Evidence & regulatory context
- Mechanism
- AP39, a mitochondria-targeted slow-release hydrogen-sulfide donor (tool compound).
- Target
- Not recorded
- Injury models
- Haemorrhage/shock
- Reported indication
- Not recorded
- First approval
- Not recorded
- Development stage
- Not recorded
- ChEMBL record
- Not recorded
- ChEMBL max phase
- Not recorded
- Synonyms
- Not recorded
- Note
- Not recorded
Clinical trials 0
0 linked trials carry an injury-indication flag. These flags support record-level exploration and sit alongside the stringent aggregate counts described in Methods.
No linked human trial in this dataset.
Preclinical evidence 1
1 studies reported at therapy level; 1 evidence entries itemised.
MouseHaemorrhage/shockControlledC57BL/6MaleIntravenous bolus100 nmol/kg (high dose) or 10 nmol/kg (low dose)At start of resuscitation, after 1 h of haemorrhage
Model: Blast wave-induced blunt chest trauma (TxT) followed by 1 h haemorrhagic shock and 4 h resuscitation
High dose AP39 attenuated systemic inflammation and reduced pulmonary iNOS and IkappaB alpha expression, but in the combined trauma plus haemorrhagic shock group it produced the lowest mean arterial pressure, highest norepinephrine requirement and higher mortality. Low dose AP39 had no haemodynamic…
Extraction: extract · Subtype source: llm · Supplied extraction confidence: 0.72. Machine-extracted fields require source verification.