CJC No Dac/Ipamorelin
CJC-1295 (no DAC) + Ipamorelin
CJC-1295 (No DAC) + Ipamorelin is the most popular growth-hormone stack in the peptide world — a GHRH paired with a GHRP that hit the GH axis through two different receptors for a bigger, cleaner pulse than either alone. This guide breaks down how CJC-1295 works, the crucial DAC vs No-DAC difference, why it's stacked with Ipamorelin, dosing references, safety and legal status.
CJC No Dac/Ipamorelin quick facts
| Reported research dosing | 200mcg-600mcg |
| Route | Subq |
| Cycle length | 3-6 Months |
| Frequency | 1-3x Daily AM/Workout/PM · 5 On 2 Off or Daily |
| Half-life | Short (both components) |
| Forms | Injectable |
| Evidence level | Human PK on components |
The classic GH-support pairing. Timing beats dose — fasted and before bed.
How CJC-1295 works
CJC-1295 is a synthetic analog of growth-hormone-releasing hormone (GHRH). It binds GHRH receptors on the pituitary's somatotroph cells, activates adenylate cyclase and raises intracellular cAMP — which prompts the pituitary to release a pulse of your own growth hormone. Because it works upstream on your own gland (rather than replacing GH like injected HGH), it preserves natural feedback regulation.
DAC vs No-DAC — the key difference
This is the single most important thing to understand about CJC-1295. DAC (Drug Affinity Complex) binds the peptide to serum albumin, stretching its half-life to roughly 6–8 days — so one dose keeps GH and IGF-1 elevated for days (dosed ~1–2× weekly). No-DAC (also called Modified GRF 1-29) has a short half-life of about 30–60 minutes, producing a sharp, brief pulse that clears fast.
Most people prefer No-DAC precisely because it's more physiologic — it creates a natural spike-and-clear pulse rather than the constant, non-physiologic GH elevation DAC produces. That pulsatile pattern is why No-DAC is the version paired with Ipamorelin.
Why it's stacked with Ipamorelin
Ipamorelin is a GHRP (ghrelin-receptor agonist) — a different receptor from CJC-1295's GHRH receptor. Combining a GHRH (CJC-1295 No-DAC) with a GHRP (Ipamorelin) produces a synergistic GH pulse larger than the sum of either alone: CJC amplifies the amount of GH released while Ipamorelin triggers the release cleanly, without the cortisol/prolactin bump of older GHRPs. That's why this specific pairing is the classic, go-to GH stack.
Dosing (research reference)
Because No-DAC CJC-1295 is short-acting, the literature references it dosed alongside Ipamorelin, often 1–3× daily and frequently timed around sleep or fasting to align with natural GH pulses. It's supplied as a lyophilized powder, reconstituted with bacteriostatic water — the calculator above converts a research amount into syringe units. This summarizes existing references for education only, not dosing advice or a recommendation for human use.
Safety & side effects
Common reported effects mirror GH-axis stimulation: water retention, tingling/numbness, head-rush or flushing (more with No-DAC's sharp pulse), and possible effects on insulin sensitivity and blood sugar. The bigger-picture caution is that raising GH and IGF-1 is not risk-free — higher IGF-1 has been linked to certain cancer risks and can fuel existing tumors, so this is not something to take casually. Long-term human safety data is limited and research-market purity varies.
Comparisons & related
This stack sits alongside the oral secretagogue MK-677 (which raises GH/IGF-1 for ~24h with more appetite and fluid retention) and the FDA-approved GHRH analogs Sermorelin and Tesamorelin. CJC + Ipamorelin is favored for its clean, synergistic, pulsatile profile.
Legal & regulatory status
CJC-1295 and Ipamorelin are not FDA-approved and are sold as research compounds (research use only). GH secretagogues are also banned in competitive sport under WADA. Compounding status is subject to ongoing FDA review. Follow the laws and sport rules that apply to you.
✅ Clinically validated
- No trial of the combination. The components are separately characterised in humans — CJC-1295 without DAC (modified GRF 1-29) has published PK, and ipamorelin reached phase 2 — but nobody has run the pair against placebo, so the synergy is inferred rather than demonstrated.
