CJC-1295: A Long-Acting GHRH Analog for Sustained Growth Hormone Stimulation

This content is provided by Superpower Health for educational and informational purposes only. Superpower Health facilitates access to GHRH-class peptides through licensed healthcare providers and compounding pharmacy partners. CJC-1295 is not FDA-approved for any indication. As of April 2026, it is classified as an FDA 503A Category 2 bulk drug substance, meaning it is prohibited for use in compounding by licensed pharmacies in the United States. This page is not a substitute for medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider. For compound reference data, see the PubChem monograph (CID 56841945).

Most adults experience a gradual decline in growth hormone output starting in the third decade of life. By middle age, the pituitary still has the capacity to secrete GH — the machinery is intact. What has changed is the hypothalamic signal telling it to fire. CJC-1295 was developed to address exactly that gap, and it does so through a structural innovation that no earlier GHRH analog could match: a covalent bond to circulating albumin that extends its half-life from minutes to days.

Here is what CJC-1295 is, how the with-DAC and without-DAC variants differ mechanistically, what the published clinical data shows, and which biomarkers matter before and during use.

Key Takeaways

• Regulatory Status: Not FDA-approved for any indication. As of April 2026, CJC-1295 is classified as an FDA 503A Category 2 bulk drug substance, prohibited for use in compounding by licensed pharmacies in the United States.
• Research Stage: Early-phase human data available (Phase 1 PK/PD); no completed Phase 2 or Phase 3 RCTs for any indication. Available outside the US through non-US licensed channels and in research contexts.
• Availability: Not available through Superpower. CJC-1295 cannot be legally obtained through a licensed compounding pharmacy in the United States as of April 2026.
• Prescribing information: View compound reference data (PubChem CID 56841945) — no FDA label exists for this compound.
• How it works: Binds GHRH receptors on the anterior pituitary, stimulating growth hormone release via Gs/cAMP/PKA signaling; the DAC variant covalently binds albumin in vivo, extending plasma half-life to approximately 6 to 8 days.
• What the research shows: A 2006 Phase 1 randomized, placebo-controlled trial by Teichman and colleagues in the Journal of Clinical Endocrinology and Metabolism reported that a single subcutaneous dose of CJC-1295 with DAC (1–30 mcg/kg) produced dose-dependent mean GH elevations of 2- to 10-fold and sustained IGF-1 elevations of 1.5- to 3-fold above baseline lasting 9 to 11 days.
• WADA Status: As of the 2026 WADA Prohibited List, CJC-1295 is classified as a prohibited substance under the S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) category, in both in-competition and out-of-competition periods.

What Is CJC-1295?

CJC-1295 is a synthetic tetrasubstituted analog of growth hormone-releasing hormone (GHRH), specifically of the first 29 residues of endogenous GHRH — the minimal sequence required for full GHRH receptor activity. It was developed to overcome the primary limitation of earlier GHRH fragments: rapid enzymatic degradation in plasma. As described in a 2005 preclinical paper by Jetté and colleagues in Endocrinology, CJC-1295 incorporates four amino acid substitutions — D-Ala at position 2, Gln at position 8, Ala at position 15, and Leu at position 27 — that confer resistance to dipeptidyl peptidase-4 (DPP-4) and other plasma proteases. These substitutions were identified through systematic screening of GHRH analogs for protease stability without loss of receptor affinity.

The compound exists in two pharmacologically distinct forms that share the same amino acid backbone but differ critically in half-life. CJC-1295 with DAC (drug affinity complex) carries a maleimidopropionyl biotin linker that covalently binds to circulating albumin after subcutaneous injection, as characterized by Jetté and colleagues. This albumin conjugation extends the plasma half-life to approximately 6 to 8 days. CJC-1295 without DAC — also called modified GRF(1-29) or mod GRF 1-29 — lacks this linker and has a plasma half-life of approximately 30 minutes. These are not interchangeable formulations: they produce fundamentally different pharmacokinetic profiles, dosing requirements, and GH release patterns.

