CJC-1295 DAC

First: confirm which CJC-1295 molecule is being discussed

“CJC-1295” is used inconsistently online. CJC-1295 DAC / with DAC / DAC:GRF is the long-acting albumin-binding GHRH analog used in the human studies on this page. CJC-1295 without DAC / Mod GRF 1-29 is a shorter-acting analog with an entirely different protocol landscape.

FDA's scientific review identified five distinct CJC-1295-related bulk substances and warned that inconsistent naming creates identity, purity, and dosing problems. Published human studies appear to concern the DAC active moiety, although the exact salt form was not consistently specified.

Any dose of 100–300 mcg given one to three times daily should not automatically be attributed to CJC-1295 DAC. That schedule usually belongs to Modified GRF 1-29 (“CJC-1295 no DAC”).

Is there an FDA-approved CJC-1295 DAC dosage?

No. CJC-1295 DAC is investigational and has no FDA-approved product or indication—therefore no approved starting dose, titration schedule, maintenance dose, treatment duration, or maximum dose.

In December 2024, FDA proposed that CJC-1295 DAC free base, acetate, and trifluoroacetate not be included on the Section 503A Bulks List. The Pharmacy Compounding Advisory Committee voted 0 yes and 13 no on inclusion. FDA's compounding safety page identifies immunogenicity, peptide-impurity, API-characterization, increased-heart-rate, and systemic-vasodilatory concerns. An advisory vote is not an approval decision, but compounded availability must not be described as FDA approval.

There is currently no FDA-approved dosage for CJC-1295 DAC. The doses below describe doses evaluated in human research rather than an established prescribing protocol.

Dosages used in human clinical research

Formal human evidence comes from healthy-adult PK/PD studies, a GH-pulsatility study, an exploratory biomarker analysis, and a terminated Phase 2 program in HIV-associated visceral obesity.

Single-dose clinical research

Teichman and colleagues assigned participants to parallel ascending cohorts: 30, 60, 125, or 250 mcg/kg subcutaneously. This was escalation across study groups—not a within-person titration.

Single administration produced dose-dependent increases in mean GH and IGF-1. Mean GH rose approximately 2- to 10-fold for at least six days; mean IGF-1 rose approximately 1.5- to 3-fold for 9–11 days. IGF-1 exceeded the age- and sex-adjusted normal range only in the 250 mcg/kg group.

These findings establish a hormonal dose response—not a dose-response curve for muscle growth, fat loss, sleep, recovery, or “anti-aging.” Those clinical outcomes were not measured.

Repeat-dose clinical research

The repeat-dose study directly compared weekly and every-two-week schedules at 20–60 mcg/kg. Maximum plasma concentrations were 29–70% higher after the day-14 dose than after the first dose, and AUC also rose. Mean IGF-1 increased within eight hours and remained above baseline through day 28—cumulative exposure after only two or three injections.

GH pulsatility study

Twelve healthy men received a single 60 or 90 mcg/kg subcutaneous dose. One week later, mean GH was 46% above baseline, trough GH was 7.5-fold higher, and mean IGF-1 was 44–45% higher. Pulse frequency and magnitude were not significantly changed; most of the increase came from a higher GH baseline between pulses. No significant response difference was observed between 60 and 90 mcg/kg in this small study.

Phase 2 escalation in HIV-associated visceral obesity

NCT00267527 enrolled 192 people with HIV-associated visceral obesity in two once-weekly escalation arms. The study was terminated after a participant experienced chest discomfort two hours after an eleventh weekly dose, had an ECG-confirmed acute myocardial infarction, and died approximately one hour later. The attending physician reportedly considered asymptomatic coronary artery disease with plaque rupture most likely. Results were never published—so causal relationship and arm-level efficacy/safety cannot be established from the public record.

Clinical dose-by-weight reference

The calculator converts published per-kilogram study exposures into total milligrams for a chosen body weight. It is mathematical context only—not a dosing chart for use. It does not account for individual risk, product identity, purity, or accumulation.

CJC-1295 DAC research dosage

People searching for a “CJC-1295 DAC research dose” usually encounter fixed weekly protocols rather than weight-based clinical dosing. These conventions are widespread enough to document, but they should not be portrayed as clinically derived.

Human trials support that subcutaneous CJC-1295 DAC has a long half-life, accumulates with repeat dosing, and increases GH and IGF-1. They do not show that 0.5, 1, or 2 mg per week improves body composition, recovery, strength, sleep, or healthy-aging outcomes.

For an 80 kg participant, even the lowest 20 mcg/kg clinical repeat dose equals 1.6 mg, while 30–60 mcg/kg equals 2.4–4.8 mg. That does not make online doses safer or ineffective—it means their effects have not been established by the original trials.

Anecdotal vs clinically studied dosing

Unlike ipamorelin, route and weekly cadence do overlap between formal and anecdotal CJC-1295 DAC protocols. Dose basis and purpose do not. Clinical studies were weight-based and primarily measured hormones; online protocols use smaller fixed doses and claim outcomes the trials did not test.

