Erinacine A and Hericenone C both come up in the same conversations; they overlap on Neurotrophins and Acetylcholine. Erinacine A: Erinacine A is the flagship cyathane diterpenoid produced by the mycelium of the culinary-medicinal mushroom Hericium erinaceus (Lion's Mane). Hericenone C: Hericenone C is an aromatic fatty-acid ester isolated from the fruiting body of Hericium erinaceus and one of the classic small-molecule inducers of nerve growth factor synthesis identified from Lion's Mane.
Erinacine A is the flagship cyathane diterpenoid produced by the mycelium of the culinary-medicinal mushroom Hericium erinaceus (Lion's Mane). It is the single most pharmacologically characterized Lion's Mane metabolite in the central nervous system, acting as a potent low-molecular-weight inducer of nerve growth factor (NGF) synthesis. Unlike the larger hericenones of the fruiting body, erinacine A is small and lipophilic enough to cross the blood brain barrier, giving it central activity after oral dosing in rodents. Preclinical work reports benefit across Alzheimer-type pathology, Parkinsonian models, ischemic stroke, metabolic-driven cognitive decline, and colorectal cancer models.
Hericenone C is an aromatic fatty-acid ester isolated from the fruiting body of Hericium erinaceus and one of the classic small-molecule inducers of nerve growth factor synthesis identified from Lion's Mane. Together with hericenones D and E it helped establish the scientific basis for the mushroom's traditional reputation as a nerve tonic. Unlike the mycelial erinacines, hericenones are relatively large and lipophilic and are thought to act largely peripherally rather than crossing the blood brain barrier efficiently.
both fingerprints on one instrument; where the marks line up the two compounds work the same lever, where a slot goes dark only one of them touches it. read straight from each entry's affinity table; nothing here is invented.
Induces transcription and secretion in glia and neurons
Induces NGF biosynthesis in cultured cells
Attenuates non-compact plaque and raises NGF:proNGF ratio
Upregulates death receptors via JNK/p300/NF-kappaB-p50
Downregulates neuroinflammatory signaling
Downstream activation via induced neurotrophins
Potentiates neurotrophin-activated cascades
NGF-dependent trophic support
strengths are the entries' qualitative ratings (strong / moderate / weak); Ki and EC50 figures appear where an entry records them.