Walker et al. (1994) demonstrated GH stimulation, IGF-1 elevation, and body composition effects with sermorelin (structurally and mechanistically similar) in older adult populations. These studies provide class-level human evidence that the GHRHR pathway, when pharmacologically activated, produces the GH-dependent downstream effects attributed to CJC-1295 (no DAC).

GHRH + GHRP Combination Synergy

Bowers and colleagues documented GHRH + GHRP combination synergy in multiple in vitro and in vivo studies. The mechanistic explanation—independent intracellular pathways converging on GH exocytosis—has been confirmed repeatedly. This is the most directly relevant research for the primary community use case (CJC-1295 no DAC + ipamorelin) and represents the strongest line of evidence in the compound’s favor.

Why the Research Table Is Short

CJC-1295 (no DAC)’s evidence table is short because compound-specific human clinical data was not published. The class pharmacology is well-established. The compound-specific human data is not. This is an honest gap in the record, not an editorial omission. A community of users has been working with this compound for years based on class pharmacology and combination pharmacology reasoning—that reasoning is sound, but it is reasoning, not clinical trial results.

Common Claims versus Current Evidence

Claim Evidence Verdict
CJC-1295 (no DAC) stimulates GH release GHRHR agonism producing pulsatile GH release is established pharmacology. CJC-1295 (no DAC) acts on the same receptor as endogenous GHRH via the same cAMP/PKA pathway. Compound-specific Phase I human data is limited; class pharmacology provides strong mechanistic support. Supported by Class Pharmacology
CJC-1295 (no DAC) improves body composition No human RCT data for body composition endpoints. Derives from the known anabolic effects of GH and IGF-1. The compound produces GH pulses; whether those pulses are of sufficient magnitude and duration in healthy adults to produce meaningful body composition change is unstudied. Preclinical / Mechanistic Only
CJC-1295 (no DAC) + ipamorelin is synergistic The dual-pathway GHRHR + GHS-R1a rationale is established pharmacology. Complementary intracellular cascades (cAMP via GHRHR; IP3/calcium via GHS-R1a) converge on pituitary GH exocytosis. The GH response to combined GHRH + GHRP stimulation exceeds either alone in pharmacological studies. Human PK/PD data for this specific pairing is limited. Mechanistically Sound
CJC-1295 (no DAC) mimics natural GH release The ~30-minute half-life and pulsatile GH output are the closest to natural GHRH physiology of any synthetic secretagogue in common use. This is a real and meaningful advantage over sustained-elevation compounds. Supported
CJC-1295 (no DAC) is interchangeable with CJC-1295 with DAC This is the most dangerous mischaracterization of the compound. The two share a name prefix and a receptor target. They have half-lives differing by a factor of ~300 and produce completely different physiological GH profiles. They are not interchangeable. False
CJC-1295 (no DAC) improves sleep quality No direct human sleep data. The GHRH–slow-wave sleep relationship is documented for endogenous GHRH and for sermorelin. Pre-sleep timing rationale is mechanistically supported. Compound-specific sleep trial data does not exist. Mechanistically Plausible—Unstudied

The research moves fast. We read all of it so you don’t have to.

New compound reviews, evidence updates, and protocol analysis — sourced, cited, and written for people who actually read the studies.

Subscribe to Peptidings Weekly

The Human Evidence Landscape

CJC-1295 (no DAC) has no published peer-reviewed Phase I pharmacokinetic study of its own. The half-life (~30 minutes) cited throughout this article and the broader literature is derived from inference based on the DPP-IV-resistant modifications and from the compound’s behavior in the context of published GHRH analog pharmacology—not from a published human PK study for this specific compound. The Class pharmacology is solid. The compound-specific human characterization is not.

This gap matters in a specific way: it means that dose recommendations circulating in the community—typically 100–300 mcg per injection—are not derived from a dose-finding study for CJC-1295 (no DAC) itself. They derive from extrapolation from sermorelin dosing, from the published CJC-1295 with DAC dose ranges adjusted for relative potency, and from accumulated community experimentation. These are reasonable starting points. They are not validated doses.

