A Ukrainian adamantane actoprotector developed outside the classic Soviet military programmes, studied mainly as a cerebroprotective candidate.
Actoprotector · Institute of Organic Chemistry, NAS Ukraine · adamantane derivative
identity
formula
adamantane derivative
labelademol|lineactoprotector|schoolIOC NAS Ukraine
No PubChem CID linked. name collisions make external IDs unreliable for this archive entry.
Formula text only; no molecule drawing. Archive identity plate.
Key takeaways
Ademol is the clearest Ukrainian branch of the actoprotector idea in our map. Institute of Organic Chemistry / Darnitsa work, not a Soviet military programme.
Mapped literature is a coherent cerebroprotective animal series: carotid occlusion, subarachnoid haemorrhage, traumatic brain injury, with suggested NMDA framing.
The densest trail is the Khodakovsky cerebroprotective series in Russian-language journals; PubChem name collisions make external lookups easy to mis-route, so this page stays tied to archive IDs.
What it is
Ademol is the odd one out among actoprotectors in this archive: it comes from Ukraine’s Institute of Organic Chemistry / Darnitsa work in the 1990s, not from a Soviet military or space programme.
It was registered as a uterotonic and later discontinued; PubChem name-traps exist (the name can resolve to an unrelated diuretic), so dossier links stay tied to our archive IDs.
We feature it because it is the clearest non-Russian branch of the actoprotector idea in our map, with a coherent cerebroprotective animal series.
What the literature describes
Themed chapters drawn only from papers already mapped on this dossier. Archive map. No medical advice.
Cerebral ischemia and haemorrhage models
In bilateral carotid occlusion in rats, ademol is reported to preserve structurally intact neurons and shift the mix of cell-death types versus control pathology.
In a subarachnoid-haemorrhage model, ademol is reported to maintain cortical blood flow above control pathology, in the same experimental conversation as nimodipine.
Authors in this series propose NMDA-receptor modulation as a candidate basis for the cerebroprotective findings (suggested mechanism, not a binding study).
The densest trail is the Khodakovsky cerebroprotective series in Russian-language journals. same research circle, repeated ischemia and trauma models. That Ukrainian organic-chemistry / pharmacology shelf is the location of the archive for this compound.
PubChem naming collisions make external lookups easy to mis-route; dossier links stay tied to our archive IDs.
Open limits
Almost entirely one Ukrainian cerebroprotective series. what would multi-lab extension inside that tradition look like?
NMDA framing is correlational suggestion, not direct binding evidence in our map.
No clear bridge from rat cerebral-blood-flow preservation to clinical stroke settings in sources we mapped.
Russian full-text papers
Open-access Russian academic PDFs on CyberLeninka. Curated PubMed retrieval for this name was all off-topic / name-collision noise and was removed.
izuchenie apoptozmoduliruyuschih svoystv ademola v usloviyah modelnogo ostrogo narusheniya mozgovogo krovoobrascheniyaRussian full text
sostoyanie energeticheskogo metabolizma golovnogo mozga krys na fone vvedeniya nekotoryh infuzionnyh rastvorov pri ishemii-reperfuziiRussian full text
vliyanie ademola na uroven faktora nekroza opuholi v golovnom mozge krys s modelnym travmaticheskim porazheniem mozgaRussian full text
Is NMDA modulation supported by direct binding work, or only by correlational suggestions in the ischemia papers?
Do the oocyte-maturation findings share a mechanism with the cerebroprotective series?
Does preserved cerebral blood flow in rat models translate to clinical stroke settings? Our map does not answer that.
Reviewed against the archive corpora on 2026-09-19. Source-grounded. No clinical claims. Archive / history / research only. No medical advice. No dosing, synthesis, sourcing, or health claims.