How CJC-1295 Works in the Body

GHRH receptor signaling at the pituitary

CJC-1295 binds the GHRH receptor (GHRHR) on the somatotroph cells of the anterior pituitary. A comprehensive 2000 review by Mayo and colleagues in Recent Progress in Hormone Research established that GHRHR is a Gs-coupled receptor: binding triggers adenylyl cyclase activation, cAMP accumulation, and protein kinase A (PKA) phosphorylation, which opens voltage-gated calcium channels and stimulates GH gene transcription via the transcription factor Pit-1. The result is pulsatile GH secretion into the portal and systemic circulation. Because CJC-1295 acts on an upstream receptor rather than delivering GH directly, the pituitary's own somatostatin-mediated feedback loop remains operational. Elevated GH triggers somatostatin release from the hypothalamus, which dampens GH output. This negative feedback is the physiological constraint that limits supraphysiological excursions.

The DAC mechanism: albumin conjugation and extended half-life

The DAC variant's extended half-life derives from a specific covalent chemistry. After subcutaneous injection, the maleimido group on the biotin linker reacts with the free thiol on cysteine-34 of circulating albumin to form a stable thioether bond. Albumin has a plasma half-life of approximately 19 days; once CJC-1295 DAC is conjugated to it, the peptide is protected from renal filtration and proteolytic clearance and circulates with albumin's pharmacokinetic profile. The 2005 Jetté paper confirmed this mechanism in rat and cynomolgus monkey models, demonstrating sustained GHRH receptor activation at the pituitary over days rather than minutes. This mechanism is structurally analogous to the albumin-binding strategies used in approved long-acting insulin and GLP-1 analogs, though CJC-1295 remains non-approved.

Pulsatile versus tonic GH release: the central pharmacological debate

Normal GH physiology is characterized by discrete high-amplitude pulses, primarily during slow-wave sleep, separated by low-trough periods. These pulses are coordinated by alternating hypothalamic GHRH and somatostatin activity. CJC-1295 without DAC mimics this pulse pattern because its 30-minute half-life limits receptor occupancy to the peri-injection window. CJC-1295 with DAC, by contrast, maintains continuous GHRHR stimulation over days, which raises a legitimate physiological question: does sustained receptor agonism produce tonic rather than pulsatile GH output?

A 2006 deep-phenotyping study by Ionescu and Frohman in the Journal of Clinical Endocrinology and Metabolism addressed this directly in healthy men aged 20–40 years receiving a single 60 or 90 mcg/kg subcutaneous injection of CJC-1295 DAC, with overnight 12-hour GH sampling before and one week after injection. Deconvolution analysis of 24-hour GH secretion profiles showed that GH pulse frequency and amplitude were unaltered, while trough GH concentrations rose approximately 7.5-fold (p < 0.0001) and mean 24-hour GH increased approximately 46% (p < 0.01). The authors concluded that sustained GHRHR agonism augments rather than replaces pulsatile secretion — likely because endogenous somatostatin continues to exert its counter-regulatory effect. This finding partially addresses the "non-physiological tonic stimulation" concern, but it also means that mean 24-hour GH is elevated throughout the dosing interval, not only during normal secretory pulses.

What CJC-1295 May Support

1. Sustained IGF-1 elevation and GH axis activation

The most direct human evidence for CJC-1295 comes from the 2006 Phase 1 program by Teichman and colleagues in the Journal of Clinical Endocrinology and Metabolism, comprising two randomized, double-blind, placebo-controlled ascending-dose trials in healthy adults aged 21 to 61 years (first trial: single subcutaneous doses of 1, 2, 4, 8, 15, or 30 mcg/kg or placebo; second trial: two or three weekly or biweekly doses). At the 2 mcg/kg dose, mean GH increased 2.4-fold above baseline. At 30 mcg/kg, the increase reached 10-fold. IGF-1 levels rose 1.5- to 3-fold above baseline and remained elevated for 9 to 11 days after a single injection. The study established the foundational PK/PD profile for CJC-1295 DAC and demonstrated dose-dependent, sustained GH axis activation from a single administration. A 2009 proteomic study by Sackmann-Sala and colleagues in Growth Hormone and IGF Research analyzed serum samples from 11 healthy men before and one week after a single CJC-1295 injection using 2D gel electrophoresis plus mass spectrometry, identifying decreases in apolipoprotein A1 and transthyretin isoforms and increases in beta-hemoglobin, albumin fragments, and immunoglobulin fragments — with the immunoglobulin/albumin fragment spot showing a linear relationship with IGF-1 levels — consistent with downstream GH axis engagement beyond the IGF-1 signal alone.

