Reference

Last reviewed: 29 Apr 2026
Sources cited: 7

Compound class~3,367 Da (with DAC); ~3,358 Da (no-DAC)

Synthetic GHRH analogue — 30-residue modified GHRH(1-29)

30-residue peptide based on the first 29 amino acids of human GHRH with four stability-conferring substitutions (D-Ala²/Gln⁸/Ala¹⁵/Arg²⁷) and C-terminal amidation. The DAC variant adds a maleimidopropionic acid–lysine residue that covalently bonds to serum albumin, extending the plasma half-life from ~30 minutes to 6–8 days.

CJC-1295

Last verified: 2026-04-29

At a glance


Also known as	DAC:GRF (with DAC); Mod GRF 1-29 / Modified GRF / “no-DAC” (without DAC); ConjuChem CJC-1295 (developmental code)
Class	Synthetic GHRH analogue (30-residue modified fragment of human growth hormone-releasing hormone, residues 1–29)
Typical route	Subcutaneous injection. With DAC: 1–2× weekly. No-DAC: 1–3× daily.
Half-life	With DAC: 6–8 days (albumin-bound). No-DAC: ~30 minutes (free in plasma).1 2
Molecular weight	~3,367 Da (with DAC); ~3,358 Da (no-DAC)
Sequence / structure	Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-NH₂ (no-DAC). DAC variant adds a maleimidopropionic acid lysine residue that covalently bonds to circulating albumin.
UK status	Not approved. Sold as a research chemical.
US status	Same regulatory pathway as ipamorelin: removed from FDA Category 2 in September 2024; July 23–24 2026 PCAC meeting will review a larger peptide batch including CJC-1295. Currently in regulatory limbo.5

What it is

CJC-1295 is a modified version of the first 29 amino acids of human growth hormone-releasing hormone (GHRH), engineered to resist enzymatic degradation. It binds the GHRH receptor on pituitary somatotrophs and asks the pituitary to release growth hormone — a different mechanism from ipamorelin (which binds the ghrelin receptor) but a complementary one.

The compound exists in two forms that biohackers treat as essentially different drugs:

CJC-1295 with DAC (Drug Affinity Complex) — adds a lysine residue that covalently binds to circulating albumin, extending the plasma half-life from minutes to 6–8 days. Produces sustained, low-amplitude GH elevation rather than discrete pulses. Dosed once or twice weekly.
CJC-1295 without DAC (also called Modified GRF 1-29, or Mod GRF) — keeps the four amino-acid substitutions that resist degradation but lacks the albumin-binding modification. Plasma half-life is ~30 minutes. Produces a sharp GHRH pulse that resolves in 2–3 hours. Dosed 1–3 times daily.

The pharmacology of these two forms is so different that the practical questions — what to stack with, when to inject, what side-effect profile to expect, what the regulatory and safety story is — diverge meaningfully. The rest of this entry treats them in parallel where they differ and unifies them where they don’t.

CJC-1295 is not human growth hormone. Like ipamorelin, it triggers your pituitary to release more of its own GH; it doesn’t replace GH itself.

Mechanism

Both forms of CJC-1295 are agonists at the growth hormone-releasing hormone receptor (GHRH-R) on pituitary somatotrophs. GHRH-R activation drives Gs-coupled cAMP elevation, which depolarises somatotrophs and triggers GH exocytosis.

Three modifications differentiate the synthetic compound from native GHRH(1-29):

D-Ala at position 2 — resists dipeptidyl peptidase-IV (DPP-IV) degradation
Gln at position 8 — resists asparagine deamidation
Ala at position 15 — resists tryptic cleavage
Arg at position 27 — improves potency

The DAC modification is independent: a maleimidopropionic acid–lysine residue at position 30 covalently bonds to a free cysteine on serum albumin. This converts a small peptide (cleared by glomerular filtration in minutes) into an albumin–peptide complex (cleared on albumin’s much slower timescale, days).

