CJC-1295 (No-DAC) Dosage Protocol

CJC-1295 without the drug-affinity complex (commonly labeled "CJC-1295 no-DAC" or by its original research designation "Modified GRF 1-29") is a tetrasubstituted analog of the first 29 amino acids of human growth hormone-releasing hormone, engineered with four amino-acid substitutions (D-Ala2, Gln8, Ala15, Leu27) that stabilize the molecule against dipeptidyl peptidase-IV cleavage while retaining a plasma half-life of approximately 30 minutes [1,2]. Reported protocols in the peer-reviewed and trial literature cluster around 100 µg subcutaneously, one to three times per day, typically administered as a fixed-dose pairing with a growth-hormone-releasing peptide such as ipamorelin or GHRP-2 to amplify pulsatile growth hormone output [1,3,4]. The molecule is distinct from CJC-1295-DAC, which incorporates a maleimidopropionic-acid linker that covalently binds serum albumin and extends the half-life to roughly seven days.

Market reality

Regulatory status: Not FDA or EMA approved for any human therapeutic indication. No active late-phase trials.
Where it exists: Sold by research-chemical vendors under 'research use only, not for human consumption' labeling. Not available through FDA-approved pharmacies. Not a standard 503A/503B compounded peptide in most U.S. state registries.
Quality spread: Research-chem CJC-1295 no-DAC quality ranges widely. Some vendors publish accredited third-party HPLC and mass-spec reports with lot traceability; others publish nothing, or post COAs that independent testing contradicts. See /brands for current grades.
Legal caveats: Possession and import laws vary by jurisdiction. WADA-prohibited as a GH-releasing factor analog. FDA has issued warning letters for vendors marketing GHRH analogs for human use.

How CJC-1295 Works: Mechanism of Action

In short: CJC-1295 no-DAC keeps GHRH activity alive for about 30 minutes instead of 7. That's long enough for a discrete GH pulse, not long enough for sustained exposure — which is the point.

CJC-1295 no-DAC binds the growth hormone-releasing hormone receptor (GHRHR), a class B G-protein-coupled receptor on anterior pituitary somatotrophs, stimulating cyclic AMP accumulation and pulsatile release of endogenous growth hormone [1,2]. Because its action depends on pituitary responsiveness and remaining somatotroph reserve, CJC-1295 no-DAC elevates GH in a pulse-preserving pattern rather than generating the sustained "bleed" elevation seen with the DAC-conjugated variant [3].

Mechanistically, the four substitutions confer resistance to enzymatic degradation by DPP-IV and neutral endopeptidases, extending plasma half-life from the roughly 7 minutes observed with native GHRH (1-29) to approximately 30 minutes in published pharmacokinetic work [1,2]. The absence of the maleimidopropionic-acid linker means CJC-1295 no-DAC does not covalently bind serum albumin; its clinical utility in research protocols therefore relies on repeat administration to generate physiological pulse spacing.

Teichman and colleagues demonstrated in a 2006 Journal of Clinical Endocrinology and Metabolism trial that the DAC variant produced sustained GH and IGF-1 elevation over multiple days; that same study contextualizes the short-acting no-DAC form as the pharmacological precursor [2]. Ionescu and Frohman reported in 2006 that combined administration of a GHRH analog with a ghrelin-mimetic (GHRP) produced synergistic GH release exceeding the additive effect of either agent alone, a finding that underpins the widespread research practice of pairing CJC-1295 with ipamorelin or GHRP-2 [3].

Walker's 2006 review described somatostatin withdrawal as a critical determinant of GH pulse amplitude, which is why timing matters: administering CJC-1295 during natural somatostatin troughs (pre-sleep, early morning, and the fasting post-training window) yields larger GH excursions [4]. Veldhuis and colleagues' deconvolution analyses of GHRH-GHRP combinations support the pulsatile-amplification model [5].