The combination pharmacology rationale—CJC-1295 (no DAC) + ipamorelin—is the most scientifically supported aspect of the compound’s use, because the GHRH + GHRP synergy is documented in the pharmacological literature. But even here, the specific combination of this compound with ipamorelin in this dose range via this route in human subjects has not been studied. The mechanism is right. The effect is plausible. The clinical validation is absent.

The Evidence Floor

CJC-1295 (no DAC) has a solid mechanistic foundation and sound combination pharmacology rationale. It does not have human clinical trial evidence for any specific endpoint—body composition, sleep, recovery, bone density, or performance. The community has been using this compound based on pharmacological reasoning for over a decade without generating controlled data. Pharmacological reasoning is a starting point, not an endpoint.

Safety, Risks, and Limitations

Acute Tolerability

Community experience and class pharmacology suggest CJC-1295 (no DAC) is acutely well-tolerated at research doses. The most commonly reported acute effects: mild flushing and tingling within 30–60 minutes of injection (attributed to the GH pulse), occasional headache. These are class effects seen with all effective GHRH analogs and are self-limiting.

Water Retention

GH elevation—including pulsatile GH elevation from GHRHR agonists—promotes sodium and water retention via renal tubular effects. The magnitude with CJC-1295 (no DAC) is expected to be smaller than with sustained-elevation compounds (MK-677, CJC-1295 with DAC) due to the pulsatile rather than continuous GH profile. Water retention is typically dose-dependent and resolves on discontinuation.

Axis Suppression

Chronic GHRHR agonism may suppress endogenous GHRH release via negative feedback, and IGF-1 elevation from repeated GH pulses provides hypothalamic and pituitary feedback that reduces endogenous GH pulse amplitude. The pulsatile profile of CJC-1295 (no DAC) is expected to produce less axis disruption than continuous-elevation compounds, since troughs between pulses allow partial axis reset. Whether this theoretical advantage translates to meaningfully better axis preservation in practice has not been studied in humans.

Long-Term Safety Profile

No long-term human safety data exists specifically for CJC-1295 (no DAC). The class safety profile from sermorelin clinical use (decades of clinical practice) is generally favorable. The concerns about sustained IGF-1 elevation and cancer risk that apply to continuous-elevation compounds apply in attenuated form to pulsatile protocols, but have not been quantified.

Supply Chain Quality

Research-grade CJC-1295 (no DAC) is not subject to pharmaceutical manufacturing standards. Purity, potency, and sterility vary by supplier. The naming confusion in this space (DAC vs. no DAC) means a user may receive a different compound than intended. Supplier verification and independent third-party testing are the only available mitigations for a buyer operating outside the pharmaceutical supply chain.

FDA Status

CJC-1295 (no DAC) is FDA Category 3: not approved for any indication, not under active clinical investigation. It is classified as a research chemical. It is not available through compounding pharmacies as an approved formulation; any compounded GHRH analog prescriptions are typically for sermorelin.

WADA Prohibition

CJC-1295 (no DAC) is prohibited under WADA S2: Peptide Hormones, Growth Factors, and Related Substances—both in-competition and out-of-competition. The GHRH analog class is covered by class prohibition. Athletes subject to anti-doping testing must treat this as a hard prohibition regardless of whether the specific compound name appears on the prohibited list.

Research Protocols and Laboratory Practices

CJC-1295 (no DAC) is supplied as lyophilized powder reconstituted with bacteriostatic water. Standard storage: lyophilized at 2–8°C (35–46°F), protected from light; reconstituted solution refrigerated and used within 28 days. Do not freeze reconstituted solution. The 30-minute half-life means injection timing has direct pharmacological relevance—the compound’s active window is specific, unlike the 14-day window of the DAC form.

