CJC-1295 W/ Dac
CJC-1295 with DAC / Drug Affinity Complex
CJC-1295 W/ Dac (CJC-1295 with DAC / Drug Affinity Complex) is a gh & growth research compound. Long-acting GHRH analog; the DAC binds albumin so it sustains GH/IGF-1 elevation for days rather than pulsing.
CJC-1295 W/ Dac quick facts
| Reported research dose (Injectable) | 1mg-2mg |
| Route | Subq |
| Frequency | 1-2x Week |
| Half-life | ~6–8 days |
| Forms | Injectable |
| Evidence level | Human PK data |
| Other forms available | Oral — dosed differently |
The 'set-and-forget' GHRH — steady elevation. Different tool than the pulsatile no-DAC version.
How CJC-1295 W/ Dac works
Long-acting GHRH analog; the DAC binds albumin so it sustains GH/IGF-1 elevation for days rather than pulsing.
Proposed benefits
Sustained GH/IGF-1 elevation for recovery, sleep and lean-mass support.
Where to get CJC-1295 W/ Dac
CJC-1295 W/ Dac is sold in 2 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.
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 W/ Dac
Graded by what exists behind each claim.
✅ Clinically validated
- Phase 1 human trials published by ConjuChem showed sustained elevation of GH and IGF-1 for up to a week or more after a single dose, with dose-related increases. Development was discontinued.
- One death occurred in a trial of a related ConjuChem compound, which is frequently cited about CJC-1295 itself and is worth stating carefully: it was not this molecule, and the causal link was never established.
📊 Correlative data
- Used far less than the no-DAC version, and the reported reason is the mechanism rather than fashion — a week-long elevation produces more water retention, more numbness and tingling, and more of the lethargy people associate with a flat GH curve.
🧪 Theoretical / extrapolated
- The Drug Affinity Complex binds the peptide to serum albumin, extending its half-life from ~30 minutes to roughly 6–8 days.
- This is the clearest mechanism-versus-marketing case in the GH category. A continuous GH elevation is not a bigger version of a pulse — it is a different physiological state, it blunts the natural pulsatility that receptor sensitivity depends on, and it is the same continuous-signaling problem that shows up as insulin resistance with MK-677.
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 W/ Dac actually does
The DAC is one chemical group, and everything that separates this product from the version without it follows from that group’s reaction chemistry. The molecule is the same tetrasubstituted GHRH(1-29) analog with a lysine added at position 30, and on that lysine’s side chain a maleimidopropionic acid group. The doping-control description is exact: a 30-amino-acid peptide carrying a reactive maleimidopropionic acid group that covalently links the peptide to free thiols on the surface of plasma proteins Timms 2019.
Read the word ‘covalently’ carefully, because it is the whole page. A maleimide and a thiol undergo Michael addition to form a thioether — a carbon–sulfur single bond that does not come apart. Human serum albumin carries exactly one free cysteine, Cys34, and it is the most abundant free thiol in plasma. So the injected drug finds albumin and stays there. The clinical paper states it plainly: CJC-1295 binds permanently to endogenous albumin after injection Ionescu 2006.
This is categorically different from every other long-acting peptide in this Vault. Survodutide, cagrilintide, amycretin and the rest of the weekly incretins carry a fatty acid that binds albumin reversibly: the drug is in equilibrium between bound and free, exchanges continuously, and can in principle be displaced. This one is welded on. There is no equilibrium and nothing to displace.
The mass arithmetic, which explains the half-life better than the word ‘albumin binding’ does. The peptide core with the extra lysine and a C-terminal amide computes to 3,496.1 Da; the maleimidopropionyl group adds 151.1 Da after losing water in the amide bond, giving the unconjugated drug at about 3,647 Da. Albumin is roughly 66,500 Da. So the moment the thioether forms, the circulating species goes from 3.6 kDa to about 70 kDa — from well below the glomerular filtration cut-off to above it. The kidney stops seeing it. That single step, not any protease resistance, is why the half-life becomes 5.8 to 8.1 days Teichman 2006 and about 8 days in the second study Ionescu 2006, against roughly thirty minutes for the same peptide without the group.
And now the consequence, which is a real argument rather than a feature. Growth hormone is normally released in discrete pulses with near-empty troughs between them. A GHRH agonist that persists for a week does not produce pulses — it produces standing stimulation. The published measurement of what that does is the most important experiment this compound has, and it is discussed in full below.
Cell, rodent, human — and where it stops
Two human studies exist, both published in 2006, and between them they contain everything anyone knows about this molecule in a person.
