CJC-1295 No Dac
Mod GRF 1-29
CJC-1295 No Dac (Mod GRF 1-29) is a gh & growth research compound. Short-acting GHRH analog — creates a clean, natural GH pulse without the sustained bleed of the DAC version.
CJC-1295 No Dac quick facts
| Reported research dose | 100mcg-500mcg |
| Route | Subq |
| Frequency | 1-3x Daily AM/Workout/PM · 5 On 2 Off or Daily |
| Half-life | ~30 min |
| Forms | Injectable |
| Evidence level | Human PK data |
Pulse, don't flood. Pair with a GHRP and time it fasted / pre-bed.
How CJC-1295 No Dac works
Short-acting GHRH analog — creates a clean, natural GH pulse without the sustained bleed of the DAC version.
Proposed benefits
A clean, pulsatile GH release for recovery, sleep and body composition.
Where to get CJC-1295 No Dac
Buy CJC-1295 No Dac at Ion Peptide →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for CJC-1295 No Dac
Graded by what exists behind each claim.
✅ Clinically validated
- Published human pharmacokinetic work exists on modified GRF (1-29) — this molecule — establishing that it raises GH and IGF-1 in humans and how long it lasts. No efficacy trial for any body-composition or ageing endpoint.
📊 Correlative data
- The GHRH half of the standard stack, used almost universally alongside a ghrelin agonist. Reported experience is of a clean GH pulse with the characteristic flush and slight lightheadedness in the first minutes.
- The naming is a persistent source of error in the community: 'CJC-1295 no DAC' and 'modified GRF 1-29' are the same peptide, and it behaves nothing like the DAC version.
🧪 Theoretical / extrapolated
- A GHRH analog with four amino-acid substitutions that resist enzymatic breakdown, giving a ~30-minute half-life rather than minutes.
- That short action is the design, not a limitation. It produces a discrete pulse that mimics physiological GH release and then clears, which is what keeps negative feedback intact — the mechanistic argument for it over the DAC version, which does not.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What CJC-1295 No Dac actually does
This molecule is Mod GRF (1-29), and its four substitutions are the entire content of the page. The parent is human GHRH(1-29) amide — Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-NH2, the shortest fragment of the 44-residue hormone that retains full activity at the receptor. This analog changes four positions: D-Ala at 2, Gln at 8, Ala at 15, Leu at 27. Run both through this site’s peptide chemistry: the native 29-mer amide is 3,357.9 Da, the substituted one 3,368.0 Da, both with an isoelectric point of 10.95 and a computed net charge of about +3.9 at blood pH. This is a strongly basic polycation, and that fact reappears in the safety section.
Each substitution has one job, and they are not interchangeable.
D-Ala at position 2 is the one that matters. Dipeptidyl peptidase-4 cuts after position 2 when position 2 is an alanine or a proline — which in native GHRH it is — releasing an inactive GHRH(3-29). Swapping the L-alanine for its D enantiomer leaves the same atoms in a mirror-image arrangement the protease active site cannot accommodate. One stereocentre closes the fastest degradation route this peptide has.
Gln at 8 removes a chemical liability rather than a proteolytic one. Native position 8 is asparagine, followed by serine at 9. Asn-Ser is a textbook deamidation hotspot: the asparagine side chain cyclizes to a succinimide and hydrolyzes to aspartate or iso-aspartate, changing the molecule’s charge in the vial without any enzyme involved. Glutamine, one carbon longer, does not cyclize the same way.
Ala at 15 is about shape. Native position 15 is glycine, the strongest helix-breaking residue in the alphabet because it has no side chain to restrict backbone rotation. The GHRH receptor is a class B1 GPCR and binds its ligand as an alpha-helix threaded into the transmembrane bundle. Replacing glycine with alanine adds a methyl group and raises helix propensity at the hinge of that helix.
Leu at 27 removes the only methionine. Methionine is the residue that oxidizes to the sulfoxide on contact with air, light or trace metals. Leucine is isosteric with methionine and cannot oxidize. The molecule loses its shelf-life liability without changing shape.
