u/ImpossibleInsect10

Cerebrolysin dosing schedule question for anyone who's run it

Ran my first 10-day block last month at 5ml IM daily, took about 3 weeks off, and i'm trying to decide what to do for round 2. The russian neurology protocol everyone references is the 10-on / break / repeat thing, but every western anti-aging clinic i've looked at seems to push 20-30 day continuous runs or even chronic low-dose. Those feel like totally different philosophies to me.

Has anyone actually tracked cognitive output across different schedules? Like cambridge brain sciences, dual n-back, quantified writing volume, whatever. I did a rough n-back baseline before my first block and want to compare but i have no idea if 10 days is even long enough to see the real curve or if i bailed too early.

Also curious if anyone noticed the effect plateau or fade on the longer western-style runs. That's my main worry with going 21+ days.

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u/ImpossibleInsect10 — 7 hours ago

Cerebrolysin dosing schedule question for anyone who's run it

Ran my first 10-day block last month at 5ml IM daily, took about 3 weeks off, and i'm trying to decide what to do for round 2. The russian neurology protocol everyone references is the 10-on / break / repeat thing, but every western anti-aging clinic i've looked at seems to push 20-30 day continuous runs or even chronic low-dose. Those feel like totally different philosophies to me.

Has anyone actually tracked cognitive output across different schedules? Like cambridge brain sciences, dual n-back, quantified writing volume, whatever. I did a rough n-back baseline before my first block and want to compare but i have no idea if 10 days is even long enough to see the real curve or if i bailed too early.

Also curious if anyone noticed the effect plateau or fade on the longer western-style runs. That's my main worry with going 21+ days.

reddit.com
u/ImpossibleInsect10 — 7 hours ago

Cerebrolysin dosing schedule question for anyone who's run it

Ran my first 10-day block last month at 5ml IM daily, took about 3 weeks off, and i'm trying to decide what to do for round 2. The russian neurology protocol everyone references is the 10-on / break / repeat thing, but every western anti-aging clinic i've looked at seems to push 20-30 day continuous runs or even chronic low-dose. Those feel like totally different philosophies to me.

Has anyone actually tracked cognitive output across different schedules? Like cambridge brain sciences, dual n-back, quantified writing volume, whatever. I did a rough n-back baseline before my first block and want to compare but i have no idea if 10 days is even long enough to see the real curve or if i bailed too early.

Also curious if anyone noticed the effect plateau or fade on the longer western-style runs. That's my main worry with going 21+ days.

reddit.com
u/ImpossibleInsect10 — 7 hours ago

Cerebrolysin vascular dementia meta-analysis thoughts

So i finally got around to reading the 2019 Cui et al Cochrane review on cerebrolysin for vascular dementia. Headline finding was that IV cerebrolysin courses improved cognition and general function with no signal of adverse effects, but the data aren't definitive, the analyses were limited by heterogeneity, and the included papers had high risk of bias. Authors basically said if benefits exist, the effects may be too small to be clinically meaningful, and there have been no new studies in vascular dementia since the previous Cochrane review. Then i saw a 2024 network meta-analysis in Neurology that put cerebrolysin ahead of rivastigmine on ADAS-Cog, which is a much rosier framing than the cochrane take.

The gap between "promising in NMAs" and "weak evidence base, mostly old trials, no new RCTs in a decade" is what's bugging me. Anyone here actually run a course of it, or know why no one's bothered to fund a clean modern trial?

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u/ImpossibleInsect10 — 4 days ago

semax vs selank. Anyone actually feel a difference running them solo vs stacked?

Been doing intranasal semax in the morning (about 600mcg total split between nostrils) for focus work, and selank around mid-afternoon (~400mcg) when my anxiety/rumination kicks up. Roughly 2 weeks in. Semax is noticeable for me, like a clean push for deep work for maybe 4-5 hours. selank is subtler, more of a "i stopped caring about the dumb thing i was spiraling on" feel.

Question for people who've run both: do you actually get more out of stacking them same-day, or do they kind of blur into each other? And has anyone found a dosing pattern that keeps the semax focus effect from tapering off after a week or two? Mine feels slightly less sharp than day 3.

Not really interested in oral, the intranasal seems to be where the effect is.

