cerebrolysin

a liquid made from pig brain, dripped into a vein in hospital after a stroke or in dementia. thousands of randomised patients have been given it. every dose in every trial is measured in millilitres, because the ampoule holds a mixture and there is no single molecule to weigh, and the only published identity test is a fingerprint match against a reference sample.

tier D · focus · 1,070 CASTA · primary missed

verdict

doctors drip this pig-brain liquid into a vein to try to keep damaged brain cells alive after a stroke or a head injury, and to hold memory and thinking together in dementia. it does half of that. the scores taken in the first two weeks improve, and the three-month score that decides whether a stroke patient gets their independence back sits flat, with CASTA putting day-90 modified Rankin 0 to 2 at 199 of 529 against 208 of 541 on placebo. two cochrane reviews and three independent syntheses read the whole literature and rate every estimate low or very low.

on whether it actually works: mixed, and the split is clean. the scores taken in the first two weeks improved. the score that decides whether a stroke patient gets their independence back at three months stayed flat. on the moving side, NIHSS at day 14 pools at a mean difference of 1.39 (95% CI 0.53 to 2.25) across 1,521 randomised patients, ESCAS moved an aphasia battery by 14.8 points, CEREHETIS cut symptomatic haemorrhagic transformation, and Cochrane's vascular dementia review reports cognition at SMD 0.36 (0.13 to 0.58) and global function response at RR 2.69 (1.82 to 3.98). the flat one is 90-day disability. CASTA at n=1,070 put day-90 modified Rankin 0 to 2 at 199 of 529 on the preparation against 208 of 541 on placebo, and the pooled estimate across 1,885 patients sits at RR 1.31 (0.90 to 1.91). mortality comes out level at moderate certainty. independent groups did reproduce a small cognitive benefit, and they rate their own finding very low certainty.

on whether the human evidence is thin: it is one of the biggest human files on the board. thousands of randomised patients sit in indexed journals, and Cochrane maintains two separate reviews on this compound, one in acute ischaemic stroke and one in vascular dementia. the stroke review pools 7 randomised trials and 1,601 participants in its compound-only version. the vascular dementia review runs 6 randomised trials and 597 people. two manufacturer trials at n=242 and n=217 have posted full results to ClinicalTrials.gov, numbers and all. what fails is the certainty attached to that volume. Cochrane rates the vascular dementia cognition estimate very low quality and writes that any benefit may be too small to be clinically meaningful.

on the positive trials, because there are real ones: there are several. CARS met its day-90 motor endpoint. ESCAS moved the Western Aphasia Battery by 14.8 points against placebo. CEREHETIS cut symptomatic haemorrhagic transformation after thrombolysis. the manufacturer's vascular dementia trial posted an ADAS-cog+ difference of -6.17 (-8.22 to -4.13). they share one pattern. whatever is measured soonest moves, and the 90-day disability endpoint stays where it started. CASTA, the largest trial ever run at n=1,070, missed its confirmatory endpoint. the manufacturer's own three-arm comparison against donepezil came back null at p=0.6348, and the repeat attempt was withdrawn before a single patient enrolled.

on what a vial sold under this name contains: nobody can say. the clinical literature never answered the question, so a vendor certificate cannot answer it either. every trial in the published record dosed one Austrian process output, measured in millilitres of preparation, given by intravenous infusion in a hospital. across the 42-study registry set the records give the article a name and stop there, with no molecular weight, sequence or purity specification anywhere in them, and the Chinese process patent in the source set defines it by manufacturing route plus a fingerprint similarity of at least 0.90 against a reference sample. a purity percentage needs one moiety to describe, and the ampoule holds a mixture. the one compositional paper in the literature reports that products sharing the cerebroprotein hydrolysate name were not comparable to each other by HPLC fingerprint.

based on published trials and primary registry records. research framing only. not medical advice.