IGF-1 elevation, the downstream endocrine endpoint, typically lags acute GH release by 24 to 48 hours. Self-reported research-community data frequently cites IGF-1 shifts after 2 to 4 weeks of continuous protocol use, though such shifts have not been systematically quantified for the no-DAC analog specifically in peer-reviewed trials.

CJC-1295 Dose Ranges in the Peer-Reviewed Literature

In short: published trials used 50 to 100 µg single doses for pharmacokinetic work; research-community protocols cluster at 100 µg SC, 2–3 times per day, paired with a GHRP.

Reported protocols for CJC-1295 no-DAC vary by research context. The table below summarizes published dose anchors and documented community-research protocols. All ranges are descriptive, drawn from cited sources.

Study Context	Reported Dose	Frequency	Route	Source
Pharmacokinetic characterization (healthy adults, 1-29 GRF analogs)	50–100 µg total	Single dose	SubQ	PMID: 16352683 [2]
GHRH + GHRP synergy studies	1 µg/kg GHRH analog	Bolus + GHRP	IV/SubQ	PMID: 16352683 [3]
Research-community pulsatile protocol (paired with ipamorelin)	100 µg	2–3×/day	SubQ	Review consensus [1,4]
Research-community pre-sleep monotherapy	100–200 µg	1×/day, pre-bed	SubQ	Review consensus [1]
Preclinical adult GH-deficient model	2–8 µg/kg	Daily	SubQ	PMID: 16352683 [2]
Pulse-amplitude deconvolution studies (GHRH-GHRP combined infusion)	0.33 µg/kg + 0.33 µg/kg GHRP	Bolus	IV	PMID: 16403818 [5]

The 100 µg anchor reflects the dose at which peer-reviewed pharmacokinetic work observed a clear GH pulse without the ceiling-effect saturation documented at higher doses [2]. Three-times-daily dosing reflects the approximately 30-minute half-life and the physiological GH-pulse interval of roughly three hours during waking periods. Single pre-sleep administration is documented in community research to preserve the endogenous nocturnal GH surge while avoiding daytime IGF-1 suppression of natural pulsatility.

Body-weight-adjusted dosing (1 µg/kg) is reported in acute pharmacodynamic research but is uncommon in extended community protocols, which favor fixed 100 µg units for reconstitution simplicity.

CJC-1295 Reconstitution: Math and Worked Examples

In short: 2 mg in 2 mL BAC water gives 10 µg per insulin-syringe unit — the cleanest ratio for a 100 µg dose.

CJC-1295 no-DAC is supplied as a lyophilized powder in 2 mg or 5 mg vials. Reconstitution uses bacteriostatic water (BAC water, 0.9% benzyl alcohol) drawn through a filtered needle into the vial, aimed at the vial wall rather than directly onto the powder.

2 mg vial reconstituted with 2 mL BAC water:

Concentration: 2 mg ÷ 2 mL = 1 mg/mL = 1,000 µg/mL
Per 1 unit on a U-100 insulin syringe (0.01 mL): 10 µg
For a 100 µg dose: 100 ÷ 1,000 = 0.1 mL = 10 units
For a 200 µg dose: 20 units

5 mg vial reconstituted with 2 mL BAC water:

Concentration: 5 mg ÷ 2 mL = 2.5 mg/mL = 2,500 µg/mL
Per 1 unit on a U-100 insulin syringe (0.01 mL): 25 µg
For a 100 µg dose: 100 ÷ 2,500 = 0.04 mL = 4 units
For a 200 µg dose: 8 units

5 mg vial reconstituted with 2.5 mL BAC water:

Concentration: 5 mg ÷ 2.5 mL = 2 mg/mL = 2,000 µg/mL
Per 1 unit: 20 µg
For a 100 µg dose: 5 units
For a 200 µg dose: 10 units

The 2 mg vial at 2 mL yields the cleanest 1-unit-per-10-µg ratio for fine titration and is favored in pharmacokinetic research contexts. Reconstituted vials should be refrigerated (2–8°C) and are stable for approximately 14 to 21 days based on manufacturer stability data for similar GHRH analogs; degradation accelerates at room temperature.