📊 Correlative data
- The most-used peptide stack in practice, by a wide margin. The reported pattern is consistent enough to be worth something: deeper sleep in the first fortnight, recovery and skin changes over one to three months, body-composition change slowest of all.
- Beyond that, the record is self-reported. Community dosing logs are real information about tolerability and nothing at all about efficacy: nobody posts the cycle where they felt no different, so what survives is a filtered sample that will always look better than the truth.
🧪 Theoretical / extrapolated
- Two different receptors, one outcome. The GHRH analogue raises the amplitude of the GH pulse; the ghrelin agonist increases pulse frequency and blunts somatostatin. Combining them is predicted to produce a bigger pulse than either alone, which is the mechanistic case for the stack and the reason it is dosed at night, when the natural pulse already occurs.
- The same logic predicts the ceiling: this amplifies a pulse, so it does little for someone whose pituitary output is genuinely gone.
These tiers tell you how much human evidence exists — not how well something works. This is the research space, and most of what’s in here is new rather than disproven. Something sitting at “theoretical” usually means nobody has funded the trial, not that the trial was run and failed.
The trap runs the other way too: something can be clinically validated and still do very little for you specifically. A statistically significant result in a study population is not a promise about your body.
- ✅ Clinically validated — human randomised trials or meta-analyses support it. The strongest footing available.
- 📊 Correlative — observational or epidemiological data. Suggestive, and genuinely useful for direction, but it cannot establish cause.
- 🧪 Theoretical / mechanistic — the mechanism is understood and often demonstrated in cells or animals, and the human trial doesn’t exist yet. Unproven is not the same as ineffective. Plenty of what’s standard practice today sat here five years ago.
✗ is a safety flag, not a grade. Where you see it, the concern is harm — not a disappointing trial. A compound tested for one purpose and found not to help there can still be worth studying somewhere else, so a negative result never gets rendered as a cross. It sits alongside the tier, because something can be both well-studied and genuinely risky.
My job is to tell you which one you’re looking at, and let you make the call. Grading something low isn’t me dismissing it — it’s me refusing to oversell it. This is the research space, and being able to reason forward from a mechanism matters as much as waiting for the trial.
CJC No Dac/Ipamorelin — safety, predicted from mechanism
Much of this compound class has never been through a human safety trial. Rather than say nothing — or print a generic warning — this is what its known mechanism predicts could go wrong, and what you can do about it. Predictions are labelled as predictions.
What the mechanism predicts
Derived from what this molecule does, not from a trial.
- Everything here follows from one fact: these raise GH and therefore IGF-1. The predicted problems are the known consequences of elevated GH/IGF-1, drawn from acromegaly and clinical GH therapy where it HAS been studied — insulin resistance and rising fasting glucose, fluid retention (puffy hands and face, and the ring that stops fitting), carpal tunnel symptoms from that same fluid pressing on the median nerve, and joint aches.
- The proliferation question is the serious one. IGF-1 is a growth signal, and growth signals do not distinguish between tissue you want to grow and tissue you do not. There is no evidence these compounds cause cancer. There is also a clear mechanistic reason not to run them with an active or recent malignancy, and that reasoning does not require a trial to be sound.
What has actually been reported
- Injection-site reactions, transient flushing, tingling and head-rush on dosing — most commonly with the GHRPs, which also release cortisol and prolactin at higher doses.
- Increased hunger is near-universal with the ghrelin-mimetic ones (GHRP-6, MK-677, Hexarelin). That is the mechanism working, not a side effect — the same receptor drives GH release and appetite.
How to reduce the risk
Each of these follows from the same mechanism as the prediction.
- Draw an IGF-1 baseline BEFORE you start. Once you are on, that number is the drug and you have permanently lost the comparison. This is the single highest-value thing on this list and it costs one blood draw.
- Watch fasting glucose and HbA1c, not the scale. Insulin resistance is the most likely thing to move and the one you cannot feel. Re-test at 8–12 weeks. If fasting glucose is climbing, that is your signal to cut the dose or come off — long before anything shows up symptomatically.