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u/ImpossibleInsect10 — 7 days ago

Anyone else pulling IGF-1 before starting a GHRH/GHRP stack? feels like the obvious move but most people i talk to just jump straight in

Context: i'm 34, been running peptides on and off for about one year. First round i did the classic CJC/ipam combo at 100/100 5 nights a week for 12 weeks and felt great, but i had no idea what my IGF-1 actually did because i never tested baseline. just vibes. second round i pulled labs first, came back at 142 ng/mL which is mid-range for my age, ran the same protocol, retested at week 10 and was sitting at 248. that's a real number i can act on.

the part that bugs me is everyone treats secretagogues like they hit the same in every body. they don't. some people are already cruising at 220 baseline and a standard ipam dose pushes them into a range i'd want to back off from. others are at 110 and need more aggressive dosing or a longer GHRH analog to actually move the needle. without the pre-test you're just guessing whether you needed it at all.

i'm also convinced the "i feel amazing on week 2" reports are mostly placebo + better sleep from the GHRP pulse, not actual axis response. IGF-1 takes weeks to climb. if you feel incredible on day 5 that's probably ghrelin agonism and cortisol blunting, not GH doing work.

so question for the sub: who here is dosing off labs vs dosing off protocol cards? and if you test, are you pulling IGF-1 only or going further (IGFBP-3, fasted glucose, prolactin on the tesamorelin/MK crowd)?

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u/ImpossibleInsect10 — 8 days ago

SURMOUNT-OSA results — tirzepatide dropped AHI by ~25 events/hr, what do we make of this?

Finally got around to reading the SURMOUNT-OSA paper in NEJM. Headline number: tirzepatide cut AHI by around 25 events/hour on average in people with moderate-to-severe OSA and obesity, vs basically nothing for placebo. That's a huge effect for what's nominally a weight-loss drug.

What i can't tell from the paper is how much of this is just the weight loss doing the work (less fat around the airway, less mechanical collapse) vs something more direct. The AHI drop tracks pretty closely with the weight loss curve, which makes me lean toward "it's mostly just the weight." But i'd love to see a comparison against a matched cohort losing the same weight through diet alone.

Anyone here running tirz primarily for sleep stuff, or got a CPAP + tirz stack going? Curious if you've seen your own AHI numbers move and how fast.

reddit.com
u/ImpossibleInsect10 — 9 days ago

Bloodwork cadence on a peptide protocol every 4 weeks feels excessive, every 12 weeks feels too slow. What's your sweet spot?

Been running a GH secretagogue stack for about 5 months now and trying to figure out a sane labs schedule. Pulled a full panel at week 4 (fasted glucose, HbA1c, IGF-1, lipids, liver) and almost nothing had moved enough to be meaningful, felt like i wasted the draw. But waiting 12 weeks between pulls feels like i could miss a glucose or IGF-1 drift until it's already a problem.

What are people actually doing? 6 weeks? 8? And are you running the full panel each time or just a cheap fasted glucose + IGF-1 check between the bigger draws?

Mostly asking because the cost adds up fast if you're doing full panels every month and i'd rather spend that on the actual compounds.

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u/ImpossibleInsect10 — 10 days ago

Semax in acute ischemic stroke: what the actual Russian registration trials show, and why the design isn't as bad as the dismissal implies

Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic ACTH(4-7) analog with a C-terminal Pro-Gly-Pro tail that blocks peptidase degradation. It has been on the Russian List of Vital and Essential Drugs and used in acute neurology wards for ischemic stroke since the 1990s. Most Western nootropic discussion either treats it as a magic BDNF booster or dismisses the stroke data outright. Neither is quite right. Here is what the actual primary literature says.

The anchor trial: Gusev et al., 1997

The Russian registration evidence rests heavily on Gusev, Skvortsova et al., Zh Nevrol Psikhiatr Im S S Korsakova, 1997;97(6):26-34, conducted at the Institute of Stroke, Russian State Medical University.

Methodology.
Efficiency of Semax was studied in 30 patients in the acute period of hemispherical ischemic stroke, with a control group of 80 patients with strokes analogous in severity and location of damage, treated with conventional therapy. Different clinical rating scales were used for objectivization of severity and estimation of neurological defect.

The control of Semax influence on the functional state of the brain included monitoring of EEG with mapping, repeated analysis of somatosensory evoked potentials and their mapping.
Add-on design (Semax + standard care vs standard care), not placebo-controlled, not blinded in the modern sense. The trial was indexed in CENTRAL by Cochrane in 2001, which is worth noting because it means independent reviewers considered it a controlled trial of sufficient quality to enter the registry, not just a case series.