Study one: dose, duration and accumulation. Healthy adults aged 21 to 61, four ascending single doses in the first protocol, then two or three weekly or biweekly doses in the second, over studies lasting 28 and 49 days. Growth hormone rose 2- to 10-fold for 6 days or more; IGF-I rose 1.5- to 3-fold for 9 to 11 days. The mean half-life was 5.8 to 8.1 days. After multiple doses, IGF-I remained elevated for up to 28 days, and the authors report evidence of a cumulative effect. Doses of 30 or 60 micrograms per kilogram were identified as safe; no serious adverse reactions were reported Teichman 2006.
Study two: the pulsatility experiment, and it is the one that should be read line by line. Healthy men aged 20 to 40, a single dose of 60 or 90 micrograms per kilogram, assessed one week after injection with 20-minute blood sampling across an overnight 12-hour period. Findings: basal GH up 7.5-fold (P < 0.0001); overall GH secretion up 46% (P < 0.01); IGF-I up 45% (P < 0.001); the frequency and magnitude of GH secretory pulses were unaltered; and no significant difference between the 60 and 90 microgram doses Ionescu 2006.
That is usually quoted as ‘pulsatility is preserved’, and it is — but look at which two numbers moved. Basal GH — the trough between pulses — went up 7.5-fold. Total GH secretion across twelve hours went up 46%. Pulse frequency and pulse height did not change at all. The extra growth hormone is almost entirely trough, not peak. The pulses are still there; the valleys between them have been filled in. That is a materially different physiological state from the one the pulses alone represent, and calling it ‘preserved pulsatility’ hides it.
Why filling in the troughs is not a neutral change — labeled as extrapolation, because that is what it is. Hepatic responses to growth hormone are pattern-sensitive as well as dose-sensitive: in rodents, the same total GH delivered in pulses versus continuously drives different hepatic gene programs, and it is the pattern rather than the amount that produces the sexually dimorphic expression difference. Nobody has tested whether a 7.5-fold trough elevation in a human shifts hepatic output in the same direction. It is a hypothesis, it is the most interesting question this compound raises, and it is answerable with markers that already exist.
The third result in that paper, which nobody quotes at all. IGF-I increases did not correlate with any parameter of GH secretion Ionescu 2006. So on this drug, IGF-1 is not a proxy for growth hormone exposure. Every protocol that tracks IGF-1 to infer ‘how much GH am I getting’ is resting on a correlation that the only study to look for it did not find.
What exists beyond those two papers is analytical. An immuno-PCR screen built specifically because conjugation to plasma protein prevents detection by top-down mass-spectrometry peptide screening detects the CJC-1295–protein conjugate down to 0.8 pg/mL, with a 50 pg/mL screening threshold in equine plasma Timms 2019; and an LC-MS/MS study of four GHRH analogs identified 19 major in vitro metabolites at limits of detection generally at or below 1 ng/mL Memdouh 2021.
The obstacles, one at a time. (1) Two human studies, both from 2006, longest 49 days Teichman 2006 Ionescu 2006. There is no modern human data, no phase 3, and no long-term follow-up of anyone. (2) The published doses are far above this site’s card. 30 to 90 micrograms per kilogram is 2.1 to 6.3 mg in a 70 kg adult; the card lists 1 to 2 mg. (3) The pulsatility study sampled one overnight window, one week after one injection Ionescu 2006 — it does not describe what twelve weeks of weekly dosing does to the same measurement. (4) Nothing has ever been measured past day 49, while IGF-1 was still elevated at day 28 after multiple doses Teichman 2006. (5) No body composition, no strength, no clinical endpoint of any kind was reported in either study.
CJC-1295 W/ Dac pharmacokinetics — how much of it actually gets in
This is the compound in this cohort whose pharmacokinetics are actually measured in humans, and the card’s ‘~6–8 days’ is close to right: the published figures are 5.8 to 8.1 days Teichman 2006 and about 8 days Ionescu 2006.
What holds it in the body, precisely. A thioether bond between the maleimide and a free plasma-protein thiol Timms 2019, with albumin’s Cys34 the overwhelmingly likely partner because it is the one free cysteine on the most abundant plasma protein. The conjugate is described as permanent Ionescu 2006. The consequence is a jump from 3,647 Da to roughly 70,000 Da, which puts the drug above the glomerular filtration threshold and removes renal clearance from the equation entirely.
