Every Peptide Bryan Johnson Has Tried — and Why He Dropped Most of Them
Bryan Johnson has trialed CJC-1295, HGH, tirzepatide, cerebrolysin, epithalon, follistatin and BPC-157. A sourced look at what he measured, kept, and dropped.
Bryan Johnson has publicly trialed CJC-1295 with DAC, recombinant HGH, tirzepatide, cerebrolysin, follistatin gene therapy, BPC-157 and an epithalon/thymosin-alpha-1 thymus pulse. He measured biomarkers on each and abandoned most within weeks to years. Everything below is his reported n=1 self-experiment data, not use guidance.
Most peptide coverage is a list of things someone started. The more useful list is what they stopped. Bryan Johnson — the entrepreneur behind Blueprint, who logs his biology in public — has run short, biomarker-tracked trials on a long roster of research peptides and abandoned most of them, often within weeks. The pattern is the interesting part: he measured, he saw the cost, and he quit. Everything below describes his reported laboratory and self-tracking figures, not use in people. Nothing here concerns human or veterinary use, and none of it is a dosing protocol.
What was actually on his list?
Johnson’s experiments span several distinct pharmacological categories that get lazily lumped together as “peptides.” A growth-hormone-releasing analog (CJC-1295). Recombinant growth hormone itself (HGH). A dual incretin receptor agonist (tirzepatide). A porcine-brain peptide mixture (cerebrolysin). A plasmid gene therapy expressing follistatin. A gastric pentadecapeptide (BPC-157). And a “thymus rejuvenation” pairing of epithalon with thymosin-alpha-1. These behave nothing alike, and separating them is the first honest step. Worth flagging up front: the topical and oral peptides in the retail Blueprint line — GHK-Cu in a serum, collagen, a TB4 cosmetic fragment — are a separate cosmetic and nutritional category, not the injectable research compounds discussed here.
2 The number of CJC-1295 doses Johnson took before stopping — he had planned a longer titration.
CJC-1295 with DAC: eight-fold GH, then out in two doses
CJC-1295 is a synthetic analog of growth-hormone-releasing hormone. The “DAC” version carries a Drug Affinity Complex that binds serum albumin, stretching its half-life to roughly 5.8-8.1 days. The pivotal characterization came from two randomized, double-blind, placebo-controlled trials in healthy adults: a single subcutaneous injection raised mean plasma GH two- to ten-fold for at least six days and IGF-1 for nine to eleven days.1 That is the “two controlled trials, roughly 7.5x GH” figure Johnson referenced when he described the pharmacology.
His own run tells the more instructive story. Across two weekly injections (1.2 mg, then 1.8 mg), he reported GH climbing about eight-fold — and then the bill arrived. REM sleep fell 23%, with his WHOOP showing roughly 40% below baseline on the second night. Fasted glucose rose 20%. Cortisol rose 12%. He described his pancreas as “working 53% harder” and estimated insulin resistance up 50%. He also reported feeling “nearly comatose” about 48 hours after the first dose.14 He stopped before reaching his target dose. Independent human evidence lines up with the direction of the glucose signal: randomized trials of supraphysiologic GH signaling in healthy aged adults repeatedly show glucose intolerance and impaired insulin handling.5
The alternative he weighed was a non-DAC CJC-1295 paired with ipamorelin. Ipamorelin matters here because it was the first selective GH secretagogue: it releases GH through a ghrelin-receptor mechanism without the ACTH, cortisol and prolactin spillover seen with older secretagogues.2 The contrast — a long-acting analog that floods the system for days versus a pulsatile, cleaner one — is the whole design tension in this class. We cover the split in CJC-1295 with DAC versus without.
He measured an eight-fold growth-hormone rise and quit anyway. The number that ended it was REM, not GH.
HGH and tirzepatide: two more short trials
Recombinant human growth hormone — the actual hormone, not a releaser — got a longer look, roughly 100-110 days in 2023. Johnson discontinued it citing symptoms he attributed to raised intracranial pressure, headaches, elevated glucose, and about a 15% drop in HRV. The controlled human literature offers little to argue with: a meta-analysis of GH in healthy older adults found small body-composition changes, no functional benefit, and significantly more adverse events — edema, arthralgia, carpal tunnel, glucose intolerance.4 A separate randomized trial reported the same glucose and edema penalties.5
Tirzepatide, the dual GIP/GLP-1 receptor agonist, was a December 2024 microdose trial: 0.5 mg per week, one-fifth of the standard starting dose. His verdict was blunt — “didn’t work for me.” The context matters: he was already, by his metrics, in the top 1% metabolically, so there was almost no deficit to correct. His reported n=1 figures were a resting heart rate up 2-3 bpm at that dose plus degraded sleep and HRV. None of that contradicts the drug’s efficacy at full dose; SURMOUNT-1 showed up to ~20.9% weight loss at 15 mg in people with obesity.3 It simply shows what a fractional dose does in someone with nothing to lose. Note the RUO framing: we describe tirzepatide only as a literature comparator here, never as a product to buy.