why D-tier

D is the grade for a file that argues with itself, and this one argues with itself in both directions. The human data is large. Two Cochrane reviews, 1,601 randomised participants in the compound-only stroke review, 597 in vascular dementia, 185 pooled in the randomised traumatic brain injury meta-analysis, 42 registered trials, and two manufacturer trials with full results posted to the registry. On volume alone this belongs high on the board. The certainty fails, and it fails from the independent side. Cochrane rates the vascular dementia cognition estimate very low quality and writes that the effects may be too small to be clinically meaningful. The stroke all-cause death estimate is moderate certainty for little to no difference. Neither review contains a pooled disability estimate. The stroke review records that no included trial reported death or dependence at the end of follow-up, early death, quality of life or time to restoration of capacity for work in a poolable form, and the vascular dementia review records that none reported quality of life or caregiver burden. Individual trials did measure it, and CASTA's day-90 modified Rankin 0 to 2 came back at 199 of 529 against 208 of 541 on placebo. The independent Glasgow synthesis puts short-term cognition at standardised mean difference -0.16 (95% CI -0.30 to -0.03) with very low certainty and substantial funnel-plot asymmetry, and reports the effect gone by three to seven months at -0.07 (p=0.32). Its own conclusion is that the effects were modest and probably less than would be considered clinically relevant. C is the grade for a compound whose preclinical work points one way and has not reached people yet. Thousands of randomised, blinded humans have been studied here, several of the trials are quadruple-masked, and two have posted their numbers in full, so C would misdescribe the literature. F requires the compound to be fake, a scam or actively harmful beyond reasonable doubt, and cerebrolysin is none of those. Four randomised trials met a pre-specified primary endpoint. The manufacturer's vascular dementia trial posted ADAS-cog+ -6.17 (-8.22 to -4.13). The rodent layer includes a properly randomised, blinded, placebo-controlled dose-response study. The non-fatal serious adverse event signal, RR 2.15 (1.01 to 4.55) in 2020 and RR 2.39 (1.10 to 5.23) in 2023, is a flag, since mortality and total serious events come out null in every synthesis including the manufacturer-independent ones. B is the real contest. B needs the words good evidence. In the 2025 vascular cognitive impairment review, cerebrolysin's Cohen's d of 0.28 (95% CI 0.03 to 0.52) sits level with galantamine at 0.28 and just below donepezil at 0.29. What sits behind that number is thinner. It is GRADE Low, it pools only 173 participants for this compound inside a review covering 22,347, it holds no poolable functional endpoint, it analyses follow-up beyond four weeks in none of the included trials, and its own text and table print different point estimates. Every synthesis here carries a low or very low rating from the people who read the trials. Voluminous, low certainty, sponsor dominated and internally contradictory is exactly what D describes. If C-RETURN reads out at 440 patients on a 90-day Glasgow Outcome Scale Extended endpoint and it separates, the tier moves. Until an adequately powered trial outside the manufacturer's orbit reports a durable endpoint, D is the ceiling.

the core tension

the endpoints measured soonest keep moving, the endpoints that matter most keep sitting still, and the trials large enough to settle it mostly belong to the company that makes the product. CASTA missed its confirmatory endpoint at n=1,070 and has posted nothing to the registry in roughly 15 years. CEREHETIS cut symptomatic haemorrhagic transformation and day-14 NIHSS, then found day-90 modified Rankin about the same in both arms. ESCAS moved the aphasia battery by 14.8 points and got only a trend on modified Rankin. the Alzheimer's meta-analysis shows cognition significant at 4 weeks and gone at 6 months. the Glasgow synthesis shows the same decay at three to seven months and reports funnel-plot asymmetry suggesting publication bias. CARS is the standout exception, and its own discussion volunteers that a poorer outcome than typically expected of the control group can explain the superiority of the treatment arm. across thousands of randomised patients, the included trials collected other endpoints, so neither Cochrane review holds a disability estimate at all.

what it is

Cerebrolysin is a liquid made from pig brain, digested with enzymes into peptides and free amino acids, and given by drip into a vein in hospital after a stroke or a brain injury and in dementia. The technical name is a brain-tissue protein hydrolysate. It is manufactured in Austria by EVER Neuro Pharma, sold as an aqueous preparation, and dosed by volume, because the liquid is a mixture and no one molecule sits underneath it to weigh. The Chinese process patent in the source set names pig brain as the source tissue and describes successive pepsin and trypsin hydrolysis followed by ultrafiltration. It has been in clinical use for decades, and its marketing authorisations are national, granted one country at a time. Across its 42 registered trials, no registry record states a molecular weight, an amino acid sequence or a purity specification. Every trial dose in the literature is expressed in millilitres of preparation: 20 mL, 30 mL, 40 mL, 50 mL.

what it does

The idea is that it keeps damaged brain cells alive after a stroke or a head injury and slows the loss of memory and thinking in dementia, so that a person recovers more movement, speech and thinking than they otherwise would. In the technical phrasing of the literature, the claim is neurotrophic and neuroprotective activity after acute brain injury and in cognitive decline. Randomised trials have run it in acute ischaemic stroke, vascular dementia, Alzheimer's disease, traumatic brain injury, post-stroke aphasia and subarachnoid haemorrhage. The proposed mechanism is that the mixture behaves like the brain's own growth factors, damping inflammation and prompting surviving tissue to make new cells. That claim rests on review articles asserting neurotrophic factor content, and on rodent work showing subventricular-zone progenitor proliferation and CREB-pathway suppression of neuroinflammation. No assay located in this sweep quantifies BDNF, GDNF, NGF or CNTF per millilitre of preparation. The one compositional paper that exists measured a neurofilament reporter and an HPLC fingerprint, and states that it did not measure neurotrophin content.

