SRS11-92

1 paper4 findings

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

On aging: the drug’s trials ARN judged to be about aging, of every trial that tests it for any use.

No results posted: trials that ended more than a year ago with no results on ClinicalTrials.gov and no paper in ARN’s record.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

1 lab in 1 country

Funders: Huazhong University of Science and Technology and 3 more

Animals1

Outcomes

Cellular senescence

downin human cells1downin mice1

1 study

SRS11-92 decreases cellular senescence in mice.
“reduced the hippocampal SA-β-gal-positive burden”
Animalshippocampus6 weeks
Neuroprotective effects of SRS11-92 against oxidative stress-induced senescence via Nrf2/HO-1/NF-κB in Alzheimer's disease models
Inflammopharmacology6 Dec 2025
SRS11-92 decreases cellular senescence in human cells.
“decreased the percentage of SA-β-gal-positive cells, and downregulated p53, p16, and p21”
Cellsin Aβ25−35-treated SH-SY5Y cells
Neuroprotective effects of SRS11-92 against oxidative stress-induced senescence via Nrf2/HO-1/NF-κB in Alzheimer's disease models
Inflammopharmacology6 Dec 2025

Latest

1 in 12 months

Inflammopharmacology6 Dec

Neuroprotective effects of SRS11-92 against oxidative stress-induced senescence via Nrf2/HO-1/NF-κB in Alzheimer's disease models

Experiments in miceAlzheimer's disease

Paper

SRS11-92

Outcomes

Latest

Neuroprotective effects of SRS11-92 against oxidative stress-induced senescence via Nrf2/HO-1/NF-κB in Alzheimer's disease models

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