What it does at the receptor, and what it cannot do. The GHRH receptor sits on pituitary somatotrophs, couples to Gs, raises cAMP, activates PKA and drives both immediate GH release and GH gene transcription. Crucially, it is a throttle, not an override: somatostatin from the hypothalamus closes the same cells, and during a somatostatin trough no amount of GHRH agonism produces a pulse. That is why a short-acting GHRH analog amplifies existing pulses instead of creating a plateau, and it is the mechanical difference between this molecule and the DAC-conjugated one on the next page. It is also a different receptor entirely from the ghrelin receptor that GHRP-2 and GHRP-6 work through.
One naming point that is a chemistry point. Doping-control chemistry treats ‘CJC-1295’ and ‘CJC-1295 with drug affinity complex’ as two different analytes, studied alongside sermorelin and tesamorelin as four distinct GHRH analogs Memdouh 2021. They are not one product at two strengths.
Cell, rodent, human — and where it stops
Say the count first: there are zero published human studies of this molecule. Not a phase 1, not a pharmacokinetic study, not a case series. Every human number attached to the name ‘CJC-1295’ belongs to the DAC conjugate Teichman 2006 Ionescu 2006, which is a different molecule with a different half-life, and this site’s own card carries ‘Human PK data’ as the evidence tier for both.
What does exist, and it is analytical rather than clinical. A liquid chromatography–tandem mass spectrometry study of sermorelin, tesamorelin, CJC-1295 and CJC-1295 with DAC identified 19 major in vitro metabolites across the four and achieved limits of detection generally at or below 1 ng/mL, the WADA required performance limit Memdouh 2021. That work establishes that the molecule exists, that it is degraded to identifiable fragments, and that it is detectable — and it measures nothing about what it does in a person.
The nearest clinical relatives, named honestly. Sermorelin is GHRH(1-29) amide with no substitutions; tesamorelin is a hexenoyl-modified GHRH(1-44) analog. Both have been through regulatory review as medicines; both were studied as GHRH receptor agonists in humans. Neither is this molecule, and the four substitutions above are exactly the difference. Borrowing sermorelin’s clinical record for Mod GRF (1-29) is the same move as borrowing the DAC conjugate’s — it just sounds more reasonable.
What a short-acting GHRH analog predicts, from the physiology. Growth hormone is released in roughly 6 to 10 pulses per 24 hours, the largest arriving in early slow-wave sleep, with near-undetectable troughs between them; the pulse pattern is generated by reciprocal GHRH and somatostatin tone. An agonist present for about 30 minutes can only act inside whichever window it lands in. That is the mechanistic case for injecting it before sleep, and it is a hypothesis rather than a result — no published study has compared bedtime with daytime administration of this molecule, because no published study has administered this molecule at all.
The obstacles, one at a time. (1) Zero human data under this molecule’s own name, so every dose, every timing rule and every expected IGF-1 response circulating for it is inference. (2) The four substitutions are argued from chemistry — DPP-4 specificity, deamidation, helix propensity, methionine oxidation — and none of them has been shown to extend this peptide’s measured half-life in any species. (3) The GHRH receptor is downstream of a pituitary that somatostatin can close, so response is expected to vary with sleep, feeding and age in ways no study of this compound has characterized. (4) The community protocol — 100 to 500 micrograms, subcutaneous — has no published dose-ranging behind it in any species.
CJC-1295 No Dac pharmacokinetics — how much of it actually gets in
The card says ~30 minutes. Here is what has to be true behind that number, and what still clears it that fast.
What was closed. D-Ala at position 2 blocks dipeptidyl peptidase-4, which is the fastest single route of attack on this sequence and the reason native GHRH(1-29) is measured in minutes rather than tens of minutes.
What was left open, and this is the part nobody states. The molecule is 3,368 Da. The glomerular filtration barrier passes molecules up to roughly 60 kDa, with efficient passage well below about 30 kDa; this peptide is nearly ten times smaller than the loosest version of that cut-off and carries a net charge of about +3.9, which the negatively charged glomerular basement membrane does not repel. So it is freely filtered, and it is not bound to anything that would hold it in the vascular compartment. Blocking one protease does not change that. Renal filtration, plus endopeptidases the substitutions do not protect against, is what sets a half-life of tens of minutes.
The exposure arithmetic, which is the useful part. If the half-life is about 30 minutes, a single subcutaneous dose is essentially gone in 2 to 2.5 hours — five half-lives. Injected once daily, the compound is present for roughly 10% of the day and absent for the other 90%. Against 6 to 10 GH pulses in 24 hours, one dose can amplify one, perhaps two of them. Every claim about this compound has to fit inside that budget, and most marketing claims do not.