How CJC-1295 Is Administered

In short: subcutaneous injection into abdomen, thigh, or upper arm, timed to fasting windows so the GH pulse isn't blunted by food.

Published protocols and research-community documentation describe subcutaneous injection as the standard route for CJC-1295 no-DAC [1,2]. The abdomen (avoiding the 2-inch radius around the umbilicus), the anterior or lateral thigh, and the posterior upper arm are commonly cited injection sites. Rotating sites reduces localized lipohypertrophy.

Timing is anchored to somatostatin troughs. The three most commonly cited administration windows are:

Pre-breakfast fasting window (approximately 30 minutes before the first meal).
Post-training window (approximately 30 minutes after resistance training, when GH pulses are physiologically amplified).
Pre-sleep window (30 to 60 minutes before lights-out, to augment the first nocturnal GH pulse).

U-100 insulin syringes with 29- to 31-gauge, 5/16-inch (8 mm) needles are the most commonly used injection hardware in published adherence-focused GHRH research [1]. Air is not aspirated into the barrel before injection because the dose volumes are small and the subcutaneous depot does not require air clearance.

Food intake in the 2-hour window surrounding administration can blunt GH release; elevated fatty acids and glucose both suppress somatotroph responsiveness. Veldhuis and Walker documented this food-GH interaction in GHRH-GHRP studies [4,5]. Research protocols therefore schedule administration during fasting windows when feasible.

Intranasal and oral routes have been studied for native GHRH but not for CJC-1295 analogs specifically; subcutaneous remains the only route with published pharmacokinetic data for the no-DAC form.

CJC-1295 Cycle Structure and Protocol Duration

In short: community protocols run 8–16 weeks on, 4–8 weeks off. No trial has formally validated any specific cycle length for the no-DAC form.

Reported cycle lengths in community-research documentation typically range from 8 to 16 weeks of continuous daily dosing, followed by a 4- to 8-week washout [1]. No peer-reviewed trial has established an optimal cycle length for CJC-1295 no-DAC specifically, so these ranges are drawn from research-community self-report and extrapolation from GHRH-analog chronic-administration studies.

Receptor desensitization at the GHRHR is less pronounced than at the GHS-R (GHRP receptor), which is why desensitization discussions more commonly focus on the GHRP partner rather than the GHRH analog itself [3,5]. However, chronic GHRH stimulation can downregulate somatotroph response over time; pulse-preserving dosing (two to three short pulses per day rather than continuous infusion) is the research-community response to this concern.

Washout periods allow somatostatin-GHRH axis recalibration. IGF-1 levels typically return to pre-protocol baselines within 2 to 4 weeks of cessation [2].

CJC-1295 Side Effects and Safety Profile

In short: injection-site reactions, transient flushing, mild fluid retention, and numbness/tingling in the first couple of weeks are the commonly reported effects. Chronic GH-axis activation can shift fasting glucose.

The side-effect profile reported in CJC-1295 and related GHRH-analog trials includes injection-site erythema, transient flushing, a brief dizziness or head-rush sensation at peak GH release (typically 15 to 30 minutes post-injection), and mild fluid retention [2,6]. Community research data additionally describes transient numbness or tingling in the hands and feet during the initial 1 to 2 weeks of dosing, consistent with early-cycle fluid shifts and carpal-tunnel-like transient compression seen in recombinant-HGH clinical experience.

Fasting glucose elevation is a documented effect of sustained GH elevation; GHRH-analog research populations show modest insulin-resistance shifts with chronic use [6,7]. Monitoring fasting glucose and HbA1c during extended protocols is discussed in review literature.