2. Body composition: visceral fat reduction

Growth hormone drives lipolysis, particularly in visceral adipose tissue, by upregulating hormone-sensitive lipase and promoting fatty acid mobilization from intra-abdominal fat stores. CJC-1295-specific controlled body composition data are limited to early-phase pharmacokinetic studies not designed to measure fat or lean mass as primary endpoints. The most relevant evidence for what sustained GHRH receptor activation can produce comes from the tesamorelin RCT program. A 2007 pivotal Phase 3 trial by Falutz and colleagues in the New England Journal of Medicine randomized 412 HIV-infected adults with abdominal lipodystrophy to tesamorelin 2 mg subcutaneous daily or placebo for 26 weeks and found visceral adipose tissue decreased 15.2% with tesamorelin versus a 5.0% increase with placebo (p < 0.001), with IGF-1 rising 81.0% on tesamorelin versus a 5.0% decrease on placebo (p < 0.001) and no significant between-group differences in glycemic measures. Tesamorelin and CJC-1295 activate the same GHRH receptor through the same Gs/cAMP/PKA pathway; this mechanistic overlap informs biological plausibility, but direct extrapolation from tesamorelin data to CJC-1295 requires explicit caution. CJC-1295-specific body composition trials have not been completed.

3. Lean muscle mass and protein synthesis

GH stimulates hepatic IGF-1 production, and IGF-1 activates mTOR signaling in skeletal muscle — the primary anabolic signaling cascade for muscle protein synthesis. In a 2006 animal study by Alba and colleagues in the American Journal of Physiology: Endocrinology and Metabolism, once-daily CJC-1295 administration normalized growth in GHRH-knockout C57BL mice that could not produce endogenous GHRH, while injections spaced every 48 or 72 hours increased body weight and length over placebo but failed to fully normalize growth; relative lean mass and subcutaneous fat body composition were preserved across treated groups, supporting the pharmacokinetic rationale for sustained receptor occupancy. This animal model demonstrates that CJC-1295 can activate the GH axis sufficiently to support anabolic processes in a GHRH-deficient system. Whether equivalent lean mass effects occur in healthy humans with intact GH secretion remains unestablished by controlled trials.

4. Synergy with GH secretagogues in the combination context

CJC-1295 is commonly used in combination with ipamorelin or other GH-releasing peptides (GHRPs). The rationale derives from receptor-level pharmacology. A landmark 1990 paper by Bowers and colleagues in the Journal of Clinical Endocrinology and Metabolism gave 18 normal adult men IV bolus GHRP at 0.1, 0.3, and 1.0 mcg/kg alone and combined with GHRH at 1.0 mcg/kg, and found peak GH rose from 1.2 ± 0.3 mcg/L on placebo to 7.6 ± 2.5, 16.5 ± 4.1, and 68.7 ± 15.5 mcg/L at ascending GHRP doses (approximately 6- to 57-fold) with submaximal GHRP plus GHRH producing synergistic — not merely additive — GH release, and no adverse clinical effects reported. A 1995 study by Popović and colleagues in the same journal gave 12 patients with hypothalamopituitary disconnection and 11 age- and sex-matched controls IV GHRH (100 mcg) and GHRP-6 (90 mcg) alone and in combination, and found the 120-minute GH area-under-the-curve for combined therapy reached 3,771.5 ± 399.6 mcg/L·min in controls versus only 745.3 ± 67.6 in disconnected patients (p < 0.01), confirming the amplification is hypothalamically mediated. A 2002 molecular mechanism paper by Cunha and Mayo in Endocrinology demonstrated at the receptor level that ghrelin/GH secretagogues potentiate GHRH-induced cAMP production when both receptor types (GHRHR and GHSR-1a, the ghrelin receptor) are coexpressed, explaining the pharmacological basis of the synergy. Ipamorelin specifically was characterized in a 1998 paper by Raun and colleagues in the European Journal of Endocrinology as the first selective GH secretagogue — equipotent with GHRP-6 for GH release but without the cortisol and prolactin stimulation seen with older GHRPs. A 1999 rat study by Johansen and colleagues in Growth Hormone and IGF Research further demonstrated that chronic ipamorelin administration increased longitudinal bone growth and body weight gain, supporting GH axis engagement.