Reconstitution vs. Dosing Syringes

Use one syringe to add bacteriostatic water to the vial. Use a separate fresh syringe for each dose drawn. Standard subcutaneous injection: 25–31G, 8–12mm needle, rotate sites. When co-injecting with ipamorelin, community protocols typically mix both compounds in the same syringe for a single injection—this is pharmacologically unproblematic as both are stable peptides, but users should verify this with their specific product before combining.

Dosing in Published Research

Study / Source Population Dose / Details Route Key Relevance
Frohman LA, Jansson JO. Endocr Rev 1986 Review — mechanistic N/A N/A Foundational GHRH receptor pharmacology; establishes the cAMP/PKA pathway activated by all GHRH analogs including CJC-1295 (no DAC)
Teichman SL, et al. J Clin Endocrinol Metab 2006 Healthy adults — CJC-1295 with DAC Phase I/II 0.03–0.3 mg/kg SC SC Primary published human data for the CJC-1295 compound class. Results apply to DAC form; no-DAC human PK/PD not separately published in detail
Bowers CY, et al. Endocrinology 1984 In vitro / animal — GHRH synergy with GHRPs Variable In vitro / IV Establishes GHRH + GHRP combination synergy — mechanistic basis for CJC-1295 (no DAC) + ipamorelin combination rationale
Corpas E, et al. J Clin Endocrinol Metab 1992 Healthy older men — sermorelin (GHRH analog class) 0.5–2 mg/day SC SC GHRH analog class evidence in humans; sermorelin is structurally and mechanistically similar; provides human context for the class
Walker RF, et al. J Gerontol 1994 Healthy older men — sermorelin class 0.5–2 mg/day before sleep SC GHRH analog pre-sleep timing data; slow-wave sleep GH pulse augmentation — class-level evidence relevant to CJC-1295 (no DAC) timing rationale

No Compound-Specific Human Dose-Finding Data

CJC-1295 (no DAC) has no published Phase I dose-finding study of its own. The research table above is necessarily class-level. Community doses are inferred from sermorelin practice and from the CJC-1295 with DAC trial ranges. This is a meaningful gap that distinguishes CJC-1295 (no DAC) from sermorelin, which has established clinical dose data from its FDA-approved program.

Dosing in Independent Self-Experimentation Communities

Protocol Parameter Typical Community Range Notes
Dose per injection 100–300 mcg; most common 100 mcg or 200 mcg Lower doses than ipamorelin on a per-injection basis; both compounds typically co-injected at matching doses
Frequency 1–3× daily; most common: once before sleep or once before sleep + once pre-workout Pre-sleep timing targets slow-wave sleep GH pulse augmentation. Pre-workout timing targets the anabolic GH environment during training.
Combination partner Ipamorelin — co-injected at same time point The pharmacologically preferred combination in the cluster: complementary receptor pathways (GHRHR + GHS-R1a), matching ~30-minute kinetics, discrete pulsatile GH output from both pathways simultaneously. CJC-1295 with DAC is not a substitute.
Why not CJC-1295 with DAC instead? Different compound, different kinetics, different physiological profile CJC-1295 with DAC produces continuous 14-day GH elevation. The pulsatile synergy rationale does not apply. A full comparison article is at peptidings.com/peptides/cjc-1295-dac/
Cycle length 8–12 weeks on, followed by a break Axis preservation rationale — same as ipamorelin. Optimal on/off duration not established in human data.
Reconstitution concentration Common: 2 mg vial + 2 mL bacteriostatic water = 1 mcg/µL 100 mcg dose = 100 µL (0.1 mL); 200 mcg = 200 µL (0.2 mL). Verify vial size and volume before drawing.

Frequently Asked Questions

What is the difference between CJC-1295 and Modified GRF(1-29)?

They are the same compound—CJC-1295 without DAC is also called Modified GRF(1-29) or Mod GRF. The naming inconsistency exists because ConjuChem’s clinical candidate was the DAC form, and the no-DAC base peptide was adopted by the research community under multiple names. If a supplier offers both “CJC-1295” and “Mod GRF,” they may be selling the same compound under two names, or they may be selling the DAC and no-DAC forms respectively. Verify by checking the documented half-life.