origin

Austrian, and the same sponsor runs through the whole literature. EVER Neuro Pharma, formerly EBEWE, manufactures the product and is lead sponsor on 10 of the 42 registered trials, including CASTA, both observational registries and both dementia trials that posted results. The independent clinical literature is largely Russian, Chinese, Romanian, Polish, Egyptian and Korean. The academic side is concentrated too. A single investigator cluster in Cluj and its collaborators authors CARS, the pooled CARS meta-analysis, the CAPTAIN trial series, the CAPTAIN prospective meta-analysis, the adverse-event meta-analysis of twelve trials, and ESCAS. Two large syntheses were produced entirely outside that orbit, the Cochrane reviews and the Glasgow analysis of animal-derived nootropics, and both land on a small effect at very low quality. Glasgow reports statistically significant benefit on short-term cognition, global function and activities of daily living, then writes that the supporting evidence is weak and the effects probably below clinical relevance.

why researchers are interested

It carries marketing authorisations in a long list of countries, which reads to a buyer as validation. It also brings thousands of randomised, blinded patients in indexed journals, which is more human data than the rest of the gray-market neuro shelf combined. The trials are real, several of them are positive, and the mechanism story is supported by properly blinded rodent work including a randomised placebo-controlled dose-response study in rats.

does it work

Mixed, and every part of that was measured. On durable function the answer is no. CASTA missed its confirmatory endpoint at n=1,070 and its day-90 modified Rankin 0 to 2 came in at 199 of 529 against 208 of 541 on placebo, with placebo numerically ahead. The 2025 fourteen-trial pool puts functional independence at RR 1.31 (0.90 to 1.91) across 6 trials and 1,885 participants. The Alzheimer's meta-analysis shows cognition significant at 4 weeks and gone at 6 months. Neither Cochrane review has a death-or-dependence pool at all, because the included trials reported other endpoints instead. On early and surrogate endpoints, several trials moved convincingly and independent groups reproduced a small benefit. NIHSS pools at a mean difference of 1.39 (0.53 to 2.25) across 1,521 participants. Cochrane's vascular dementia review reports cognition at SMD 0.36 (0.13 to 0.58) and global function response at RR 2.69 (1.82 to 3.98), and writes that courses of the preparation improved cognition and general function, at very low quality. The independent Glasgow synthesis finds short-term cognition, global function and daily living all significantly in the compound's favour, at very low certainty, and gone by three to seven months. That split is what makes it a D.

key facts

• molecular formula: undefined; it is a hydrolysate, a mixture of many peptides and free amino acids
• molecular weight: none stated in any of the 42 registry records. manufacturer and review descriptions carry roughly 15 percent peptides under 10 kDa and 85 percent free amino acids; several vendor pages instead print 25 percent and 75 percent
• amino acids: a mixture. the Chinese process patent specifies 16 amino acids plus nitrogen content
• half-life: not characterised; no human pharmacokinetic study was located in this sweep
• type: brain-tissue protein hydrolysate, dosed by the millilitre of preparation
• CAS: no CAS number for a defined active moiety appears anywhere in the trial record
• 1,070 patients in CASTA, confirmatory endpoint missed
• 3/42 registered trials with posted results
• 10/42 registered trials sponsored by the manufacturer
• 0 human pharmacokinetic studies located

frequently asked questions

What is cerebrolysin?

Cerebrolysin is a liquid made from pig brain, broken down with enzymes into peptides and free amino acids, and given by drip into a vein in hospital, to people who have had a stroke or a brain injury or who have dementia. Where it is authorised it is a prescription drug sold under the Cerebrolysin name by its Austrian maker, formerly called EBEWE. Other preparations circulate under the name cerebroprotein hydrolysate, and the one compositional comparison in the literature found that products sharing that name were not comparable to each other. The technical description is a brain-tissue protein hydrolysate manufactured in Austria by EVER Neuro Pharma and supplied in ampoules, dosed by the millilitre. The Chinese process patent in the source set names pig brain as the source tissue. It is not FDA approved. Its marketing authorisations are national, granted one European country at a time, and one of them is documented in a primary record: Romanian authorisation number 4610/2004/03, with the substance registered only as CEREBROLYSIN CONCENTRATE under EU substance number SUB74627. Across its 42 registered trials, no registry record states a molecular weight, an amino acid sequence or a purity specification.