The pharmacological consequence is the difference between the two forms:

No-DAC drives a brief GHRH receptor pulse that the pituitary translates into a discrete GH spike. The pituitary fully recovers between doses. Stack synergy with a GHRP (ipamorelin) is large because the two pulses arrive together and add through non-overlapping intracellular pathways.3
With DAC keeps GHRH-receptor occupancy elevated continuously for days. The pituitary shifts into a “GH bleed” state — sustained low-amplitude release rather than discrete pulses. This produces higher 24-hour mean GH and IGF-1 but flattens the natural pulsatile rhythm. The synergy with GHRP is smaller because the GHRH receptor is already partly desensitised when the GHRP pulse arrives.

This is the technical reason the standard stack pairs ipamorelin with no-DAC, not with DAC. The pulsatile GH pattern that drives the synergy depends on the GHRH receptor being available at injection time, which the no-DAC variant preserves and the DAC variant doesn’t.

Routes of administration

Subcutaneous injection (the standard route)


Bioavailability	Sufficient to drive GHRH pulse / sustained albumin-bound elevation depending on form
Onset (no-DAC)	GH pulse peaks ~30 min post-injection; resolves 2–3 hours
Onset (DAC)	Plasma elevation builds over ~24 hours; steady state ~3–4 weeks of weekly dosing
Duration (no-DAC)	2–3 hours per dose
Duration (DAC)	Continuous over 6–8 days per dose
Typical dose (this route)	No-DAC: 100–300 mcg per injection, 1–3× daily. DAC: 1–2 mg per injection, 1–2× weekly.
Equipment	Insulin syringe (29G–31G, U-100), bacteriostatic water, alcohol wipes
When this route makes sense	Default and standard. Both forms were studied subQ in clinical work.

For no-DAC, bedtime or pre-bed dosing dominates the same way it does for ipamorelin — fasted, aligned with the natural night-time GH pulse, paired with ipamorelin.

For DAC, timing matters less per-injection because the half-life smooths the elevation across days. Some users inject Sunday and Wednesday for steadier coverage; others inject once weekly and accept slightly higher peak-to-trough variation.

Intramuscular injection


Bioavailability	Comparable to subQ; absorption faster
Onset	Slightly faster
Duration	Same total elimination window
Typical dose (this route)	Same as subQ
When this route makes sense	Rarely chosen. SubQ is easier and equivalent in effect.

Oral / sublingual / intranasal

Not viable for either form. CJC-1295 is GI-degraded; sublingual absorption is unreliable for a 30-residue peptide; intranasal absorption is too low to deliver effective doses.

Cross-route comparison

SubQ for both forms. The route question for CJC-1295 is not which administration route to use; it’s which form (DAC vs no-DAC) to use, what to pair it with, and when to inject relative to meals.

What the evidence says

Honest summary: the GHRH-receptor pharmacology is well-characterised and short-term studies showed dose-dependent GH/IGF-1 elevation with adequate tolerability. The DAC variant’s Phase 2 lipodystrophy program was discontinued after a death from myocardial infarction in a treated patient, and no further sponsor-led clinical development has been brought forward for either form.

Pharmacokinetic and short-term efficacy data (well-supported)

ConjuChem’s original work (Teichman et al., 2006) characterised CJC-1295 with DAC in healthy adults: weekly subQ dosing produced sustained dose-dependent increases in GH and IGF-1 over 28 days, with the 60 mcg/kg dose producing roughly 2–3× baseline IGF-1 elevation. The compound was tolerated at this duration.2

PK is dose-proportional, half-life is consistent across studies (~5.8–8.1 days for DAC; ~30 minutes for no-DAC), and the GHRH-receptor selectivity is mechanistically clean.