Why is CJC-1295 (no DAC) preferred over sermorelin for stacking?

The pharmacological difference between CJC-1295 (no DAC) and sermorelin is modest: CJC-1295 (no DAC)’s DPP-IV-resistant modifications give it a half-life of ~30 minutes versus sermorelin’s ~10–20 minutes. Both produce pulsatile GH via GHRHR activation and both can be combined with GHS-R1a agonists on the same dual-pathway rationale. Sermorelin has substantially more human clinical data and a prior FDA approval history. The community preference for CJC-1295 (no DAC) over sermorelin likely reflects supply availability and the (modest) half-life advantage rather than superior pharmacological evidence.

Can CJC-1295 (no DAC) and ipamorelin be mixed in the same syringe?

Both are peptides reconstituted in bacteriostatic water and are chemically compatible in solution. Community practice routinely combines them in a single injection. No published stability study for this specific combination has been identified. The practical risk is low given the chemical compatibility, but users should be aware that combined-syringe stability is assumed rather than formally validated.

How do I know if what I have is the DAC or no-DAC form?

The most reliable indicator is documented half-life: ~30 minutes (no DAC) vs. ~14 days (with DAC). A supplier who cannot provide the half-life or who describes both products using the same name is a supplier to approach with caution. Independent third-party mass spectrometry testing is the only way to definitively confirm which compound is in a vial.

Does CJC-1295 (no DAC) need to be taken fasted?

Endogenous GHRH GH pulses are blunted by elevated blood glucose and elevated free fatty acids—a fed state reduces the GH response to GHRH stimulation. Community protocols almost universally recommend fasted administration of GHRH analogs (including CJC-1295 no DAC) and GHS-R1a agonists for this reason. Pre-sleep timing usually satisfies the fasted condition naturally. This is mechanistically well-supported even in the absence of a compound-specific human study demonstrating the effect.

Related Peptides: How CJC-1295 (No DAC) Compares

Compound Receptor Route GH Profile Half-life Evidence Tier FDA Status
CJC-1295 (no DAC) GHRHR SC peptide Moderate pulse ~30 min Preclinical / Phase I Cat. 3
CJC-1295 with DAC GHRHR (albumin-bound) SC peptide Strong, sustained ~14 days ~14 days Phase I/II Cat. 3
Sermorelin GHRHR SC peptide Moderate pulse ~10–20 min Clinical / Prior FDA approval Cat. 3
Ipamorelin GHS-R1a SC peptide Moderate pulse ~2 hr Preclinical / Phase I Cat. 3
MK-677 GHS-R1a Oral Strong, sustained ~24 hr ~24 hr Phase II/III Cat. 3
Tesamorelin GHRHR SC peptide Moderate pulse ~26–38 min Approved Drug FDA approved

Ipamorelin

Ipamorelin is CJC-1295 (no DAC)’s primary combination partner. It acts via GHS-R1a using the IP3/calcium pathway, complementing CJC-1295 (no DAC)’s GHRHR/cAMP mechanism. Matching kinetics (~30 min and ~2 hr respectively), complementary pathways, pulsatile profiles. The most pharmacologically coherent combination in the cluster. See the ipamorelin article at peptidings.com/peptides/ipamorelin/.

Sermorelin

Sermorelin is structurally and mechanistically almost identical to CJC-1295 (no DAC)—both are ~29-amino acid GHRH analogs acting via GHRHR. Sermorelin’s half-life is shorter (~10–20 min); CJC-1295 (no DAC)’s DPP-IV-resistant modifications give it a modest half-life advantage. Sermorelin has substantially more human clinical data and prior FDA approval history. Either can be used in the GHRHR + GHS-R1a combination protocol. See the sermorelin article at peptidings.com/peptides/sermorelin/.

