SCIENCE
S-nitrosylation (SNO) is one of many post-translational modifications pathways that regulate protein function. Malfunctions in these pathways can result in disease. Unlike phosphorylation and ubiquitination, the SNO pathway has received relatively little attention from drug developers despite its role in many diseases.
prior drug discovery efforts have focused on NO synthases and NO-mediated cGMP signaling
Protein S-nitrosylation requires the coordinated operation of three classes of enzymes: NO synthases to generate NO, SNO synthases that convert NO into SNO, and transnitrosylases to transfer NO groups to target proteins. SNO synthases and transnitrosylases are both protein S-nitrosylases
Denitrosylases remove NO from SNOed proteins
Our novel therapeutics targets these proteins regulating nitrosylation and denitrosylation
SNO biology is implicated in a wide variety of diseases
Theraputic Areas:
- Sickle Cell
- Muscular Dystrophy
- Pulm HTN
- Pancreatic
- Melanoma
- TNBC
- Hepatocellular Cancers
- Parkinson
- Alzheimer’s
- Autism
- ALS
- Huntington
- Atherosclerosis
- Asthma
- Multiple Sclerosis
- Coronary Disease
- Heart Failure
- Arrhythmia
- NASH
- Diabetes
- Hypercholesterolemia
- Kidney Injury
- Tissue Preservation
Platform discovers enzymes & matches enzymes + substrates to SNO sites validated in disease
Drug discovery engine powering SNO bio pipeline
Publications and Presentations
SNO Biology
Protein S-Nitrosylation: Determinants of Specificity and Enzymatic Regulation of S-Nitrosothiol-Based Signaling
The manifold roles of protein S- nitrosylation in the life of insulin
SNO Biology & Cancer
Decreased tumorigenesis in mice with a Kras point mutation at C118
S-Nitrosylation in Tumor Microenvironment
Exploiting S-nitrosylation for cancer therapy: facts and perspectives
SNO Biology & Neurodegeneration
S-nitrosylated TDP-43 triggers aggregation, cell-to-cell spread, and neurotoxicity in hiPSCs and in vivo models of ALS/FTD
S-Nitrosylation of p62 Inhibits Autophagic Flux to Promote α-Synuclein Secretion and Spread in Parkinson’s Disease and Lewy Body Dementia
Protein S-nitrosylation and oxidation contribute to protein misfolding in neurodegeneration
Protein Transnitrosylation Signaling Networks Contribute to Inflammaging and Neurodegenerative Disorders