Phase 2 lipodystrophy trial in HIV patients (2006; one death; discontinued)

ConjuChem ran a 12-week Phase 2 trial of CJC-1295 with DAC in 192 HIV patients with lipodystrophy. One patient died of acute myocardial infarction approximately 2 hours after receiving the 11th weekly dose. Investigation found the patient had asymptomatic coronary artery disease with plaque rupture and occlusion. The attending physician concluded the death was most likely unrelated to treatment.2

The program was discontinued. ConjuChem did not bring CJC-1295 to Phase 3. No subsequent sponsor has run a registrational program for either form.

This matters editorially for the same reason ipamorelin’s failed ileus trial does: the most-completed clinical work for CJC-1295 ended at Phase 2, with a serious cardiac event in the active group, and no sponsor has been willing to take the next step. Officially the death is attributed to pre-existing CAD; the timing is also consistent with a treatment-related effect. Both reads are honest; the regulatory record is silent on which is correct.

What the evidence does NOT show

No long-term human safety data. The longest published controlled study is 28 days (DAC) or single-dose (no-DAC). Multi-month or multi-year safety is unknown.
No outcome trials in healthy biohackers. No body composition, recovery, sleep, or longevity outcome data exists for either form.
No head-to-head with HGH.
No characterisation of receptor desensitisation with chronic use, especially for the sustained-elevation DAC profile, where the mechanism would predict it most strongly.
No comparative trial of DAC vs no-DAC. The choice between forms is mechanistically argued but not empirically measured.

The compound’s pharmacology is real. The downstream claims — body composition, recovery, sleep depth, longevity — rest on inference from GH biology generally, not on direct evidence for CJC-1295.

Typical use patterns

No-DAC + ipamorelin (the dominant stack)

This is the standard GH-secretagogue protocol in the biohacker space. Pairing the GHRH-receptor pulse from no-DAC with the ghrelin-receptor pulse from ipamorelin produces 3–5× higher GH release than either alone at the same doses.3

Standard bedtime stack:

No-DAC CJC-1295: 100–300 mcg
Ipamorelin: 100–300 mcg
Same syringe, same injection
2–3 hours after the last meal
1× daily, usually before bed

Many users start at 100 mcg of each, twice daily (morning fasted + bedtime fasted) and stay there for a full cycle before considering 200 mcg per injection. The morning dose is harder to keep fasted in practice; users who can’t reliably fast in the morning typically drop to once-daily bedtime dosing rather than dose fed.

Cycling: 5 days on, 2 days off weekly, plus longer cycles of 3–6 months on / 1–2 months off. Same precaution as ipamorelin against theoretical receptor desensitisation; same lack of evidence for whether it’s necessary.

DAC monotherapy (the sustained-GH approach)

Users who want continuous GH/IGF-1 elevation rather than discrete pulses run CJC-1295 with DAC alone, typically:

1–2 mg subQ once or twice weekly
No ipamorelin co-injection (the synergy doesn’t apply once the GHRH receptor is sustainably occupied)
Cycle length: 8–16 weeks per protocol, with 4–8 week breaks

This pattern is less common than no-DAC + ipamorelin. The case for it is convenience (one injection a week vs daily) and stronger 24-hour mean IGF-1 elevation; the case against it is the loss of natural pulsatility, the larger fluid-retention side-effect profile that comes with sustained elevation, and the cardiac signal from the discontinued Phase 2 trial.

DAC + ipamorelin (uncommon, mechanistically weaker)

Rare and not generally recommended. The sustained GHRH-receptor occupancy from DAC desensitises the pathway that makes GHRP synergy work. Some users layer DAC weekly with ipamorelin daily, but the GH-pulse arithmetic favours no-DAC for the same total injection burden.

Duration and monitoring

8–12 week cycles for body-composition or recovery-focused use; longer for sustained sleep-quality / longevity-focused protocols. IGF-1 testing every 8–12 weeks is a useful concrete marker for users who want to see whether their stack is doing anything measurable — this is the most accessible objective signal.