Several reviews place this combination in broader context. A 2018 systematic review by Sigalos and Pastuszak in Sexual Medicine Reviews summarized the class-wide safety and efficacy record for GH secretagogues; a 2017 retrospective case series by Sigalos and colleagues in the American Journal of Men's Health of 14 men on testosterone therapy receiving 100 mcg of GHRP-6, GHRP-2, and a SERM three times daily for approximately 134 days documented a mean IGF-1 rise from 159.5 to 239.0 ng/mL (p < 0.0001), providing observational magnitude context; the small uncontrolled cohort and off-label regimen limit generalization; and a 2020 review by Sinha and colleagues in Translational Andrology and Urology addressed GH secretagogues — including CJC-1295 by name — in the management of body composition in hypogonadal males, while flagging the gap between marketed claims and controlled trial evidence. This selectivity profile is why ipamorelin became the preferred combination partner for CJC-1295. The combination article covers this clinical and pharmacological context in depth; the discussion here is intentionally brief.

CJC-1295 With DAC vs. Without DAC: The Critical Distinction

The two forms of CJC-1295 are structurally related but pharmacologically different compounds, and conflating them produces serious misunderstandings about dosing, timing, and risk.

CJC-1295 with DAC has a plasma half-life of approximately 6 to 8 days, as established by the Teichman 2006 trial. A single subcutaneous injection produces IGF-1 elevation lasting 9 to 11 days. Dosing is typically once or twice weekly precisely because the albumin conjugation extends duration of action. The extended half-life produces the elevated mean 24-hour GH pattern documented by Ionescu and Frohman — elevated troughs alongside maintained pulses — rather than discrete peaks at injection time only.

CJC-1295 without DAC (modified GRF 1-29) has a plasma half-life of approximately 30 minutes. After subcutaneous injection, GH pulses occur within 15 to 30 minutes and return to baseline shortly thereafter. Dosing requires multiple daily injections, typically timed immediately before sleep to coincide with the natural nocturnal GH secretory window. Without the albumin-binding linker, there is no sustained receptor occupancy, no chronic IGF-1 elevation, and no associated concerns about persistent tonic GH stimulation.

The two variants are not interchangeable. Providers who work with GHRH analogs evaluate the DAC versus no-DAC distinction explicitly. Research referencing "CJC-1295" without specifying DAC status is ambiguous; the Teichman 2006 trial and the Ionescu 2006 study both used the DAC formulation.

CJC-1295 vs. Sermorelin vs. Tesamorelin: Comparator Context

CJC-1295, sermorelin, and tesamorelin all belong to the GHRH analog class and bind the same receptor. They differ in half-life, structural modification strategy, clinical evidence base, and regulatory status.

Sermorelin is the native 29-amino acid GHRH fragment. It has a plasma half-life of approximately 10 minutes, requires nightly subcutaneous injection to achieve sustained GH stimulation, and received FDA approval in 1997 for pediatric GH deficiency before voluntary market withdrawal by 2008. As a 2006 review by Walker in Clinical Interventions in Aging noted, sermorelin's short half-life preserves the physiological pulsatility pattern and maintains somatostatin feedback, which is one argument for preferring it over longer-acting analogs for physiological GH restoration. CJC-1295 differs from sermorelin by its four stabilizing substitutions and, in the DAC form, by the albumin-binding chemistry that extends half-life by more than 40-fold. Both compounds produce similar downstream effects via GHRH receptor activation, but CJC-1295 DAC produces a chronically elevated mean GH exposure that sermorelin's kinetics do not replicate.

Tesamorelin is a GHRH analog with a trans-3-hexenoic acid modification at the N-terminus, extending its half-life to approximately 25 to 30 minutes. It is the only FDA-approved GHRH analog, with approval for HIV-associated lipodystrophy specifically. The 2007 Phase 3 RCT by Falutz and colleagues in the New England Journal of Medicine and a 2014 RCT by Stanley and colleagues in JAMA constitute the strongest controlled body composition evidence for the GHRH class. Stanley and colleagues enrolled 48 HIV-infected adults with central adiposity and randomized 28 to tesamorelin 2 mg daily and 22 to placebo for 6 months, finding a treatment-effect reduction in visceral fat of 42 cm² (p = 0.005) and a reduction in hepatic lipid-to-water ratio of 2.9% (p = 0.003); fasting glucose rose transiently at 2 weeks (9 vs. 2 mg/dL, p = 0.03) but normalized by month 6. A 2020 review by Miller, Velazquez, and Yuen in the Journal of Clinical Endocrinology and Metabolism surveys long-acting GH preparations more broadly; CJC-1295 with DAC represents one of several albumin-conjugation strategies discussed in that literature. Tesamorelin is positioned as the evidence benchmark for the class: it has the most rigorous RCT data, an FDA-approved indication, and a published safety profile. CJC-1295 has no FDA approval for any indication and no completed Phase 2 or Phase 3 efficacy trials in any population. For individuals evaluating GHRH analogs, the tesamorelin clinical record is the most informative comparator for understanding what the class can achieve under controlled conditions.