- Dose at night, on an empty stomach. GH release is pulsatile and largest during early sleep; food, and carbohydrate in particular, blunts the pulse through insulin. This is not a ritual — it is the same mechanism working with you rather than against you.
- Don't run a secretagogue through a high-carbohydrate surplus. The predicted problem is insulin resistance; adding a large carb load is pushing the same lever from the other end.
- Cycle rather than run continuously. Most of the predicted problems — fluid retention, carpal tunnel, glucose drift — are dose-and-duration dependent and reverse on cessation. Time off is the cheapest safety intervention available.
- If fluid retention is the issue, it usually resolves on a dose reduction long before it needs anything else. Reach for the dose before you reach for a diuretic.
What it does to your bloodwork
A fact about the assay, not a guess about the drug.
- IGF-1 drawn on-cycle is not your baseline — it is the drug working, and it will read high. If you want a real baseline, draw before starting or after a proper washout.
- Watch fasting glucose and HbA1c, because insulin resistance is the most likely thing to move and the one you will not feel.
- GHRP-6 and Hexarelin can raise prolactin and cortisol; if you are chasing an unexplained prolactin result, this is a candidate.
What it overlaps with
- Stacking two secretagogues that work by the same route is redundancy, not synergy. A GHRH analogue (CJC-1295, Sermorelin, Tesamorelin) plus a ghrelin mimetic (Ipamorelin, GHRP-2, GHRP-6) is the deliberate pairing — two different levers on the same axis. Two GHRH analogues together is paying twice for one lever.
Don't run this if
- Active or recent malignancy — the IGF-1 reasoning above.
- Diabetes or poor glycaemic control, unless you are monitoring fasting glucose and HbA1c and know what you are looking at.
- Untreated diabetic retinopathy.
The honest unknown
- Nobody has run long-term studies of intermittent secretagogue use in healthy adults. The specific unmeasured thing is what years of repeatedly pushing IGF-1 above your natural set point does — not whether a single cycle is tolerable, which it evidently is.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Fasted — and pre-bed is the best of the windows
Food is the problem here, and specifically carbohydrate and fat. Both trigger somatostatin release, and somatostatin is the brake on growth hormone — eating before the injection pharmacologically cancels it. Two clear hours either side.
Pre-bed is the strongest window because the largest natural GH pulse happens in the first hours of deep sleep, so you are stacking with it rather than asking the pituitary for something it is not primed for. Fasted pre-training is the second-best, for the same reason in a different rhythm.
Derived from half-life, route and mechanism — not from a dosing trial. Reasoned, and labelled as reasoned.
CJC No Dac/Ipamorelin reconstitution calculator
Research reconstitution calculator
Where to get CJC No Dac/Ipamorelin
Buy CJC No Dac/Ipamorelin at AminoWell USA →CJC No Dac/Ipamorelin — interference & stacking
Predicted from mechanism, not from an interaction study. There are no trials of these combinations — what follows is what the biology implies, so treat it as a reason to watch something, not as a finding.
What CJC No Dac/Ipamorelin moves on your bloodwork
These are the markers this compound is expected to move, and which direction. Knowing that in advance is mostly about NOT panicking: some of these moving is the compound working.
- IGF-1 (Insulin-like Growth Factor 1) — ↑ expected to rise
This is the point. IGF-1 rising is the compound doing its job — it is the stable downstream readout of a GH pulse.
What to do: Test it before you start and again at 6–8 weeks. It is the only number that tells you whether the product was real and the dose was enough. - Growth Hormone, Serum — ✕ unreliable here
A random GH level is close to meaningless here. GH is secreted in pulses during deep sleep and sits undetectable between them, so a daytime draw catches a trough almost every time — including when the compound is working perfectly.
What to do: Do not use GH to judge a secretagogue. Read IGF-1 instead. - Fasting Insulin — ↑ expected to rise
GH is a counter-regulatory hormone: it opposes insulin. Fasting insulin and glucose drifting up is the predicted trade-off, not a surprise.
