Evidence Grade B — Strong clinical evidence. 628 published studies, 322 human. 42 registered clinical trials.
Medically reviewed by a licensed medical professional
Cerebrolysin is a mixture of peptide fragments derived from pig brain tissue, used in some countries (mainly Central/Eastern Europe, Asia, and Latin America) for stroke and dementia. Unlike most compounds in this database, it is not a single defined molecule — it is a complex biological mixture whose exact composition varies between batches.
Cerebrolysin is also known by these brand and alternate names:
628 published studies: 322 human, 203 animal, 47 in-vitro, 95 reviews
Cerebrolysin has been studied in over 200 clinical trials involving more than 15,000 patients, primarily for stroke and Alzheimer's disease. The largest stroke trial (CASTA, 1,070 patients) showed no significant benefit on its primary endpoint. A Cochrane systematic review concluded that evidence was insufficient to support its routine use in stroke or dementia.
Cerebrolysin is approved in some non-FDA/non-EMA jurisdictions for neurological conditions. Its clinical evidence base, despite being extensive in volume, has not met the standards required for FDA or EMA approval. The undefined molecular composition makes batch-to-batch consistency and quality standardisation inherently challenging compared to defined single-entity pharmaceuticals.
Research suggests the peptide mixture may interact with neurotrophic factor pathways. However, as an undefined mixture of unknown composition, the active component(s), their receptor targets, and their mechanism cannot be precisely characterised in the way that a defined single-entity drug can be. This is a fundamental limitation of mixture-based biologics.
Research suggests cerebrolysin has been studied in over 200 clinical trials involving more than 15,000 patients, primarily for stroke and Alzheimer's disease. However, the largest and most rigorous trials — particularly the CASTA stroke trial (1,070 patients) — failed their primary endpoints. Cochrane systematic reviews consistently rate the evidence as low to very low quality and have flagged a possible increase in non-fatal serious adverse events. Positive findings emerge mainly from smaller trials, post-hoc subgroup analyses, and meta-analyses partially associated with the manufacturer — patterns that do not meet the standards required for FDA or EMA approval. The undefined molecular composition makes batch-to-batch consistency inherently challenging compared to single-entity drugs. Despite extensive study, no positive Phase III trial on a primary endpoint exists for any indication.
PeptideTrace tracks 42 registered clinical trials for Cerebrolysin sourced from ClinicalTrials.gov.
Cerebrolysin Compared to Donepezil in Patients With Mild to Moderate Dementia of Alzheimer's Type (DAT)
Safety and Feasibility of Using Cerebrolysin in the Treatment of Primary Intracerebral Hemorrhage - a Prospective Randomized Open Blinded End-point Trial
Cerebrolysin in Early Stroke Rehabilitation - Tertiary Study
Effects of Cerebrolysin on Language Ability in Non-fluent Aphasia Patients After Stroke: A Randomized, Placebo-controlled, Double-blinded, Single Center Study
Cerebrolysin as an Add-On Therapy to Standard Treatment of Basilar Artery Occlusion
Cerebrolysin (FPF-1070) is a porcine brain-derived preparation consisting of approximately 25% low-molecular-weight neuropeptides and 75% free amino acids, produced through standardized enzymatic proteolysis of purified porcine brain proteins. Peptide fragments are typically <10 kDa, enabling BBB crossing. Identified constituents include fragments mimicking BDNF, NGF, GDNF, and CNTF, plus active fragments of enkephalins, orexin, and galanin. Manufactured by EVER Neuro Pharma GmbH (Austria). Available in 1-30 mL ampoules for intravenous infusion or intramuscular injection. Approved in approximately 44-50 countries including Austria, Germany, Russia, China, and South Korea for cerebrovascular disorders, Alzheimer's disease, vascular dementia, and traumatic brain injury. Not approved in the United States, United Kingdom, Canada, or Australia.
Research suggests Cerebrolysin acts through multimodal neurotrophic mechanisms: mimicking endogenous BDNF, NGF, CNTF, and GDNF signaling; activating PI3K/Akt survival pathways and Sonic hedgehog signaling; exerting anti-apoptotic, anti-oxidant, anti-excitotoxic, and anti-inflammatory effects; promoting neuroplasticity, synaptogenesis, neurogenesis, and angiogenesis; reducing neocortical amyloid plaque load in transgenic models; modulating GABAergic and cholinergic pathways; and enhancing BDNF expression synergistically when combined with donepezil in preclinical models.
Cerebrolysin has been studied in over 200 clinical trials involving more than 15,000 patients. In stroke, the CASTA trial (N=1,070), the largest RCT, showed no significant difference on its primary combined endpoint versus placebo; post-hoc analysis in severe strokes (NIHSS >12, N=252) showed mortality of 10.5% versus 20.2% favoring Cerebrolysin (p=0.0497). The 2023 Cochrane stroke review (7 RCTs, N=1,773) concluded Cerebrolysin 'probably adds no benefit' on mortality and 'probably increased' non-fatal serious adverse events. In Alzheimer's disease, the Gauthier et al. (2015) meta-analysis of 6 RCTs showed significant cognitive benefit at 4 weeks (SMD -0.40, p=0.003) but not at 6 months (SMD -0.37, p=0.17). In vascular dementia, the 2019 Cochrane review (6 RCTs, N=597) rated all outcomes as 'very low quality evidence.' In TBI, the CAPTAIN trials showed improvements on specific neuropsychological tests but with very small sample sizes. Approved in approximately 44 countries but not in the US, UK, Canada, or Australia.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
Compare prices from 3 vendor listings
View pricing data across vendors and countries for Cerebrolysin
P21 has no marketing authorisation. No human clinical trials have been conducted. The evidence base consists entirely of studies in transgenic Alzheimer's disease mouse models, conducted primarily by a single research group. Animal studies reported behavioural and biochemical changes in AD mouse models following chronic oral administration. The translation of results from transgenic mouse models of Alzheimer's disease to human disease has historically been extremely poor — the vast majority of compounds showing efficacy in such models have failed in human trials. Products available through unregulated channels lack pharmaceutical quality assurance.
Semax is approved in Russia for stroke recovery and cognitive conditions. It has not been approved by the FDA, EMA, or other major Western regulatory agencies, and the clinical evidence base has not undergone Western regulatory review. Published clinical studies are predominantly Russian. The largest published study (110 stroke patients) reported correlations between treatment and BDNF levels. The evidence does not meet the standards typically required for FDA or EMA approval. Its regulatory status is limited to Russia and certain former Soviet states.
FGL has no marketing authorisation. A Phase I trial (24 healthy volunteers) of intranasal FGL demonstrated tolerability with only mild adverse events. Preclinical studies reported effects on memory in animal models. The compound has progressed further through formal development than many research peptides, having completed a Phase I safety study. However, no efficacy trials have been conducted in patients, and clinical development beyond Phase I has not been reported.
Evidence Reviews
This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