Cerebrolysin: the subjective-versus-measured gap
Cerebrolysin is a mixture of low-molecular-weight peptides derived from porcine brain, given by injection. Johnson ran an intramuscular trial of about three months and said it felt like the best subjective neuro-enhancer he had tried. And yet — this is the useful part — he measured no biomarker improvement. That gap between “feels like it works” and “the data moved” is exactly why n=1 self-report is fragile. The controlled evidence is thin in the same direction: a Cochrane review of cerebrolysin for vascular dementia found only limited, low-certainty cognitive-outcome evidence.11
The one he kept — and why it’s the weakest bet
In November 2023 Johnson announced a “thymus rejuvenation” protocol: epithalon paired with thymosin-alpha-1, framed as targeting thymic regeneration, telomere lengthening and epigenetic-age reduction, and citing a “66% all-cause-mortality risk reduction from 6 years of usage.” What he described was a Khavinson-style pulse — a short course repeated only a couple of times a year, echoing the ‘five days on, then months off’ cadence of the original Soviet bioregulator studies (we do not reproduce the injectable doses here).
Epitalon (epithalon) is a pineal tetrapeptide, Ala-Glu-Asp-Gly; we describe it in what is epitalon. Thymosin-alpha-1 is a genuine immunomodulator with real T-cell and thymic activity, covered in our thymosin alpha-1 research guide. But the mortality figure is where the honesty has to kick in, and it is the throughline of this whole piece: he adopted this on the thinnest evidence of anything on his list.
| Compound | Johnson’s trial length | Outcome he reported (n=1) | Independent human evidence |
|---|---|---|---|
| CJC-1295 + DAC | 2 doses | ~8x GH; REM -23%, glucose +20% | 2 RCTs of PK/GH-IGF-1 kinetics1 |
| Recombinant HGH | ~110 days | ICP symptoms, glucose, HRV -15% | Meta-analysis: no functional benefit, more harms4 |
| Tirzepatide (0.5 mg/wk) | Short | “Didn’t work”; HR +2-3 bpm | SURMOUNT-1 (full dose)3 |
| Cerebrolysin | ~3 months | Best subjective, zero measured | Cochrane: low-certainty11 |
| Follistatin (Minicircle) | One-time | Serum FST >2x, ambiguous clocks | Company preprint only12 |
| Epithalon + TA-1 | Kept (pulsed) | Cited “66% mortality reduction” | Single-lineage, unreplicated7 |
All “outcome” figures are Johnson’s own unblinded, uncontrolled n=1 self-report. The “independent evidence” column reflects in-vitro and human literature only, not any endorsement of use. Materials named are Research Use Only.
Two more experiments: follistatin and BPC-157
In late 2023 Johnson underwent follistatin gene therapy through Minicircle — a plasmid expressing FST-344. He reported serum follistatin roughly doubling (the Minicircle preprint cites 8.58 to 24.03 ng/ml) with an ambiguous multi-clock epigenetic readout and no lasting protocol. The mechanism is real: follistatin antagonizes myostatin to drive muscle hypertrophy, which is why the axis is a target at all.12 We unpack the molecule in what is follistatin-344. The data source, however, is a company preprint from an open-label offshore clinic, not a controlled trial.
BPC-157 shows up in an April 2025 post as a past experiment, paired with cerebrolysin, described as “effective when used precisely” — not a current protocol. Its evidence base is almost entirely rodent, much of it from the peptide’s originating research group, with essentially no controlled human trials.13
An honest read of the evidence
Start with what’s weak on both sides. Johnson’s CJC-1295 and tirzepatide “results” are a single person, unblinded, uncontrolled, on a narrow biomarker panel, with no washout confirmation reported at the time. They are directional and admirably transparent, but they are not evidence of population effects. Read strictly as his data, they are still useful — a self-experimenter watching his own REM crater and stopping is a cleaner signal than most marketing — but they cannot carry more weight than that.
Now the sharp tension. The subtractions on his list are backed by real independent data or by his own instrumented measurements: he dropped HGH after ~110 days on side effects the literature predicts,4 quit CJC-1295 in two doses on his own glucose and REM numbers, and shelved rapamycin after roughly five years despite the strongest mouse-lifespan evidence in the field — the NIA Interventions Testing Program showed rapamycin extends median and maximal lifespan in genetically heterogeneous mice.6 He cited a since-flagged October 2024 preprint suggesting raised epigenetic age across 16 clocks, and noted himself it might be methodologically flawed. That is a person letting data override a strong prior.
