Semax

All ten papers cited here are preclinical, published between 2020 and 2025. Three examine the same rat model of cerebral ischaemia-reperfusion, measuring gene transcripts and brain proteins after a temporary interruption of blood flow. Two are chemistry studies of how Semax interacts with copper and amyloid-beta, one using cultured SH-SY5Y neuroblastoma cells and one using artificial membrane models. The other five used a mouse model of spinal cord injury, an animal model of Alzheimer's disease, rat hippocampal neurons, rats exposed to fluvoxamine early in life, and rats under restraint stress.

In the ischaemia model, the authors reported that Semax suppressed transcripts for pro-inflammatory mediators and offset expression changes caused by ischaemia-reperfusion, and linked this at the protein level to reduced inflammatory and cell-death processes. In the chemistry studies, Semax prevented copper from forming complexes with amyloid-beta, reduced copper-catalysed production of reactive oxygen species and aggregation, and lowered cytotoxicity in neuroblastoma cells. In the Alzheimer's model, animals given Semax or its derivative had fewer amyloid inclusions in the cortex and hippocampus. The spinal cord study in female mice reported greater functional recovery and traced it to the μ-opioid receptor gene, USP18 and deubiquitination of the FTO protein. In rats, Semax lessened behavioural and biogenic amine changes after early fluvoxamine exposure and prevented stress-induced shifts in colon microbiota, while the hippocampal study recorded intracellular calcium responses to locate the peptide's first cellular targets.

No study here involves people, so the findings describe rodent, cell and membrane systems only. The ischaemia results rest on expression data from a single rat model, and one of those papers discussed the limits of RNA-Seq, compared with real-time RT-PCR, for measuring less abundant transcripts. Outside that work, most models appear only once in this list, so those findings are not replicated here, and mechanisms such as the μ-opioid route in spinal injury come from single studies. The entries do not state group sizes.