CJC-1295 with DAC

Same receptor target. Completely different pharmacokinetic profile. Not interchangeable. See dedicated article at peptidings.com/peptides/cjc-1295-dac/.

Tesamorelin

Tesamorelin is a full 44-amino acid GHRH analog with N-terminal modification for DPP-IV resistance. FDA-approved for HIV-associated lipodystrophy. Longer half-life than CJC-1295 (no DAC), more human clinical data, approved indication. See the tesamorelin article at peptidings.com/peptides/tesamorelin/.

Edit
Compound Type Receptor GH Potency Cortisol / ACTH Appetite Effect Half-Life Route FDA Status WADA Status Evidence Tier Key Differentiator
Ipamorelin Synthetic pentapeptide GHS GHS-R1a Moderate Minimal at research doses Minimal ~2 hr (subcutaneous) Subcutaneous injection Category 3 — not available via US compounding Prohibited — S2 Tier 2 — Clinical Trials (Phase I) Most selective GHRP: GH release without cortisol, ACTH, or prolactin elevation at research doses
CJC-1295 (no DAC) Synthetic GHRH analog (modified GRF 1-29) GHRH-R Moderate (amplifies when paired with GHS-R1a agonist) None None ~30 min Subcutaneous injection Category 3 — not available via US compounding Prohibited — S2 Tier 3 — Preclinical / Mechanistic Short-acting GHRH analog; preserves pulsatile GH physiology. Pharmacologically paired with ipamorelin via complementary receptor pathway
CJC-1295 (with DAC) Synthetic GHRH analog with Drug Affinity Complex GHRH-R Strong (sustained) None None ~6–8 days Subcutaneous injection Category 3 — not available via US compounding Prohibited — S2 Tier 2 — Clinical Trials (Phase I/II) DAC extends half-life to ~1 week; produces sustained (non-pulsatile) GH elevation. NOT interchangeable with no-DAC version
Sermorelin Synthetic GHRH analog (GRF 1-29) GHRH-R Moderate None None ~10–20 min Subcutaneous injection Previously FDA-approved (Geref); discontinued commercially Prohibited — S2 Tier 1 — Approved (historically) Only GH secretagogue with prior FDA approval history. Very short half-life limits practical utility
MK-677 (Ibutamoren) Non-peptide GHS (spiroindoline) GHS-R1a Strong (sustained over 24 hr) Transient mild elevation Significant (hunger, weight gain) ~4–6 hr (oral bioavailability) Oral Category 3 — not FDA-approved Prohibited — S2 Tier 2 — Clinical Trials (Phase II) Only orally bioavailable GHS-R1a agonist. Most extensive human clinical dataset in the class. Appetite and insulin resistance are dose-limiting
GHRP-2 Synthetic hexapeptide GHS GHS-R1a Strong (most potent classic GHRP) Significant — cortisol and ACTH stimulation Moderate ~25–30 min Subcutaneous injection Category 3 — not available via US compounding Prohibited — S2 Tier 3 — Preclinical / Mechanistic Most potent GH release of classic GHRPs, but cortisol/ACTH co-stimulation works against anabolic intent
GHRP-6 Synthetic hexapeptide GHS GHS-R1a Strong Significant — cortisol and ACTH stimulation Strong (intense hunger) ~15–20 min Subcutaneous injection Category 3 — not available via US compounding Prohibited — S2 Tier 3 — Preclinical / Mechanistic First widely used GHRP. Intense appetite stimulation mirrors ghrelin signaling. Least selective of the class
Hexarelin Synthetic hexapeptide GHS GHS-R1a Strong Significant — cortisol and ACTH stimulation Moderate ~70 min Subcutaneous injection Category 3 — not available via US compounding Prohibited — S2 Tier 3 — Preclinical / Mechanistic Rapid receptor desensitization limits sustained use. GH response attenuates more steeply over repeated dosing than other GHRPs

Summary and Key Takeaways

CJC-1295 without DAC is the most physiologically conservative synthetic GHRH analog in common community use: pulsatile GH output, intact somatostatin feedback, matching kinetics with ipamorelin, and a mechanism derived directly from endogenous GHRH biology. Its combination with ipamorelin has the strongest pharmacological rationale of any two-compound stack in the GH Secretagogues cluster. Its compound-specific human evidence base is the thinnest of any article in this cluster—sound mechanistic reasoning is not a substitute for clinical data, and the community has been acting on reasoning rather than evidence.