Side Effects and Safety Considerations

The safety signal for CJC-1295 is informed by the Teichman 2006 Phase 1 trial, the Ionescu 2006 deep-phenotyping study, and the broader GHRH analog class literature. Most reported effects in early-phase studies were injection-site reactions and vasodilatory symptoms consistent with GH release.

Common (reported in clinical studies):

• Injection-site redness, swelling, or pain (most frequently reported in the Teichman 2006 trial; typically self-limiting)
• Flushing and warmth (vasodilatory effects of GH release; typically occurring within 30 minutes of injection)
• Headache (reported in the Teichman 2006 trial, dose-related)
• Water retention and peripheral edema (consistent with GH-driven IGF-1 elevation promoting sodium and water retention)

Less common but mechanistically relevant:

• Insulin resistance and elevated fasting glucose: GH directly antagonizes insulin action at liver and muscle, reducing peripheral glucose uptake. A 2017 review by Kim and Park in the Annals of Pediatric Endocrinology and Metabolism established this mechanism; it applies to any compound that sustains GH elevation. The Sigalos and Pastuszak systematic review specifically identified decreased insulin sensitivity and elevated blood glucose as consistent adverse signals across the GH secretagogue class, including GHRH analogs. Sustained GH elevation from CJC-1295 DAC may amplify this concern relative to shorter-acting analogs. Fasting glucose and HbA1c monitoring is standard clinical practice.
• Carpal tunnel syndrome: GH promotes soft tissue expansion and fluid retention; carpal tunnel syndrome is a well-established adverse effect of GH replacement and has been reported with other GH secretagogues.
• Dizziness or orthostatic changes: vasodilatory effects may transiently affect blood pressure shortly after injection.

Safety context: the acromegaly analogy

Acromegaly — chronic GH and IGF-1 excess caused by a GH-secreting pituitary adenoma — provides the most informative negative-control model for what sustained non-physiological GH elevation produces. A 2019 comprehensive review by Vila and colleagues in Frontiers in Endocrinology documented that acromegaly patients develop insulin resistance, type 2 diabetes, cardiomyopathy, and increased all-cause mortality, with metabolic normalization occurring only after GH excess is controlled. Acromegaly represents extreme, decades-long GH elevation, not what CJC-1295 is designed to produce. However, it establishes the directional risk: the higher and more sustained GH elevation climbs above physiological range, the more consequential the metabolic effects. A 2019 review by Holt and Ho in Endocrine Reviews on GH abuse in sport reached a similar conclusion, noting limited evidence for athletic benefit from exogenous GH-elevating compounds alongside consistent signals of insulin resistance and soft tissue adverse effects.

Who Is CJC-1295 Typically Evaluated For?

CJC-1295 has no FDA-approved indication. In research and off-label contexts, it has been evaluated primarily in adults with documented age-related GH decline — characterized by low or low-normal IGF-1 for age, symptoms consistent with somatopause (reduced lean mass, increased visceral fat, poor recovery), and absence of active malignancy or other contraindications. The Teichman 2006 Phase 1 trial enrolled healthy men aged 21 to 61 years; it did not evaluate a specific symptomatic population. Providers who consider CJC-1295 evaluate IGF-1 levels relative to age-adjusted reference ranges as the primary candidacy biomarker, typically alongside fasting glucose, HbA1c, and a comprehensive metabolic panel to establish a safety baseline. CJC-1295 requires a prescription from a licensed provider where it is legally accessible; as of April 2026, it cannot be compounded in the United States.