Results.
Including Semax in combined intensive therapy of acute ischemic stroke had some influence on the rate of restoration of damaged neurological functions in terms of increasing the regress of general cerebral and focal, especially motor disorders.
The EEG mapping and somatosensory evoked potential data was the more interesting piece, because it gave an objective physiological correlate to the clinical rating scale changes, which is harder to fake than a Barthel score.

The 2018 follow-up: BDNF as mechanistic bridge

Gusev, Martynov, Kostenko et al., 2018 tested Semax in the rehabilitation phase rather than the hyperacute window.

One hundred and ten patients after ischemic stroke (43 men, 67 women, mean age 58.0±9.7) were divided into early (89±9 days) and late (214±22 days) rehabilitation groups. Each group was subdivided into semax+ and semax- subgroups. Standard regimen of semax included 2 courses (6000 mcg/day) for 10 days with 20 day interval.
Primary endpoints: plasma BDNF, MRC motor scale, Barthel index.

Administration of semax, regardless of the timing of rehabilitation, increased BDNF plasma levels which remained high during the whole study period. In semax- subgroups high BDNF plasma levels were positively correlated with early rehabilitation.

Administration of semax and high BDNF levels accelerated improvement and ameliorated the final outcome of Barthel score index. There was a positive correlation between BDNF plasma levels and Barthel score, as well as between early rehabilitation and motor performance improvement. The correlation between BDNF plasma levels and Barthel score was modified by the timing of rehabilitation. Early rehabilitation and administration of semax increase BDNF plasma level, speed functional recovery, and improve motor performance.

Translation: the peptide raised peripheral BDNF, and the BDNF rise tracked with functional recovery. This is a mechanistic bridge, not just a clinical claim.

Methodological caveats (the honest part)

  1. No modern placebo-controlled double-blind RCT exists in the English-language literature. As of late 2023, no published human Semax trials have been conducted outside Russia and post-Soviet states. The registration trials are Russian-language, add-on design, with unequal group sizes (30 vs 80 in the 1997 trial).
  2. Outcome measures vary across studies. Some use Barthel and MRC, others use Scandinavian Stroke Scale or local Russian scales. Cross-study comparability is weak.
  3. No NIHSS primary endpoint in the original registration trial. Some secondary sources cite NIHSS/mRS for Semax, but the foundational 1997 paper used a mixed clinical and electrophysiological panel.
  4. Replication has been mechanistic, not clinical. The transcriptomic work, including Medvedeva et al., BMC Genomics 2014 showing immune and vascular gene modulation after pMCAO, and Dmitrieva et al., Cell Mol Neurobiol 2010 showing induction of Bdnf, Ngf, TrkB, TrkC, and TrkA transcription in the ischemic cortex, is solid and reproducible. The clinical replication is thinner.
  5. Regulatory status is changing. Semax is scheduled for FDA Pharmacy Compounding Advisory Committee review on July 24, 2026 for the Section 503A Bulks List, with cerebral ischemia as one of the indications under evaluation. How PCAC handles non-English clinical data will be the deciding factor.

So what does this change for protocol thinking

For the nootropic-curious reader who is not a stroke patient: the stroke data is not directly portable to healthy-cognition use cases. What does port is the mechanism. The 2018 trial demonstrated that intranasal Semax at 6 mg/day raised plasma BDNF and that the rise was functionally meaningful in a damaged-brain context. That is a much stronger BDNF-elevation signal in humans than most nootropics can claim. The dose range used in stroke care (clinically 6,000-12,000 mcg/day for moderate stroke per Russian protocols) is roughly 10-20x what recreational nootropic users typically take, which should temper extrapolation in both directions.

At Klarovel, the editorial position has been that Semax's stroke literature is the most defensible part of its evidence base, but the 1990s trial design ceiling means it should be read as suggestive-with-mechanism rather than confirmatory.

What's the question this leaves you with: if a 1997 add-on trial plus a 2018 BDNF-correlation study is enough for Russian registration but not enough for FDA, where do you personally set the bar between "interesting peptide with mechanistic plausibility" and "actually use it"?

u/ImpossibleInsect10 — 11 days ago