Cerebrolysin

Cerebrolysin is a mixture of free amino acids and low-molecular-weight peptides made by enzymatic breakdown of pig (porcine) brain proteins (Hartbauer et al., 2001). Japanese studies use the code FPF-1070 (Satou et al., 2000).

The studies below used that licensed medicine, which Disguised Alpha's research material is not.

PubChem has no compound record (CID) for Cerebrolysin and so gives no formula or weight; its substance records, such as SID 135307256 from ChemIDplus, list the name, FPF 1070, the UNII and the CAS number. The 10 kDa limit and a 75% amino acid, 25% peptide split are from Hartbauer et al., 2001.

Cerebrolysin research falls into six areas, each summarized with its model. The trials used the licensed medicine, its manufacturer supported several, and part of the rodent literature has been retracted.

Composition: a mixture, not a single peptide

Mass spectrometry identified 638 unique peptides in an Internet-obtained Cerebrolysin sample, mostly fragments of tubulin, actin and myelin basic protein, and no fragments of known neurotrophic factors such as NGF, BDNF or CNTF; the authors proposed that unidentified peptides account for its reported activity (Gevaert et al., 2015). A 2024 study compared it with 11 other preparations, most listing cerebroprotein hydrolysate as their active ingredient. Their HPLC peptide profiles differed significantly, and they lacked relevant activity in a PC12 cell differentiation assay (Seidl and Aigner, 2024). Models: mass spectrometry, HPLC and PC12 cells.

Neurotrophic-like activity in cultured neurons

In chicken embryo explants, FPF-1070 promoted neurite outgrowth from dorsal root ganglion and sympathetic neurons, less than nerve growth factor did and with an inverted U-shaped concentration response, but not from ciliary ganglion neurons (Satou et al., 2000). In chick telencephalon neurons in low serum, Cerebrolysin and an artificial amino acid mix both promoted outgrowth at 4 days; by 8 days the networks had degenerated with the amino acid mix but not with Cerebrolysin, which the authors credited to the peptide fraction (Hartbauer et al., 2001). Model: chick embryo neurons.

Rodent models and retracted mouse studies

In rats with embolic middle cerebral artery occlusion, Cerebrolysin at 2.5 or 5 mL/kg from 24 hours after stroke increased progenitor cells and neuroblasts in the subventricular zone at 28 days. It did not reduce infarct volume, but the rats scored better on behavioral tests at 21 and 28 days, and blocking PI3K/Akt abolished the progenitor response in culture (Zhang et al., 2010).

In mice expressing mutant human amyloid precursor protein, a University of California San Diego laboratory reported fewer water-maze deficits in younger mice and 27% to 43% less amyloid-beta after three months (Rockenstein et al., 2003). Journals retracted four later Cerebrolysin papers from that laboratory in 2025 and 2026, on tau, Pick's disease, Rett syndrome and CNTF-peptide models, including Rockenstein et al., 2014 and Doppler et al., 2008 (our P21 guide covers the CNTF paper), and a 2009 tau paper carries a 2026 expression of concern (Ubhi et al., 2009). Models: rats and transgenic mice.

Acute ischemic stroke trials

CASTA randomized 1,070 people with acute ischemic stroke in Asia to daily intravenous infusions of Cerebrolysin or saline placebo for 10 days, started within 12 hours. Its primary endpoint, a combined test of the modified Rankin Scale, Barthel Index and NIH Stroke Scale at day 90, showed no significant difference; the authors said a post hoc trend favoring Cerebrolysin in severe strokes needed confirmation (Heiss et al., 2012).

The smaller, exploratory CARS trial, started 24 to 72 hours after stroke alongside rehabilitation, reported a large effect favoring Cerebrolysin on its primary endpoint, the Action Research Arm Test at day 90 (Muresanu et al., 2016). The 2023 Cochrane review of seven trials (1,773 participants, one testing the similar mixture Cortexin) found probably little to no difference in all-cause death or total serious adverse events, and, with moderate certainty, more non-fatal serious adverse events with Cerebrolysin (risk ratio 2.39); the manufacturer supported three of the trials (Ziganshina et al., 2023). Model: randomized trials in people.

Traumatic brain injury trials

The CAPTAIN trials added Cerebrolysin or saline to standard care after moderate to severe traumatic brain injury and scored an ensemble of outcome scales. In CAPTAIN I (46 participants), the primary ensemble just missed statistical significance in the full analysis and reached it per protocol (Poon et al., 2020). In the single-center CAPTAIN II (139 analyzed), it showed a statistically significant small-to-medium effect favoring Cerebrolysin at day 90 (Muresanu et al., 2020). Model: randomized trials in people.

Dementia trials

In a 24-week trial, 279 people with mild to moderate Alzheimer's disease received intravenous infusions of placebo or one of three infusion amounts over 12 weeks. At week 24, global clinical impression (CIBIC+) favored all three Cerebrolysin arms, but cognition (modified ADAS-cog) differed from placebo only at the lowest amount (Alvarez et al., 2006).

The 2019 Cochrane review of six vascular dementia trials (597 participants) found pooled scores favoring Cerebrolysin but rated the evidence very low quality, with high risk of bias, and said any effects may be too small to be clinically meaningful (Cui et al., 2019). Model: randomized trials in people.