A practical consequence people get wrong. Because it is gone in about two hours, a serum growth hormone drawn three hours after an injection is measuring the pituitary’s baseline, not the drug. If you want to see this peptide work, the draw is at 20 to 30 minutes. And because IGF-1 integrates GH exposure over roughly a day, a peptide occupying two hours of that day moves it far less than the DAC form does.
The oral barrier. Absolute. A 29-residue peptide carrying four positive charges meets gastric acid, pancreatic endopeptidases, brush-border peptidases and hepatic first-pass extraction; the charge alone rules out passive transcellular absorption. No oral or nasal bioavailability figure has ever been published for it.
The injectable route. Subcutaneous, which removes gut and first-pass liver and does not remove plasma peptidases or the kidney. Nothing published states the absorption rate from a subcutaneous depot for this molecule, so even the 30-minute figure is an expectation rather than an observation.
What would have to be true, and how you would know it was not
Three predictions. The first one says this compound will barely move the marker everybody buys it to move.
1. IGF-1 will move much less than people expect, and that cuts against the product. Draw IGF-1 at baseline and after 6 weeks, from the same laboratory, at the same time of day, because between-assay variation on this analyte is large enough to invent a result on its own. The prediction is a change of well under the 1.5- to 3-fold rise the DAC conjugate produced in humans Teichman 2006 — because IGF-1 is an integral of GH exposure across the day and this molecule occupies about a tenth of it. A user who sees a doubling of IGF-1 on a 30-minute peptide should ask what is actually in the vial before congratulating themselves.
2. The identity test, and it is decisive. Draw serum growth hormone immediately before an injection and again 20 to 30 minutes after it. A GHRH analog that is present and active produces a visible rise inside that window; a vial of bacteriostatic water does not. This is the one measurement on this page that distinguishes a working product from an empty one in a single morning, and it is not on anybody’s protocol sheet.
3. Fasting insulin and HbA1c should not move, and if they do the form is wrong. Growth hormone antagonizes insulin action, so sustained GH elevation raises fasting insulin and can nudge HbA1c. A peptide present for two hours a day should not produce sustained elevation at all. Draw fasting insulin and HbA1c at baseline and 12 weeks and expect a flat line. Movement here is the signature of continuous GH exposure — which is what the DAC conjugate produces and what this molecule is specifically chosen to avoid.
What nobody has tested yet
Five experiments, and the first is embarrassing in how easy it would be.
1. Nobody has ever measured this peptide in human plasma. There is no published time to peak, no maximum concentration, no half-life and no bioavailability for Mod GRF (1-29) by any route. The analytical chemistry is already solved — the same laboratories that detect it for doping control have the assay and reach 1 ng/mL or better Memdouh 2021. Eight volunteers, one dose, ten timepoints, and the number that this whole compound’s protocol rests on would exist.
2. Nobody has run it against sermorelin head-to-head. Sermorelin is the identical 29-residue sequence without the four substitutions. One crossover study with GH sampling would say what the substitutions actually buy in a person, and it would settle whether the chemistry argument on this page translates into anything.
3. Nobody has tested the timing rule. Injecting before sleep to catch the dominant slow-wave pulse is the standard instruction and it has never been compared with morning dosing in a controlled way for this molecule. Overnight 20-minute GH sampling — the exact design already used on the DAC form Ionescu 2006 — would answer it in one night per arm.
4. Nobody has published a mass spectrum of a vendor vial. Native GHRH(1-29) amide is 3,357.9 Da and the substituted analog is 3,368.0 Da — a 10 Da difference that any modern mass spectrometer resolves easily, and the DAC conjugate is 3,647 Da, which is not even close. Three lots from three vendors would produce the first compositional data this product has ever had.
5. Nobody has asked whether repeated daily pulses desensitize the somatotroph. The receptor is a class B1 GPCR and every one of them internalizes after agonist exposure. Whether a once-daily 30-minute stimulus at 100–500 micrograms leaves the pituitary less responsive after twelve weeks is unmeasured, and it is the mechanism by which a compound stops working without anybody being able to say so.