The thing he kept inverts that discipline. The “66% all-cause-mortality reduction over 6 years” traces to the Khavinson and Anisimov group in St Petersburg — the thymalin/epithalamin cohort work — a single research lineage, largely in low-impact or regional venues, with no independent Western RCT replication.7 The supporting human trials are small and single-lab.8 Epitalon’s telomerase-activation and epigenetic-age claims lean heavily on in-vitro assays and the same group’s studies; a 2025 review is explicit that robust independent human RCT evidence is lacking.9 Thymosin-alpha-1 is a real immunomodulator, but even its best-studied clinical application — sepsis — rests on low-quality, heterogeneous, mostly single-region trials.10 So the honest summary is uncomfortable: the compound he adopted rests on the thinnest evidence of anything he tried, while the compounds he dropped were often better supported. The follistatin gene-therapy data has the same problem in a different costume — a company preprint from an offshore clinic with mixed epigenetic results and an obvious conflict of interest. BPC-157 and cerebrolysin belong in the “research-only signal” bin, not the “established human benefit” one.1311
All materials supplied by Condor Research are Research Use Only (RUO). Everything above summarizes Johnson’s self-reported self-experiment data alongside published in-vitro and literature findings; it is not a dosing protocol, clinical guidance, or a safety assessment for any organism. Nothing here should be read as encouraging administration of any compound to any person or animal.
Condor Research · Scientific desk
Atrio Sciences s.r.o., IČO 57 669 651, Nitra (SK) · info@condorresearch.com
- CJC-1295 with DAC lasted two doses: Johnson reported ~8x growth hormone but a 23% REM drop, +20% fasted glucose, +12% cortisol and +50% insulin resistance before stopping.
- Recombinant HGH ran ~110 days and was dropped for symptoms he attributed to raised intracranial pressure, headaches, elevated glucose and an HRV decline.
- Tirzepatide at 0.5 mg/week (one-fifth the starting dose) 'didn't work' for an already metabolically top-1% subject; he reported resting heart rate up 2-3 bpm and worse sleep.
- Cerebrolysin felt like the best subjective neuro-enhancer he had tried, yet produced no objective biomarker change — the subjective-versus-measured gap in miniature.
- Rapamycin ran ~5 years and was discontinued in 2024 after no perceived benefit, recurrent soft-tissue infections, lipid and glucose shifts, and a preprint suggesting raised epigenetic age.
- The one peptide protocol he kept — an epithalon plus thymosin-alpha-1 thymus pulse — rests on the thinnest evidence base of all: a single St Petersburg research lineage with no independent Western replication.
- All figures are his unblinded, uncontrolled n=1 data. The materials named here are Research Use Only; nothing below is a dosing protocol or a use recommendation.
Is Bryan Johnson's peptide data reliable?
It is transparent but structurally limited. Everything he reports is a single-subject, unblinded, uncontrolled self-experiment on a narrow biomarker panel. That makes it honest and directional — you can watch him measure and quit — but it is not evidence of what a compound does across a population. Treat every figure as his n=1, not as a result.
Why did he drop rapamycin after five years?
He announced discontinuation on 28 September 2024, citing no perceived benefit plus intermittent skin and soft-tissue infections, lipid abnormalities, glucose elevations and raised resting heart rate. He also flagged an October 2024 preprint showing raised epigenetic age across 16 clocks, while noting it might be flawed. The mouse-lifespan case remains strong; the human longevity case is unproven.
What is the difference between CJC-1295 and HGH?
CJC-1295 is a growth-hormone-releasing hormone analog — it prompts the pituitary to release your own GH in a somewhat pulsatile way. HGH is the recombinant hormone itself, delivered directly. Johnson tried both and dropped both, but the mechanisms and the side-effect profiles differ, and the DAC version of CJC-1295 has an unusually long half-life of days rather than minutes.
What is epithalon and why did he keep it?
Epithalon (epitalon) is a pineal tetrapeptide, Ala-Glu-Asp-Gly, studied mainly by the Khavinson group in St Petersburg for proposed telomere and epigenetic-aging effects. Johnson kept it as part of a thymus pulse. The candid caveat is that this is the least-replicated item on his list — independent human RCT evidence is lacking.
Did follistatin gene therapy work for him?
He reported serum follistatin roughly doubling after a one-time Minicircle plasmid treatment, with an ambiguous multi-clock epigenetic result and no lasting protocol. The mechanism — follistatin blocking myostatin to allow muscle growth — is well established. The data source, a company preprint from an open-label offshore clinic, is not a controlled trial, so read the outcome cautiously.
Are these the same peptides in the Blueprint retail products?
No. The injectable research peptides discussed here — CJC-1295, HGH, tirzepatide, cerebrolysin, epithalon, thymosin-alpha-1, follistatin, BPC-157 — are distinct from the topical and oral peptides in the retail Blueprint line, such as a GHK-Cu serum or collagen. Those are a cosmetic and nutritional category and should not be conflated with the experiments above.