Stacking beyond ipamorelin

BPC-157 / TB-500: common pairing during recovery phases. No documented interactions.
NAD+ precursors, MOTS-c: common in longevity stacks. No documented interactions.
Other GHRH analogues (sermorelin, tesamorelin): redundant — same receptor — and the longer-acting tesamorelin is closer pharmacologically to DAC than to no-DAC.
HGH: redundant; users with HGH access don’t need a secretagogue.

For sensitive systems

CJC-1295 sits in similar tolerability territory to ipamorelin for sensitive-systems users — better than older GHRPs because it doesn’t drive cortisol/prolactin, but with its own profile to watch.

Form choice matters here. No-DAC’s pulsatile pattern is closer to physiological; DAC’s sustained elevation is more likely to drive water-retention symptoms, sustained joint stiffness, and the broader profile of “chronic mild GH/IGF-1 elevation.” For sensitive-systems users who want to try a GHRH-class compound, no-DAC is the more cautious starting point.

Start dose for sensitive users.

No-DAC: 100 mcg subQ at bedtime, paired with 100 mcg ipamorelin. Hold for 1–2 weeks.
DAC: not recommended as a starting compound for this audience. If trying DAC anyway, 0.5 mg weekly (half the standard 1 mg starting dose) for 4 weeks before considering increase.

Ramp. No-DAC follows the ipamorelin ramp pattern: 200 mcg / 200 mcg after 1–2 weeks if tolerated. DAC: from 0.5 mg → 1 mg weekly with a 4-week hold at each step. Receptor adaptation to DAC is slower than to no-DAC because the elevation is sustained rather than pulsatile.

Expected adjustment profile (both forms):

Mild headache in the first few days — vasoactive, GH/IGF-1-driven fluid shifts. Usually resolves in a week.
Tingling, numbness, or carpal-tunnel-like sensations — same fluid-retention mechanism as ipamorelin. More common with DAC than no-DAC because the elevation is sustained.
Joint stiffness or fullness in the morning — fluid retention plus IGF-1-driven soft-tissue effects. Reverses with dose reduction.
Vivid dreaming in the first 1–2 weeks — common.
Mild flushing at injection — usually local, transient.
DAC-specific: blood pressure modest elevation in some users — has been reported in community use; not consistently quantified.

What’s not normal and warrants stopping: sustained headache, persistent paraesthesia that doesn’t reverse on dose reduction, blood pressure elevation that doesn’t normalise, chest discomfort or atypical chest sensations (the cardiac signal from the discontinued Phase 2 program means this needs to be taken seriously, especially in the DAC variant). Users with any cardiovascular risk factors should treat new chest symptoms as a stop signal.

For MCAS / histamine-sensitive users. No specific histamine activity documented. The receptor target (GHRH-R) is not directly mast-cell-relevant.

For POTS users. Fluid retention is the relevant concern, more so with DAC. Monitor for orthostatic worsening in the first 2 weeks of any new dose level. POTS users should strongly prefer no-DAC over DAC because the pulsatile pattern produces less sustained fluid-retention pressure.

For UARS / chronic fatigue / ME/CFS. Same logic as ipamorelin: GH-pulse-driven sleep architecture changes are the most defensible benefit. No-DAC + ipamorelin is the protocol with the best community-reported sleep-quality signal in this audience. DAC’s flattened pattern produces less of the night-time pulse architecture.

For cardiovascular risk. Special caution for both forms. The 2006 trial death was a CAD-related MI — officially attributed to pre-existing disease, but the timing was treatment-related. Users with known coronary artery disease, prior MI, significant CAD risk factors (especially uncontrolled hypertension, hyperlipidaemia, diabetes), or strong family history of premature MI should treat CJC-1295 — particularly the DAC variant — as a relative contraindication in the absence of cardiac workup.

For active or recent cancer history. Same relative contraindication as ipamorelin. GH/IGF-1 axis stimulation is theoretically mitogenic for some tumour types. No specific cancer evidence either way for CJC-1295, but the mechanism warrants cautious posture, particularly for breast, prostate, colon, and GH/IGF-1-responsive endocrine tumours; MEN syndromes; and strong family history without active screening.