CJC-1295 No Dac — its own safety story, not its class's
The class block on this page is written for growth-hormone secretagogues generally. Four things here are specific to a short-acting, strongly basic GHRH analog with no human record.
1. The flush has a mechanism, and it is the peptide’s charge. Computed isoelectric point 10.95, net charge about +3.9 at blood pH. Strongly cationic peptides are the classic trigger for non-immunological mast cell degranulation through MRGPRX2, which releases histamine without any antibody being involved. That is a coherent explanation for the warmth, facial flushing and head-rush reported within a minute or two of injection, it explains why the reaction is immediate rather than delayed and why it happens on the first exposure, and it predicts that injecting more slowly and in a smaller volume reduces it. It is an inference from peptide chemistry, not a published finding for this molecule.
2. The real risk is that the dose is set by nothing. With zero published human studies of this molecule, the 100 to 500 microgram protocol has no dose-ranging behind it. That is a different kind of risk from toxicity: the compound may be too small a dose to do anything, or several times more than needed, and the published record cannot distinguish those.
3. The identity risk, and it is unusually consequential here. The market uses ‘CJC-1295’ for both this molecule and the DAC conjugate, which doping chemistry treats as separate analytes Memdouh 2021 — the conjugate carrying a maleimidopropionic acid group that bonds it covalently to a plasma protein thiol Timms 2019. Getting the conjugate when you wanted this one converts a 30-minute exposure into a 5.8-to-8.1-day one Teichman 2006 at whatever dose you had planned for the short form. The masses differ by 279 Da and no vendor publishes one.
4. What the GH axis makes off-limits, and why it applies less here. The standard cautions for this axis — active malignancy, proliferative retinopathy, uncontrolled diabetes — are driven by sustained IGF-1 elevation, and sustained elevation is precisely what a two-hour daily exposure is least likely to produce. That is an argument for this form being lower risk than the conjugate, not for it being risk-free, and it is undermined entirely if the vial contains the conjugate.
Sources read for this page
- Memdouh S, et al. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Testing and Analysis 2021 · PMID 34665524
- Timms M, et al. An immuno polymerase chain reaction screen for the detection of CJC-1295 and other growth-hormone-releasing hormone analogs in equine plasma. Drug Testing and Analysis 2019 · PMID 30489688
- Teichman SL, et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. Journal of Clinical Endocrinology and Metabolism 2006 · PMID 16352683
- Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. Journal of Clinical Endocrinology and Metabolism 2006 · PMID 17018654
CJC-1295 No Dac — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not 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
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.
- 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 analog (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 analogs together is paying twice for one lever.
Don't run this if
- Active or recent malignancy — the IGF-1 reasoning above.
- Diabetes or poor glycemic 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.
CJC-1295 No Dac — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What CJC-1295 No Dac moves on your bloodwork
Expected direction, not a measured one.
- 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.
Everything above follows from one fact: these raise GH and therefore IGF-1. Nothing here needs a trial of the specific molecule.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- 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
Everything above is free and stays free. Skool is where it becomes a plan — CJC-1295 No Dac in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside CJC-1295 No Dac
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| IGF-1 (Insulin-like Growth Factor 1) | Short half-life preserves pulsatility — a smaller rise than DAC, by design |
| Fasting Insulin | Still the trade, just a smaller one than with DAC |
| HbA1c (Hemoglobin A1c) | Slower confirmation |
| Comprehensive Metabolic Panel (CMP) | Fasting glucose and organ 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 103 markers A–Z
CJC-1295 No Dac — frequently asked questions
What is CJC-1295 No Dac?
CJC-1295 No Dac (Mod GRF 1-29) is a gh & growth research compound. Short-acting GHRH analog — creates a clean, natural GH pulse without the sustained bleed of the DAC version.
Is the full CJC-1295 No Dac protocol on this page?
The reported research dose is on this page, along with how CJC-1295 No Dac works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of CJC-1295 No Dac?
CJC-1295 No Dac has an approximate half-life of ~30 min, which is part of what determines how often it's dosed.
What's the evidence behind CJC-1295 No Dac?
Current evidence level: Human PK data. CJC-1295 No Dac is offered for research purposes only and is not an approved medicine.
What CJC-1295 No Dac is used for
CJC-1295 No Dac appears under 2 goals in the goal router.
Related GH & Growth compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.