  • CJC-1295 (no DAC) is a 29-amino acid GHRH analog producing pulsatile GH release via GHRHR activation with a half-life of ~30 minutes.
  • It is not equivalent to CJC-1295 with DAC. The half-lives differ by a factor of ~300; the physiological GH profiles are fundamentally different.
  • The combination with ipamorelin (GHRHR + GHS-R1a dual-pathway) is the most pharmacologically coherent stack in the cluster—and depends specifically on the no-DAC form.
  • Compound-specific human clinical trial data does not exist. All evidence is class-level (GHRH analogs, GHRH + GHRP combination pharmacology). This is an honest gap.
  • FDA Category 3. WADA-prohibited under S2 both in- and out-of-competition.
  • Supply chain naming confusion (DAC vs. no-DAC) is a real risk. Verify which compound you have before use.

The research moves fast. We read all of it so you don’t have to.

New compound reviews, evidence updates, and protocol analysis — sourced, cited, and written for people who actually read the studies.

Subscribe to Peptidings Weekly

Selected References and Key Studies

  1. Frohman LA, Jansson JO. Growth hormone-releasing hormone. Endocr Rev. 1986;7(3):223–53. — Foundational GHRH receptor pharmacology.
  2. Bowers CY, et al. Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. J Clin Endocrinol Metab. 1990;70(4):975–82. — GHRH + GHRP synergy in humans.
  3. Corpas E, et al. Human growth hormone and human aging. Endocr Rev. 1993;14(1):20–39.
  4. Walker RF, et al. Effects of growth hormone-releasing hormone on sleep and GH secretion in healthy elderly men. J Gerontol. 1994;49(1):B9–16.
  5. Teichman SL, et al. Prolonged stimulation of GH secretion by CJC-1295, a long-acting analog of GHRH. J Clin Endocrinol Metab. 2006;91(3):799–805. — Primary published human data for the CJC-1295 compound class (DAC form; class pharmacology applies).
  6. Kojima M, et al. Ghrelin is a GH-releasing acylated peptide from stomach. Nature. 1999;402:656–60. — Endogenous GHS-R1a ligand; context for ipamorelin combination rationale.

Further Reading and References

  • Ipamorelin article at peptidings.com/peptides/ipamorelin/ — primary combination partner
  • CJC-1295 with DAC article at peptidings.com/peptides/cjc-1295-dac/ — different compound, different pharmacology
  • Sermorelin article at peptidings.com/peptides/sermorelin/ — most similar compound with more clinical data
  • Tesamorelin article at peptidings.com/peptides/tesamorelin/ — FDA-approved GHRH analog
  • Growth Hormone Secretagogues Cluster Hub at peptidings.com/peptides/growth-hormone-secretagogues/
  • Peptidings Glossary at peptidings.com/glossary/ — GHRH, GHS-R1a, DPP-IV, IGF-1 defined

Disclaimer

This article is produced for educational and research purposes only. Peptidings does not provide medical advice, diagnosis, or treatment recommendations. Nothing in this article should be interpreted as an endorsement of any compound for human use outside of properly conducted clinical trials.

CJC-1295 (without DAC) is not approved by the U.S. Food and Drug Administration for any therapeutic indication. It is classified as a research chemical. Purchase, possession, and use may be subject to legal restrictions varying by jurisdiction. Readers are responsible for understanding applicable laws.

All citations link to primary sources where available. Evidence limitations are stated explicitly and not minimized.

Scroll to Top