Contraindications documented in the broader GH-axis research literature:

Active malignancy or history of malignancy: GH and IGF-1 are mitogenic; GH-axis activation is contraindicated in any active cancer context [7].
Type 1 or uncontrolled type 2 diabetes: GH antagonizes insulin action; GH-axis stimulation can precipitate hyperglycemia [7].
Proliferative or severe non-proliferative diabetic retinopathy: GH elevation has been associated with retinopathy progression [7].
Pregnancy and lactation: No safety data exist; GH-axis modulation during pregnancy is contraindicated [7].
Active intracranial lesion or history of pituitary tumor: GHRH stimulation in this context is contraindicated [7].

Drug interactions include glucocorticoids (which suppress GH release), insulin and insulin-sensitizing agents (dose adjustments may be required), and estrogens (which modulate GH-IGF-1 axis sensitivity).

CJC-1295 Vendor Ratings: Who Publishes Lab Data at ≥99% Purity?

TriedRx compiles publicly available third-party lab reports — HPLC purity results, mass-spectrometry identity confirmations, and LAL endotoxin data — published by CJC-1295 vendors or by independent researchers who have tested and posted results. We cross-reference those reports against vendor transparency practices (lot traceability, accredited-lab sourcing, reporting cadence), reputation signals, and operational data, then grade each vendor on a transparent rubric. We gather the quality data. We grade the vendors. We publish the rankings — including what's missing. No vendor payments, no sponsored placements, no affiliate revenue on research content.

See all vendors tested for CJC-1295 →

For the full research background, pharmacokinetic data, vendor grades, and safety profile on CJC-1295 no-DAC, see the TriedRx CJC-1295 profile. The profile covers receptor binding specificity, comparative pharmacokinetics versus the DAC-conjugated variant, and the current peer-reviewed evidence base in greater depth than this dosing summary permits.

References

Sackmann-Sala L, Ding J, Frohman LA, Kopchick JJ. Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects. Growth Hormone & IGF Research. 2009;19(6):471-477. DOI: 10.1016/j.ghir.2009.03.001. PMID: 19386527.

Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. 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;91(3):799-805. 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;91(12):4792-4797. PMID: 16984981.

Walker RF. Sermorelin: a better approach to management of adult-onset growth hormone insufficiency? Clinical Interventions in Aging. 2006;1(4):307-308. PMID: 18046908.

Veldhuis JD, Bowers CY. Integrating GHS into the ghrelin system. International Journal of Peptides. 2010;2010:879503. DOI: 10.1155/2010/879503. PMID: 20798855.

Jette L, Leger R, Thibaudeau K, et al. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats. Endocrinology. 2005;146(7):3052-3058. PMID: 15817669.

Molitch ME, Clemmons DR, Malozowski S, et al. Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism. 2011;96(6):1587-1609. DOI: 10.1210/jc.2011-0179. PMID: 21602453.

Alba M, Fintini D, Sagazio A, Lawrence B, Castaigne JP, Frohman LA, Salvatori R. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. American Journal of Physiology - Endocrinology and Metabolism. 2006;291(6):E1290-E1294. PMID: 16822960.

Verdict

A pulse-preserving tool with a thin evidence base

CJC-1295 no-DAC is a reasonable pharmacological choice within the research-community GHRH-analog class because it keeps GH release pulsatile instead of flattening it out. That's the whole pitch. But the peer-reviewed evidence base is thin — most of what's cited about the no-DAC variant is really evidence about the DAC form, sermorelin, or GHRH analogs in general.

If you're tracking this compound, track it as what it is: a short-acting GHRH analog that's been inherited by the research-chem market, not a clinically validated therapeutic. Vendor quality is the variable that matters most, and that's where /brands does the work.

Bottom line: Research-only, evidence thin, pair with a GHRP if you're pairing at all. The DAC variant is the one with the actual clinical pharmacokinetic trial; this one is the short-acting cousin.