Interactions worth considering:

HGH: redundant; do not stack.
Other GHRH analogues: redundant.
GHRP-2, GHRP-6, hexarelin: redundant with ipamorelin and remove its selectivity advantage.
Insulin / metformin / GLP-1 agonists: GH transiently raises blood glucose. In well-controlled users this is usually subclinical.
Steroids: exogenous corticosteroids blunt GHRH-driven GH pulse response.
SSRIs, SNRIs, LDN, beta-blockers: no documented interactions.

Reasonable expectations

Onset. Both forms produce measurable GH elevation within hours of the first injection. Subjective sleep quality changes (deeper, more vivid dreams, easier wake-ups) typically appear within 1–2 weeks of consistent dosing. Body composition or recovery effects, if they appear, take 6–12 weeks.

Response rate. Sleep-quality signal is the most consistently reported subjective effect across the GH-secretagogue category — rough community signal of ~70% reporting clear sleep change with no-DAC + ipamorelin. Body-composition response is more variable.

What the evidence actually supports.

GH and IGF-1 elevation in healthy adults — strongly supported in published short-term work (28 days for DAC; single-dose for no-DAC).
Dose-proportional kinetics — supported.
Tolerability over weeks — supported with the cardiac caveat above.

What the evidence does not support.

Body composition outcomes at any specific magnitude — not measured.
Recovery, sleep, or training-adaptation outcomes — not measured.
Anti-ageing or longevity claims — entirely speculative.
Comparative claims between DAC and no-DAC — argued mechanistically; not measured.

What not to expect.

HGH-equivalent effects. Both forms produce a GH pulse pattern; HGH delivers sustained elevation at therapeutic doses. The body-composition effects of HGH are larger and faster.
Effects without proper timing (no-DAC). Fed dosing blunts the GH pulse substantially.
Effects without the stack (no-DAC). No-DAC alone produces less effect than no-DAC + ipamorelin; the synergy is the reason for the pairing.

Cost

CJC-1295 is not available through licensed UK pharmacy channels. No NHS or private-prescription pricing to quote.

On the grey market:

No-DAC 5 mg vials: ~£20–55. 10 mg vials: ~£35–80.
With-DAC 2 mg vials: ~£25–60. 5 mg vials: ~£50–110.
Combined ipamorelin + CJC-1295 no-DAC blend vials (typically 5 mg + 5 mg or 10 mg + 10 mg): ~£35–100.

Monthly cost at standard doses (research-chem, vendor-neutral estimate):

No-DAC + ipamorelin stack at 200 mcg of each daily, 5 days/week: ~£40–100/month
DAC monotherapy at 1 mg weekly: ~£25–55/month

The DAC monotherapy path is generally cheaper than the no-DAC + ipamorelin stack because of the dosing frequency, but the cost difference is small compared to the pharmacological differences and the cardiac-signal concern that should drive the choice.

Sensitive-start economics. A user starting at 100 mcg of no-DAC + 100 mcg ipamorelin once daily uses half the compound, extending vial life proportionally.

Reconstitution

This section covers reconstitution of research-chemical CJC-1295 (both forms). The math is the same as ipamorelin; the differences are in target dose ranges, vial sizes, and how often the dose is delivered.

What’s in the box

Research-chemical CJC-1295 ships as lyophilised white powder in a glass vial:

No-DAC: typically 5 mg or 10 mg per vial.
With DAC: typically 2 mg or 5 mg per vial (smaller vials are more common because per-injection doses are larger and weekly dosing means a vial gets used up fast).

You’ll also need the same equipment as for ipamorelin: BAC water, U-100 insulin syringe, larger transfer syringe, alcohol wipes.