Research protocol variations

1. Once weekly vs twice weekly. Formal research used weekly or every-14-day dosing—not two injections in the same week. Twice-weekly splits are anecdotal. A ~1-week half-life means dividing a weekly amount may change peak-to-trough variation but is not proven to improve efficacy or tolerability.
2. Fixed vs weight-based dosing. All clearly reported formal human doses were weight-based. Most online protocols use a fixed weekly milligram amount. Some PK parameters were weight-independent in studies—that does not validate a universal fixed chronic dose.
3. Continuous use vs cycling. 8–16 weeks on / 4–8 weeks off is commonly repeated. Published PK studies did not compare cycling strategies. Phase 2 planned 12 treatment weeks and 6 weeks of follow-up as trial design—not proof of an optimal cycle.
4. Monotherapy vs combination. Pairing with ipamorelin has a complementary-receptor rationale, but no controlled human trial established optimal dose, timing, ratio, or safety. Many “CJC-1295/Ipamorelin” vials contain Modified GRF 1-29 rather than DAC.
5. Bedtime or fasted timing. Often inherited from short-acting peptide protocols. DAC produced measurable exposure for 10–13 days and elevated IGF-1 for weeks. No trial showed a particular time of day or meal interval improves DAC outcomes.

Animal / preclinical research dosage

Animal doses must remain separate from human research and should not be converted casually into human protocols. Efficacy models show GH-pathway stimulation; toxicology identified injection-site hemorrhage/inflammation/necrosis, altered food intake and activity, reduced hemoglobin, altered cholesterol, and genotoxicity signals. These data cannot determine a safe or effective human dose.

Why these research doses and schedules appear

1. Albumin binding and long half-life. The DAC maleimide binds albumin cysteine-34. Estimated human half-life 5.4–9.2 days supports weekly or biweekly clinical-study schedules.
2. Cumulative exposure. Repeat-dose research showed rising Cmax/AUC and progressively greater IGF-1 peaks. Effects or adverse reactions can persist; rapid escalation can occur before prior exposure clears.
3. Dose-response and tolerability. GH/IGF-1 rose with dose; 125 and 250 mcg/kg had more adverse effects. The original paper described 30–60 mcg/kg as relatively better tolerated—that does not validate the modern 0.5–2 mg fixed-dose range.
4. Different research endpoints. Healthy-adult studies were short PK/PD experiments. Phase 2 targeted HIV-associated visceral obesity. None established a dose for bodybuilding, athletic recovery, sleep, general fat loss, or longevity.

Dosage evidence ladder

CJC-1295 DAC has more human PK/PD dosing data than many research peptides, but it still has no established treatment dose. Published studies demonstrate long-acting hormonal effects and accumulation across 20–250 mcg/kg exposures, while smaller 0.5–2 mg weekly protocols online have not been validated. Long-term efficacy and safety evidence is particularly weak because the only larger Phase 2 program was terminated and unpublished.

Dose escalation

Formal clinical escalation is documented only for the terminated Phase 2 HIV visceral-obesity study (once-weekly SC escalation over three weeks to a final assigned regimen). It was not designed for general research use.

Anecdotal escalation often starts at 0.5–1 mg weekly then moves to 1–2 mg. No original dose-finding source was identified. Because human research found roughly one-week half-life and cumulative exposure, an early increase may occur before steady exposure is apparent.

Safety findings relevant to dosage

In Teichman Study 1, adverse events were reported by 94% of active-drug participants and 29% of placebo participants. Most adverse effects were more common at 125 or 250 mcg/kg. FDA also highlighted potential immunogenicity, nonclinical DNA-damage signals, absence of long-term carcinogenicity studies, and theoretical pituitary hyperplasia/tumor risk from prolonged somatotroph stimulation. Because CJC-1295 DAC raises GH and IGF-1, available evidence is insufficient to rule out risks associated with other GH-axis drugs.

Editorial bottom line

The most defensible answer to “What is the CJC-1295 DAC dosage?” is that no approved treatment dose exists. Human research establishes a long half-life, dose-dependent GH/IGF-1 elevation, and accumulation at weight-based subcutaneous exposures. Smaller fixed weekly protocols online are real conventions—but not validated substitutes for trial doses—and must never be mixed with the short-acting “CJC-1295 no DAC” protocol landscape.

Confirm DAC vs no-DAC identity first. Then separate weight-based clinical exposures from anecdotal fixed weekly milligram conventions.

CJC-1295 DAC dosage FAQ

Primary and authoritative sources

• FDA

  Scientific Review of CJC-1295-Related Bulk Drug Substances

  December 2024.

• FDA PCAC

  December 4, 2024 Pharmacy Compounding Advisory Committee Meeting Minutes

  0–13 vote against 503A Bulks List inclusion for DAC forms.

• FDA

  Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks

  CJC-1295 compounding safety summary.

• Teichman SL et al.

  Prolonged stimulation of GH and IGF-1 secretion by CJC-1295

  Journal of Clinical Endocrinology & Metabolism, 2006.

• Ionescu M, Frohman LA

  Pulsatile GH secretion during continuous CJC-1295 stimulation

  Journal of Clinical Endocrinology & Metabolism, 2006.

• Sackmann-Sala L et al.

  GH/IGF-1-axis activation and serum protein changes

  Growth Hormone & IGF Research, 2009.

• ClinicalTrials.gov

  NCT00267527

  Phase 2 HIV visceral obesity; terminated; results unpublished.

• Jetté L et al.

  Identification of CJC-1295 as a long-lasting GRF analog

  Endocrinology, 2005.

• Alba M et al.

  CJC-1295 administration in GHRH-knockout mice

  American Journal of Physiology—Endocrinology and Metabolism, 2006.