Frederick Sachs

After completing his formal education, Sachs taught organic chemistry at Chaminade College School followed by a position as a staff fellow at the National Institutes of Health. In 1978, he accepted an assistant professor position in the University at Buffalo's Department of Pharmacology.[1] In this role, Sachs discovered mechanosensitive ion channels which are sensors for systems including the senses of hearing, touch, and balance. As a result of his discovery, he also created the only drug to inhibit these channels.[3] Sachs believed that spider venom could contain molecular compounds that could block the ion channels.[4]

After discovering the possibility of a drug, he was contacted by several large pharmaceutical companies but none offered to adopt the drug. He eventually co-launched Rose Pharmaceuticals in 2009, which was named after Sachs’ pet tarantula and grandmother, with a stockbroker named Harvey whose grandson had had Duchenne muscular dystrophy.[5] The following year, the Food and Drug Administration designated the firm’s peptide, called GsMTx4, as an orphan drug for Duchenne muscular dystrophy.[6]

In 2012, Sachs and Harvey opened their first-ever headquarters in UB’s New York State Center of Excellence in Bioinformatics and Life Sciences and re-named the company Tonus Therapeutics.[7] Within two years, the company sold the rights to their drug to Akashi Therapeutics.[8] He also began studying AT-300’s effectiveness in dystrophic mice.[9] By 2018, Sachs demonstrated that the drug significantly reduced loss of muscle mass and susceptibility to muscle damage from repeated stimulation in an advanced animal model of DMD.[10]

In 2001, Sachs led a research team at UB which found that a chemical isolated from the venom of the Chilean tarantula could calm abnormal rhythms induced in rabbit hearts.[11] Sachs said the result of this study showed that the protein could be herald a new class of compounds that could be targeted at treating the causes, rather than the symptoms, of atrial fibrillation.[12] Following this discovery, Sachs was named a UB Distinguished Professor and honored by Buffalo Business First for his invention.[13]

In 2013, Sachs and his research team identified that familial xerocytosis causes symptoms, such as the shortness of breath seen in anemic patients. This identification marked the first time defects in a mechanosensitive ion channel were implicated as the cause of a disease.[14]

Beyond spider venom, Sachs also conducted the first voltage clamp studies of isolated adult heart cells.[15] He was also responsible for the first single-channel recording from tissue cultured cells.[3]

Sachs won the 2013 Kenneth S. Cole Award from the Biophysical Society "for his significant contributions to the understanding of cell membrane biophysics."[3] Sachs also received an Entrepreneurial Spirit Award at UB’s annual Inventors and Entrepreneurs Reception in 2015.[16]