The math

No-DAC, 5 mg vial, 2 mL BAC water (the standard for the ipamorelin stack)

Concentration: 2.5 mg/mL (2,500 mcg/mL)
100 mcg = 0.04 mL = 4 units (right at the readability floor; consider 1 mL BAC for sensitive-start)
200 mcg = 0.08 mL = 8 units
300 mcg = 0.12 mL = 12 units

No-DAC, 10 mg vial, 4 mL BAC water (for users running 200 mcg twice daily)

Concentration: 2.5 mg/mL (same as the 5/2 setup, just more total drug per vial)
200 mcg = 0.08 mL = 8 units

With DAC, 5 mg vial, 2 mL BAC water

Concentration: 2.5 mg/mL
1 mg weekly = 0.4 mL = 40 units
1.5 mg weekly = 0.6 mL = 60 units
2 mg weekly = 0.8 mL = 80 units

With DAC, 2 mg vial, 1 mL BAC water

Concentration: 2 mg/mL
1 mg weekly = 0.5 mL = 50 units
The whole vial is two weekly doses.

Combined no-DAC + ipamorelin blend, 10 mg vial (5 mg of each), 3 mL BAC water

Concentration: ~1.67 mg/mL of each (~3.33 mg/mL total)
200 mcg of each = ~0.12 mL = 12 units delivers both peptides in one draw.

The Peptrax Vial Plan calculator handles the same math interactively — enter your vial size, BAC volume, and dose, and it returns draw volume and doses per vial.

Reconstitution procedure

Wipe the rubber stopper of the lyophilised vial and the BAC water vial with alcohol.
Draw the chosen volume of BAC water into the larger syringe.
Insert the needle into the lyophilised vial at an angle, with the tip touching the inside wall above the powder. Inject the water slowly down the inside of the vial, not directly onto the powder. Forcing water onto lyophilised peptide can denature it.
Leave the vial undisturbed for 1–2 minutes. Do not shake. Gently swirl if needed; the powder dissolves on its own.
Once the solution is clear, label the vial: compound, form (DAC vs no-DAC), concentration, reconstitution date. The label matters — a no-DAC dose injected from a DAC vial is a 30× overdose of the DAC compound.
Store refrigerated (2–8°C / 36–46°F).

Some practitioners pass the reconstituted solution through a 0.22 µm syringe filter as a belt-and-braces sterility step. Optional rather than standard.

Storage and stability

Both forms reconstituted with BAC water are stable for roughly 4 weeks refrigerated, with the same conservative/middle/optimistic spread:

Conservative: 14–21 days
Middle: 28 days (the most commonly cited figure)
Optimistic: ~30 days

The honest middle is 28 days at 2–8°C. Store at the back of the refrigerator. Do not freeze.

If you reconstitute with plain sterile water instead of BAC water, the vial is single-use — discard within 24 hours.

For no-DAC at 200 mcg/day stacked daily, a 5 mg vial is 25 doses ≈ 5 weeks of theoretical doses, just over the 4-week stability window. Buy smaller vials or accept some product loss. For DAC at 1 mg/week, a 5 mg vial is 5 weeks; small loss expected at conservative stability windows.

What gets miscalculated

Confusing no-DAC and DAC. The dose ranges differ by 10× (mcg vs mg). Mistakenly drawing a no-DAC dose volume from a DAC vial delivers roughly 10× the intended dose. Label vials clearly with the form.
mg vs mcg. No-DAC dosing is in mcg. 200 mcg = 0.2 mg, not 200 mg.
Reading “units” as mg. 8 units on a U-100 syringe is 0.08 mL of solution.
Ignoring the fasted-dosing requirement (no-DAC). Same as ipamorelin: a fed dose blunts the GH pulse substantially.
Stacking DAC with ipamorelin. Mechanically possible but mechanistically weaker than no-DAC + ipamorelin; users who stack DAC with ipamorelin often blame poor results on the GHRP rather than on the form mismatch.