What sets the ceiling, and why the observed half-life is shorter than that ceiling. Albumin itself turns over with a half-life of roughly 19 days. If the conjugate were cleared only by albumin turnover, the drug would last about that long. It lasts 5.8 to 8.1 days Teichman 2006, which means the peptide portion is being chewed off the carrier by plasma and tissue peptidases while the carrier itself survives. That difference — roughly two- to threefold — is the quantitative signature of proteolysis operating on a protected substrate.
What accumulation means in practice, with the published number. After multiple doses, IGF-I stayed elevated up to 28 days and the authors describe a cumulative effect Teichman 2006. At a 7-day half-life, weekly dosing reaches steady state at roughly twice the concentration a single dose produces, and four to five weeks are needed to get there. Two consequences follow directly: the first month under-represents the protocol, and stopping leaves a month of tapering exposure during which the axis is still being stimulated.
What degrades it. Peptidases acting on the peptide arm of the conjugate; no cytochrome involvement, so no metabolic drug interaction. The 19 major in vitro metabolites identified across this analog family Memdouh 2021 are the fragments of that process.
A chemistry point that belongs in a pharmacokinetics section. The maleimide is only reactive while it is intact. In water at neutral or slightly alkaline pH, maleimides hydrolyze to the corresponding maleamic acid, which no longer adds to a thiol. A vial reconstituted in bacteriostatic water and kept for weeks is therefore losing conjugation capacity on a clock nobody measures — and a molecule whose DAC has hydrolyzed is not a week-long drug at all. It is the short-acting peptide, at a dose chosen for the long one.
The oral barrier and the route. Absolute; subcutaneous. There is no oral form and there could not be one: the maleimide would react with the first thiol it met in the gut.
What would have to be true, and how you would know it was not
Four predictions. The second and third both argue against the way this compound is used.
1. IGF-1 should rise and stay risen for weeks after stopping. Draw IGF-1 at baseline, at day 7 after the first dose, at 6 weeks on protocol, and — the important one — at 4 weeks after the last injection. The published behavior is a 1.5- to 3-fold rise lasting 9 to 11 days from a single dose and elevation persisting up to 28 days after multiple doses Teichman 2006. A person who stops and retests a week later has not measured their off-drug baseline; they have measured the tail.
2. IGF-1 will not tell you how much growth hormone you are getting, and that cuts against the standard protocol. The only study that looked reported that IGF-I increases did not correlate with any parameter of GH secretion Ionescu 2006. So the falsifiable version is: if IGF-1 tracked GH exposure on this drug, people with the largest IGF-1 rises would report the largest effects, and the 2006 data predict they will not. Track both a symptom log and IGF-1 and expect them to disagree.
3. Fasting insulin should rise, and this is the cost of filling in the troughs. Growth hormone opposes insulin action at liver and muscle, and the physiological trough between pulses is when insulin sensitivity recovers. This drug raises basal GH 7.5-fold Ionescu 2006, which is precisely an attack on that recovery window. Draw fasting insulin and HbA1c at baseline, 6 and 12 weeks. A rising fasting insulin with a flat HbA1c is the early picture; it is the most predictable adverse metabolic consequence of this molecule and almost nobody measures it.
4. The trough test, which is the one experiment a single person can run that would be new. Draw serum growth hormone at a fixed mid-afternoon time — deliberately between expected pulses — before starting and again seven days after a dose. The prediction from the published data is a large rise in that trough value Ionescu 2006. A single random GH is uninterpretable on a normal person for exactly the reason that makes it interpretable here: the pulses are unchanged and only the baseline has moved.
What nobody has tested yet
Five experiments. The third one is a quality-control question that affects every vial sold and nobody has ever asked it.
1. Nobody has repeated the pulsatility study on a chronic protocol. The 20-minute overnight sampling was done once, one week after a single injection Ionescu 2006. Whether twelve weeks of weekly dosing still leaves pulse frequency and amplitude untouched, or whether the somatotroph flattens out under standing stimulation, is unmeasured — and it is the single most important question about a drug whose selling point is that it does not abolish pulses.
2. Nobody has measured the pattern-sensitive hepatic markers. If continuous GH signaling drives a different hepatic program from pulsatile GH, the human read-outs would be IGFBP-3, the acid-labile subunit, and SHBG, all of which are ordinary laboratory tests. None of them appears in either 2006 paper. Adding three assays to a design that already exists would turn a rodent hypothesis into a human result.
3. Nobody has measured the conjugation efficiency of a real vial. The DAC works only while the maleimide is intact, and maleimides hydrolyze in aqueous solution to a species that cannot conjugate. Nothing published describes how much intact maleimide survives lyophilization, shipping and two weeks in a refrigerator after reconstitution. A thiol-titration assay would answer it in an afternoon and would tell buyers whether they are receiving an 8-day drug or a 30-minute one at eight-day pricing.
