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Suritozole took the opposite approach from a sleeping pill; instead of boosting GABA-A signaling like a benzodiazepine, Marion Merrell Dow (via the MDL research code) built it as a partial inverse agonist at the benzodiazepine site, a molecule meant to dial GABA-A activity down just enough to sharpen memory and arousal without tipping into the anxiety or seizures that full inverse agonists cause. It moved into clinical evaluation for both depression and Alzheimer's-related memory loss in the 1990s, backed by animal data showing it could blunt cognitive impairment after traumatic brain injury in rats. The clinical program quietly stopped without ever producing published efficacy results, leaving it as a research reagent rather than a medicine.
- did not worsen cognitive impairment after traumatic brain injury in rats, unlike some comparator compounds
- no anxiogenic or convulsant effects reported at tested doses, unlike classic full inverse agonists
- clean, predictable pharmacokinetics in normal human volunteers
- Suritozole is still sold today as a laboratory reagent for probing GABA-A receptor pharmacology, decades after its clinical program went quiet.
Mechanism
Partial inverse at the benzodiazepine binding site on the -A receptor complex; unlike full inverse agonists, it lacks convulsant or strongly anxiogenic effects at tested doses while still nudging cognitive performance upward in animal models.
Safetyrisks and cautions, not medical advice
Blood levels rise faster than the dose does. Across a 230-fold single-dose range in healthy male volunteers, peak concentrations and total exposure climbed disproportionately while apparent oral clearance fell from roughly 53 to 14 liters per hour, so each increment buys more drug in the blood than the last one did. For a compound that works by turning GABA-A signaling down that matters, because the class failure mode at high exposure is anxiety and seizure. Repeat dosing at up to 120 mg twice daily ran for 28 days without a reported tolerability problem, and no adverse-event data from either clinical program was ever published.
History
Developed by Marion Merrell Dow in the late 1980s and 1990s; entered clinical evaluation for depression and Alzheimer's-associated memory loss, with supporting rat traumatic-brain-injury studies published through the mid-1990s, then discontinued with no published human efficacy data.
Resources
This entry is here for reference.
Research
- 1.Pharmacokinetics of MDL 26479, a novel benzodiazepine inverse agonist, in normal volunteers
- 2.Chronic postinjury administration of MDL 26,479 (Suritozole), a negative modulator at the GABAA receptor, and cognitive impairment in rats following traumatic brain injury
2 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is suritozole a benzodiazepine?
No, it binds the same benzodiazepine site on the GABA-A receptor but acts as a partial inverse agonist, pushing receptor activity down slightly rather than up, the opposite of a classic benzodiazepine.
What was suritozole supposed to treat?
It was evaluated clinically for depression and for Alzheimer's-related memory loss, but no efficacy results were ever published before the program ended.
Limitations of the evidence
- no published human tolerability profile beyond early pharmacokinetic volunteer studies
- as a GABA-A negative modulator, an anxiogenic ceiling effect at higher doses cannot be ruled out