Areas of concern ⚠

The cardiac signal from the discontinued Phase 2 program

A patient died of acute myocardial infarction approximately 2 hours after the 11th weekly dose in the 2006 ConjuChem Phase 2 lipodystrophy trial in HIV patients. The attending physician concluded the death was most likely unrelated to treatment, attributing it to pre-existing asymptomatic CAD; the program was discontinued anyway.2 For the DAC variant especially, this single trial event is the central safety story — no Phase 3 has been brought forward by any sponsor since.

The official attribution is “pre-existing CAD with plaque rupture, unrelated to treatment.” The timing — a treated patient, 2 hours post-dose, eleventh weekly dose meaning steady-state albumin-bound peptide — is also consistent with a treatment-mediated effect. The trial was not large enough or long enough to disambiguate. No subsequent sponsor has run a registrational program for either form, so the cardiac safety question has not been re-examined under controlled conditions.

For users with known CAD, prior MI, significant cardiovascular risk factors, or strong family history of premature MI: the DAC variant in particular should be treated as relative contraindication in the absence of cardiac workup. No-DAC’s much shorter duration of action makes the per-dose exposure smaller but does not eliminate the underlying GH/IGF-1 cardiovascular question.

Long-term safety is uncharacterised

Longest published controlled study is 28 days. Multi-month or multi-year safety in healthy users is unknown for either form. Mechanistic concerns from sustained GH/IGF-1 elevation:

IGF-1 elevation is broadly anabolic but theoretically mitogenic for GH/IGF-1-responsive tumour types.
GH transiently antagonises insulin; chronic effects on insulin sensitivity in healthy users not characterised.
Sustained GHRH-receptor occupancy (DAC variant) may downregulate receptors over months. The rationale for cycling is theoretical.

Cancer / tumour-growth concern

Same framing as ipamorelin: the mechanism (GH/IGF-1 elevation) is plausibly mitogenic for some tumour types. CJC-1295 specifically has not been studied in cancer populations, but the mechanism is the same as exogenous HGH, which is contraindicated in active or recent cancer.

Treat as a relative contraindication for:

Active malignancy of any type
Recent (within ~5 years) malignancy of GH/IGF-1-responsive types — breast, prostate, colon, certain endocrine tumours
Multiple Endocrine Neoplasia syndromes
Strong family history of GH/IGF-1-responsive cancers without screening in place

Quality and sourcing

Standard research-chem caveats. No batch testing at point of sale, variable purity, occasional under-potency or contamination, no MHRA oversight. Combined ipamorelin + no-DAC blend vials are widely sold and convenient but obscure the per-peptide concentration; users tracking dose precisely should reconstitute separately.

The DAC variant is also sometimes mis-supplied as no-DAC by careless or fraudulent vendors — meaning a user attempts no-DAC daily dosing using actual DAC powder, which would produce sustained elevation. The reverse error (DAC supplied as no-DAC) is rarer because DAC is generally more expensive per mg. Lab-test certificates from third-party mass spec are the meaningful quality signal where available.

Populations where CJC-1295 is contraindicated or high-risk

Active or recent cancer history (relative contraindication; see above)
Active or significant cardiovascular disease — special concern for DAC variant; relative contraindication without workup
Active acromegaly or known pituitary adenoma
Pregnancy and breastfeeding — no safety data
Under 18 — endogenous GH is already at peak; no use case
Type 1 diabetes — GH antagonises insulin
Severe insulin resistance / poorly-controlled type 2 diabetes — same concern, smaller margin
Sleep apnoea (untreated) — GH/IGF-1 effects on soft tissue may worsen airway collapse

Measurement and dosing pitfalls

DAC vs no-DAC confusion is the highest-impact dosing error specific to this compound. Label vials clearly. Per-injection doses differ by ~10×.
mg vs mcg confusion — 1 mg = 1,000 mcg.
Reading units as mg — units are a volume mark on the syringe, not a mass.
Skipping the form difference in dosing schedules — applying DAC weekly cadence with no-DAC produces underdosing; applying no-DAC daily cadence with DAC produces overdose stacking.
Stacking DAC with ipamorelin and expecting the synergy — the mechanism doesn’t apply.