Who Should Not Use CJC-1295

A licensed provider will evaluate individual risk factors before any prescribing decision. The following represent general clinical contraindications based on the compound's mechanism and the GHRH class literature:

• Active or history of malignancy: GH and IGF-1 are mitogenic; CJC-1295's GH-promoting mechanism may stimulate proliferation in existing tumor tissue. The GHRH class is contraindicated in active cancer across all compounds in this class.
• Uncontrolled diabetes or significant insulin resistance: sustained GH elevation worsens peripheral insulin sensitivity; CJC-1295 is not appropriate in individuals with poorly controlled blood sugar.
• Hypothyroidism: untreated hypothyroidism blunts GH axis response; thyroid status should be assessed and addressed before initiating any GH secretagogue.
• Pregnancy or breastfeeding: safety not established in these populations; GH axis stimulation during pregnancy is not clinically evaluated.
• Known hypersensitivity to CJC-1295 or to albumin-binding agents (for the DAC formulation specifically).
• Individuals not willing to undergo baseline and follow-up IGF-1 and metabolic monitoring: responsible use of any GH secretagogue requires objective tracking of GH axis response and metabolic parameters.

This is not an exhaustive list. A licensed provider will conduct a full clinical evaluation, including baseline bloodwork, before determining eligibility.

Biomarkers to Monitor With CJC-1295

CJC-1295's mechanism is GH axis activation. The markers below directly track whether that mechanism is engaged and whether the resulting GH and IGF-1 elevation remains within a physiologically appropriate range.

• IGF-1: The primary efficacy and safety monitoring marker. IGF-1 is the main downstream effector of pulsatile GH release and the most reliable serum index of GH axis activity over time. Baseline IGF-1 confirms GH axis status before starting. On-therapy IGF-1 tracks response and ensures levels remain within the age-adjusted reference range rather than trending toward acromegalic values. A 2021 review by Bailes and Soloviev in Biomolecules emphasized the importance of interpreting IGF-1 within age- and sex-specific reference ranges due to binding-protein interference — a single result without a baseline is difficult to act on.
• Fasting glucose: GH's insulin-antagonizing effect on liver and peripheral muscle is well established; CJC-1295 elevates GH, which in turn suppresses peripheral glucose uptake. Baseline fasting glucose establishes metabolic status before therapy begins and provides a reference point for detecting insulin resistance signals during use.
• HbA1c: Reflects mean blood glucose over the prior 2 to 3 months. More informative than a single fasting glucose draw for detecting chronic glycemic effects; recommended at baseline and at the 3- to 6-month follow-up interval.
• Fasting insulin: Pairs with fasting glucose to calculate insulin sensitivity indices (HOMA-IR). An elevated fasting insulin in the context of normal fasting glucose can be an early signal of developing insulin resistance, making it a more sensitive early indicator than glucose alone.
• Comprehensive metabolic panel: Covers liver function markers (ALT, AST, alkaline phosphatase, bilirubin) and kidney function (creatinine, BUN). CJC-1295 is metabolized via endopeptidase cleavage and renal filtration; baseline organ function matters for safety interpretation.
• Thyroid panel (TSH, Free T4): GH secretagogue use can unmask or worsen subclinical hypothyroidism; an untreated thyroid deficiency also blunts GH axis response. Baseline thyroid status should be assessed.
• Growth hormone (serum): Direct measurement of GH is technically challenging due to its pulsatile, short-lived nature in circulation, but a morning fasting GH alongside an IGF-1 draw provides useful baseline context in individuals with suspected GH deficiency.

Is CJC-1295 Legal?

As of April 2026, CJC-1295 is not FDA-approved for any indication. It is classified as an FDA 503A Category 2 bulk drug substance under the Consolidated Appropriations Act of 2023, which prohibits its use in compounding by licensed 503A pharmacies in the United States. The regulatory basis for this classification was detailed in a 2024 position statement FAQ by Bays and colleagues in Obesity Pillars from the Obesity Medicine Association, which outlined the FDA's approach to 503A compounding eligibility and the consequences of Category 2 designation — specifically, that compounds in Category 2 lack USP monographs and have not received FDA-approval, making them ineligible for compounding regardless of prescription status.

With that regulatory context established, it is worth noting that CJC-1295 does not fall under any REMS program or controlled-substance scheduling. It is not a controlled substance in the United States. Individuals outside the United States may encounter it through licensed healthcare providers in jurisdictions with different compounding regulations; legal status varies by country.