What to do: Check fasting insulin and HbA1c at baseline and again at 8–12 weeks. This is the marker that decides whether you keep running it. - HbA1c (Hemoglobin A1c) — ↑ expected to rise
Same mechanism, longer window — a slow drift rather than a jump.
What to do: Pair it with fasting insulin; either alone can mislead. - Free T4 (Thyroxine) — ↓ expected to fall
GH accelerates the peripheral conversion of T4 to T3, so free T4 can fall while free T3 holds or rises. Read alone it looks like new hypothyroidism, and it usually isn't.
What to do: Run a full thyroid panel rather than TSH alone before concluding anything.
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Get the complete breakdown for CJC No Dac/Ipamorelin — inside the Academy alongside the full interactive Vault.
Unlock in the Academy — $10/mo →Everything above follows from one fact: these raise GH and therefore IGF-1. Nothing here needs a trial of the specific molecule.
Bloodwork to run alongside CJC No Dac/Ipamorelin
Run these before you start, and again after 8–12 weeks. A baseline you didn’t take is one you can never go back for.
| Marker | What it’s watching for |
|---|---|
| IGF-1 (Insulin-like Growth Factor 1) | The number that actually tracks your GH exposure — dose by this, not by feel |
| Fasting Insulin | GH raises insulin resistance; this moves before glucose does |
| HbA1c (Hemoglobin A1c) | The slower confirmation that the insulin change is real |
| Comprehensive Metabolic Panel (CMP) | Fasting glucose, and liver and kidney at baseline |
The Running GH Peptides or MK-677 panel covers these in one order — 9 markers, $132.30 with the discount applied.
Check results you already have → · All 102 markers A–Z
CJC No Dac/Ipamorelin — frequently asked questions
What is CJC-1295 / Ipamorelin?
It's a growth-hormone stack: CJC-1295 is a GHRH analog that tells the pituitary to release GH, and Ipamorelin is a GHRP that triggers a clean GH pulse. Together they act on two receptors for a larger, synergistic pulse of your own growth hormone.
What's the difference between CJC-1295 with DAC and no DAC?
DAC binds the peptide to albumin, extending its half-life to ~6–8 days (constant, non-physiologic GH). No-DAC has a ~30–60 minute half-life, giving a sharp, natural pulse. No-DAC is preferred for being more physiologic and is the version paired with Ipamorelin.
Why stack CJC-1295 with Ipamorelin?
They hit different receptors — CJC (GHRH) amplifies how much GH is released, Ipamorelin (GHRP) triggers the release cleanly. The combination produces a bigger GH pulse than either alone, without the cortisol/prolactin spike of older GHRPs.
How is CJC-1295 / Ipamorelin dosed?
The No-DAC version is short-acting, so the literature references dosing it with Ipamorelin 1–3× daily, often around sleep or fasting. It's reconstituted with bacteriostatic water — use the calculator above. This is educational, not dosing advice.
What are the side effects of CJC-1295 / Ipamorelin?
Reported effects include water retention, tingling, and flushing, plus possible effects on blood sugar. The key caution is that raising GH/IGF-1 carries theoretical cancer-related risk, so it isn't casual. Long-term human data is limited.
Is CJC-1295 / Ipamorelin FDA-approved?
No — both are sold as research compounds and are not FDA-approved. GH secretagogues are also banned in competitive sport under WADA.
References & further reading
- CJC-1295 with DAC vs without DAC — differences (Revolution Health)
- CJC-1295 protocol, dosage & research guide (Path to Peptides)
- CJC-1295: complete guide to the GHRH analog (No DAC vs DAC)
Want Coach Cam's exact CJC No Dac/Ipamorelin protocol?
Dosing schedules, stacking, cycle timing and my personal notes live inside the Academy — plus the full interactive Vault of 237 compounds & 350 supplements.
Join the Academy — $10/mo →What CJC No Dac/Ipamorelin is used for
CJC No Dac/Ipamorelin appears under 3 goals in the Vault’s goal router, grouped by the mechanism it works through rather than by how much trial evidence exists. Each link opens that pathway in full, with the alternatives beside it and the bloodwork that tests it.