What the community gets wrong

“DAC is just longer-lasting CJC.” It’s pharmacologically a different mode of GH stimulation — sustained elevation rather than pulsatile spikes. The downstream physiological effects are not equivalent.
“No-DAC and DAC are interchangeable, just dose different amounts.” They’re not. Stack pairing differs. Side-effect profiles differ. Cardiac-risk profiles plausibly differ.
“The 2006 death was definitely unrelated.” It was officially attributed to pre-existing CAD. The trial was not large enough to settle the question. “Probably unrelated, but the program ended there and no one has rerun it” is the honest read.

FDA / regulatory status

Jurisdiction	Status	Last verified
US (FDA)	Compounding grey zone. Removed from Category 2 in September 2024. July 23–24 2026 PCAC meeting scheduled to review a larger peptide batch including CJC-1295 (Federal Register notice published April 16 2026). Active legal challenge: Evexias and Farmakeio lawsuit under the Administrative Procedure Act. As of late April 2026, compounding pharmacies operate in regulatory uncertainty pending PCAC review.	2026-04-29
UK (MHRA)	Not approved. No licensed product. Sold as a research chemical under “research use only / not for human consumption” labelling, which permits sale of the raw peptide but does not authorise human use.	2026-04-29
EU (EMA)	Not approved. No licensed product.	2026-04-29
WADA (sport)	Prohibited. Listed under S2 (Peptide Hormones, Growth Factors, and Related Substances). In and out of competition. Detection: GHRH analogues are detectable in urine via mass spectrometry; the DAC variant’s albumin-bound form has a longer detection window.	2026-04-29

Narrative. The US compounding-pharmacy pathway for CJC-1295 (and ipamorelin) is in active flux. The September 2024 Category 2 removal narrowed legal compounding access; the July 2026 PCAC meeting is the next inflection point. For UK readers, no licensed pathway exists in any direction — research-chemical purchase remains the only access route, with the standard legal grey area. For athletes, both forms are clearly prohibited; the DAC variant’s detection window is longer than no-DAC’s.

What to track in Peptrax

A “CJC-1295” entry without DAC vs no-DAC specification is missing the single most important attribute — the two forms have different dosing schedules, different side-effect profiles, and different stack pairings. Logging the form first, then concentration and dose schedule (daily for no-DAC; weekly for DAC), is the bare minimum for any CJC-1295 protocol to be meaningfully reviewable later.

For most users, the highest-signal log overlaps with ipamorelin: subjective sleep quality and morning state across the first 4–8 weeks. Because no-DAC + ipamorelin is the dominant stack, the question the app should help answer is “is this stack doing anything for me, and is it the synergy or one of the components?” Users who run no-DAC alone for 2–3 weeks and then add ipamorelin (or vice versa) get the cleanest read on whether the pairing matters for their physiology specifically — sequential rather than simultaneous introduction makes the attribution possible.

For sensitive-systems users, the priority log shifts to the first 2–3 weeks of dosing: water-retention symptoms (rings tighter, hands puffy, carpal-tunnel-like tingling), morning joint stiffness, blood-pressure changes, any chest or cardiovascular symptoms. The cardiac-signal concern from the discontinued Phase 2 program means new chest discomfort or pressure is a stop signal, not a wait-and-see. A written stop criterion before starting matters for both forms.

For users running DAC, an objective IGF-1 measurement at 8–12 weeks gives the most accessible “is this working” signal. IGF-1 elevation is the most-measured outcome in the published short-term work and the easiest biomarker to track at home with a private blood test. Logging the dose, the cycle position, and the IGF-1 result alongside subjective notes is the closest a research-chem CJC-1295 user can get to outcome data on themselves.

For personal tracking and informational purposes only — not medical advice.