For competitive athletes, there is a separate regulatory consideration. As of the 2026 WADA Prohibited List, CJC-1295 is prohibited both in and out of competition as a member of the S2 Peptide Hormones, Growth Factors, Related Substances and Mimetics class. A 2021 analytical study by Memdouh and colleagues in Drug Testing and Analysis developed LC-MS/MS methods capable of detecting CJC-1295 and CJC-1295 DAC in urine at the WADA-required threshold of 1 ng/mL, with detection windows extending several days after the last dose. A 2018 immuno-PCR assay developed by Timms and Ganio in the same journal demonstrated detection at 0.8 pg/mL in equine plasma, underscoring the scale of anti-doping surveillance for this compound across both human and equine sport.

Understanding Your Baseline Before Starting a GHRH Analog

A single IGF-1 result captures one moment in a dynamic hormonal system. What makes it clinically useful is comparison: where does your IGF-1 sit relative to age-adjusted reference ranges, and does it change in a predictable direction when a GHRH analog is introduced? The same principle applies to fasting glucose and HbA1c. Without pre-treatment values, on-therapy results lack context. An IGF-1 of 180 ng/mL means something different at age 30 than at age 55, and something different again if your baseline was 120 ng/mL versus 210 ng/mL. Establishing the baseline is what makes the numbers meaningful.

That principle — test first, then evaluate — is central to Superpower's approach to preventive health: every clinical decision should begin with knowing where your biomarkers actually stand. Understanding your IGF-1, fasting glucose, and metabolic baseline is the first step in any informed evaluation of a GH secretagogue.

If you are working with a licensed provider to evaluate any GHRH-class compound, start with a clinician assessment and a baseline IGF-1 before any therapeutic decision is made.

IMPORTANT SAFETY INFORMATION

CJC-1295 is not FDA-approved for any indication. As of April 2026, it is classified as an FDA 503A Category 2 bulk drug substance, prohibited for use in compounding by licensed pharmacies in the United States. Superpower Health does not prescribe, sell, compound, or facilitate access to CJC-1295. This page is provided for educational and informational purposes only and does not constitute medical advice, diagnosis, or treatment.

Contraindications: Active or history of malignancy (GH and IGF-1 are mitogenic); uncontrolled diabetes or significant insulin resistance (GH worsens insulin sensitivity); untreated hypothyroidism; pregnancy or breastfeeding (safety not established); known hypersensitivity to CJC-1295 or albumin-binding excipients.

Warnings: Insulin resistance and elevated fasting glucose (consistent adverse signal across the GH secretagogue class); carpal tunnel syndrome (GH-driven soft tissue expansion); water retention and peripheral edema; injection-site reactions (redness, pain, swelling); flushing and headache post-injection; potential for supraphysiological IGF-1 elevation with the DAC formulation if not monitored.

Common side effects: Injection-site reactions, flushing, headache, water retention.

WADA status: As of the 2026 WADA Prohibited List, CJC-1295 is prohibited in and out of competition under S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Athletes subject to anti-doping testing should not use this compound.

Long-term safety data: No Phase 2 or Phase 3 controlled efficacy or safety trials for CJC-1295 have been completed in any population. Long-term safety is unknown. The acromegaly literature provides a relevant negative-control model for the consequences of sustained GH/IGF-1 excess; chronically supraphysiological IGF-1 carries documented risks of insulin resistance, cardiomyopathy, and increased mortality.

Full compound reference data at PubChem CID 56841945. No FDA-approved prescribing information exists for this compound.

Additional Questions

What is the FDA peptide reclassification and how does it affect CJC-1295?

The Consolidated Appropriations Act of 2023 required the FDA to create a list of bulk drug substances eligible for compounding under Section 503A. CJC-1295 was placed in Category 2 — the designation for substances that present significant safety risks or lack adequate evidence for use in compounding. Category 2 designation means licensed pharmacies cannot legally compound CJC-1295 regardless of whether a patient has a prescription. This is distinct from controlled-substance scheduling; CJC-1295 is not a controlled substance, but its compounding is prohibited under the 2023 framework.

Is CJC-1295 the same as sermorelin?

No. Both are GHRH analogs that bind the same pituitary receptor, but their structures and pharmacokinetics differ substantially. Sermorelin is the native 29-residue GHRH fragment with a half-life of approximately 10 minutes. CJC-1295 incorporates four amino acid substitutions that confer protease resistance, and the DAC formulation additionally conjugates to albumin for a half-life of 6 to 8 days. The practical difference is dosing frequency and duration of GH stimulation per dose. Sermorelin requires nightly injection; CJC-1295 with DAC is typically dosed once or twice weekly.