What does cerebrolysin do?

In hospital it is dripped into a vein after a stroke or a brain injury, or in dementia, with the intention of protecting brain cells so that a person recovers more movement, speech and thinking than they otherwise would. It is claimed to be neurotrophic and neuroprotective, and it has been tested in acute ischaemic stroke, vascular dementia, Alzheimer's disease, traumatic brain injury, post-stroke aphasia and subarachnoid haemorrhage. The published record splits by how soon the endpoint is measured. Early and surrogate measures moved in several randomised trials: CARS met its day-90 arm-function endpoint, ESCAS moved the Western Aphasia Battery by 14.805 points (95% CI 9.521 to 20.089), CEREHETIS cut symptomatic haemorrhagic transformation to odds ratio 0.248 (0.072 to 0.851). Durable measures mostly held still. CASTA missed its confirmatory endpoint at n=1,070 and put day-90 modified Rankin 0 to 2 at 199 of 529 against 208 of 541 on placebo, CEREHETIS found day-90 modified Rankin about the same in both arms, and the independent Glasgow synthesis reports cognition at standardised mean difference -0.16 (-0.30 to -0.03) short term, where negative favours the compound in that paper's coding, decaying to -0.07 (p=0.32) at three to seven months.

How is cerebrolysin dosed in the published trials?

Always in millilitres of preparation, because there is no single active substance to weigh in milligrams, and always by intravenous infusion in a clinical setting. The common stroke schedule is 30 mL daily for 10 days, used in CASTA and in the Cochrane subgroup analyses. CARS used 30 mL daily for 21 days on top of a standardised rehabilitation programme. The vascular dementia trial with posted results used 20 mL. CAPTAIN used 50 mL daily for 10 days followed by two further cycles of 10 mL. The Alzheimer's dose-ranging trial compared 10 mL, 30 mL and 60 mL and found the lowest dose the only one significant on cognition at 24 weeks. There is no approved dosing protocol outside the countries holding national authorisations, and no FDA label exists to quote.

What are the side effects of cerebrolysin?

There is no FDA label, so there is no adverse-reactions table or contraindications section to quote, and the picture has to be built from the trials. Total serious adverse events come out null across every synthesis: Cochrane 2020 puts them at RR 1.15 (95% CI 0.81 to 1.65) and all-cause death at RR 0.90 (0.61 to 1.32), the twelve-trial adverse-event meta-analysis reports serious events at RR 0.99 (0.74 to 1.32), and the 2025 fourteen-trial pool reports RR 1.08 (0.84 to 1.40). The signal sits in one subset. Cochrane 2020 reports non-fatal serious adverse events at RR 2.15 (1.01 to 4.55), p=0.047, across 4 trials and 1,435 participants, rising to RR 2.86 (1.23 to 6.66) on the 30 mL for 10 days schedule, and the 2023 update puts the same estimate at RR 2.39 (1.10 to 5.23). Fatal and non-fatal events move in opposite directions and cancel when pooled, so quoting the null on total serious events as an all-clear misses where the signal is. Mild agitation is described in the CEREHETIS report as a known effect. Nothing here characterises long-term or non-clinical exposure, because no trial studied it.

Is cerebrolysin FDA approved?

No. There is no FDA approval, no NDA or BLA, and no label. The sourcing behind that answer needs stating. The regulatory register connector assigned to this sweep was blocked by an account quota and returned zero records, so the absence of an FDA application was not confirmed against a primary register here. What is documented in primary records runs the other way. The product holds national authorisations in Europe, granted country by country, and the Romanian authorisation 4610/2004/03 appears in the CTIS registration for the C-RETURN trial. Cochrane's 2023 update records that its 2020 version informed two joint European Stroke Organisation and European Academy of Neurology guidelines on post-stroke cognitive impairment, and that both advise against use.

How much does cerebrolysin cost?

No verified price appears in the retrieved record. Where it is authorised it is a prescription product supplied in ampoules and administered by infusion, so any price is set market by market and no US clinical price exists at all. What circulates on the research market is priced by unrelated suppliers, and identity, concentration and contamination status stay unverified unless a lot-specific certificate of analysis reports them. The harder problem sits upstream of any price. A purity percentage needs one defined molecule to describe, and this is a mixture.

related peptides

• semax: the other eastern-european neuro peptide with a domestic-literature-heavy file, graded higher
• selank: same regulatory geography, same problem with independent replication
• dihexa: neurotrophic claim with the opposite evidence profile: rodents only, no human trials

reptides grades the research record and cites the literature behind every call. research reference only; not medical advice.