Roughly 20 clinical trials are underway, and at least 10 more are planned or have published some results. There are trials on senolytics for osteoarthritis, COVID-19, Alzheimer’s, and Parkinson’s diseases.  Another trial is treating grafts from older donors with senolytics before transplant. Amid these investigations, emerging evidence shows that senolytics can reduce senescence in humans and provide other benefits. The results of a study published in 2024 showed  a senolytic called foselutoclax benefited people with advanced diabetic macular edema. A single injection in the back of the eye improved their sight, especially in the dark, for at least 6 months. The drug works by inhibiting a protein that regulates cell death, leading to a removal of senescent cells that researchers believe spurs healing in the eye.

Another standout senolytic is known as D+Q, a combination of dasatinib (a US Food and Drug Administration [FDA]–-approved chemotherapy drug) and quercetin (a flavonoid found naturally in many foods). Dasatinib targets certain classes of receptors on the surface of some — but not all — senescent cells, triggering “a natural death process” . 

Research published in 2017 and 2018 found that D+Q improved bone density, lifespan, and physical function in older mice. A phase 1 clinical trial showed that intermittent doses of D+Q improved physical function in 12 older people with idiopathic pulmonary fibrosis, a serious lung disease. And a phase 2 trial in 60 healthy postmenopausal women showed that D+Q boosted formation of new bone tissue, but did not reduce bone resorption (the breakdown and removal of old bone tissue). Importantly, 10 women with the highest baseline biomarkers for senescent cell burden benefited more — with increases in bone formation, less bone resorption, and enhanced wrist bone mineral density. 

The major roadblock is the heterogeneity of senescent cells.

The senescent cells are extremely heterogeneous, and researchers are still determining what that looks like in a broad sense.

 A big problem is, we can’t really differentiate between them. We don’t have good markers that separate them, but it seems that functionally, if you treat with senolytics in an old animal, that’s beneficial. There’s conflicting data in young animals about whether there’s good or bad effects of trying to clear these cells.

But not all senescent cells are bad. In fact, senescence has sort of evolved as an anticancer mechanism. Some senescent cells are linked to tumor suppression, wound healing, and tissue repair. Generally speaking, the immune system clears these cells not long after detecting them but immune dysfunction and other factors like old age may prevent that and the cells can become pro-inflammatory and not so friendly. Senescent cells are damaged and unable to repair themselves, but not so damaged that they self-destruct — a process called apoptosis. For reasons scientists don’t fully understand, senescent cells upregulate pathways that keep them from dying. It could be that the body has an “immune memory” against senescent cells.