4. Nobody has asked what else the maleimide reacts with. Its chemistry is not selective for albumin — it adds to any accessible thiol Timms 2019, and the plasma pool includes free cysteine, homocysteine, glutathione and the surface thiols of circulating cells. What fraction of an injected dose ends up on something other than albumin, and what those adducts do, has never been reported for this drug in any species.
5. Nobody has followed anyone past 49 days. Both human studies stopped there Teichman 2006, with IGF-1 still elevated at day 28 after multiple dosing. The community protocol is months to years. There is no published data on what a year of standing GHRH receptor stimulation does to the pituitary, to glucose handling, or to anything else.
CJC-1295 W/ Dac — its own safety story, not its class's
The class block on this page is written for growth-hormone secretagogues. Five things below belong to a covalently albumin-conjugated, week-long GHRH analog.
1. You cannot take it back. Every other long-acting peptide in this catalog binds albumin reversibly. This one forms a covalent thioether Timms 2019 and is described as binding permanently Ionescu 2006. If a person reacts badly to it, the response is not a matter of hours or of stopping the next dose: the drug is chemically attached to a carrier with a multi-day residence and IGF-1 stays elevated up to 28 days after multiple doses Teichman 2006. That asymmetry — fast to start, weeks to leave — is the defining safety property of this molecule and it is never stated on a vendor page.
2. The doses that were actually studied are two to three times the ones circulating. 30 to 90 micrograms per kilogram Teichman 2006 Ionescu 2006 is 2.1 to 6.3 mg in a 70 kg adult. This site’s card says 1 to 2 mg. The card is the conservative one here, and anyone scaling up toward the ‘studied’ dose should know that the study was 28 to 49 days long and reported no outcome beyond hormone levels.
3. The trough elevation is the risk, not the peak. Basal GH up 7.5-fold with pulses unchanged Ionescu 2006 means the insulin-sensitizing window between pulses has been closed. The predictable consequences of sustained GH exposure — rising fasting insulin, fluid retention, carpal tunnel symptoms, joint aching — are consequences of standing exposure specifically, and this is the form that produces it. The short-acting version on the previous page is not.
4. Maleimide chemistry is indiscriminate. The reactive group adds to free thiols on plasma proteins Timms 2019, and albumin is the most abundant target rather than the only one. Injecting a thiol-reactive electrophile weekly for months has no published safety characterization in humans at all — the two 2006 studies ran 28 and 49 days Teichman 2006.
5. What the record is, stated plainly. Two studies, one year, twenty years ago, in healthy adults, with hormone levels as the only endpoints, and no development program since. The compound is detectable in anti-doping testing down to 0.8 pg/mL as a protein conjugate Timms 2019, which matters for anyone competing. ‘Human PK data’ is a fair evidence tier for it — and PK data is not efficacy data, not safety data at duration, and not a reason to run it for a year.
Sources read for this page
- 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
- 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
- Memdouh S, et al. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Testing and Analysis 2021 · PMID 34665524
CJC-1295 W/ 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 W/ Dac — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What CJC-1295 W/ 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
- How the forms differ in dose
- 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 W/ Dac in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside CJC-1295 W/ Dac
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| IGF-1 (Insulin-like Growth Factor 1) | Multi-day half-life means SUSTAINED elevation, not pulses — IGF-1 runs higher |
| Fasting Insulin | Continuous GH costs more insulin sensitivity than pulsatile does |
| HbA1c (Hemoglobin A1c) | The three-month confirmation that the change is real |
| 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 W/ Dac — frequently asked questions
What is CJC-1295 W/ Dac?
CJC-1295 W/ Dac (CJC-1295 with DAC / Drug Affinity Complex) is a gh & growth research compound. Long-acting GHRH analog; the DAC binds albumin so it sustains GH/IGF-1 elevation for days rather than pulsing.
Is the full CJC-1295 W/ Dac protocol on this page?
The reported research dose is on this page, along with how CJC-1295 W/ 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 W/ Dac?
CJC-1295 W/ Dac has an approximate half-life of ~6–8 days, which is part of what determines how often it's dosed.
What's the evidence behind CJC-1295 W/ Dac?
Current evidence level: Human PK data. CJC-1295 W/ Dac is offered for research purposes only and is not an approved medicine.
What CJC-1295 W/ Dac is used for
CJC-1295 W/ Dac appears under 1 goal 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.