At Satya, we're dedicated to creating Big Drugs for Big Diseases - developing transformative therapies for major health challenges that impact millions. Our mission is to deliver high-impact solutions across diseases, ensuring patient benefit through innovative approaches.
Using AI-driven insights, we target patient populations by modulating key biological processes, such as the cell cycle, DNA repair, and cell metabolism, to address diseases across oncology, inflammation, and metabolic disorders.
In the DNA damage repair (DDR) space our focus is on inhibiting Homologous Recombination (HR) via RAD51: BRCA2 disruption; we are also generating differentiated PARG inhibitors through covalent mechanisms that exhibit sustained PD; SOS1 inhibitors can have a broad impact across KRAS and EGFR driven tumors either as a single agent or in combinations
A novel and hitherto undrugged class of biology is being explored as a platform for oncology and inflammatory disorders through an academic collaboration
In the metabolic disorders space we have an abiding interest in generating alternative obesity treatments for emerging markets as well as supportive therapeutics for improved outcomes such as preservation of lean muscle mass or to mitigate gastrointestinal effects
Satya leverages its deep expertise in traditional drug discovery, enhanced by AI, to gain profound insights into target biology. Our teams access extensive literature, curate public databases, and develop models to study ligand-protein interactions, focusing on pathways that significantly impact large patient populations.
We select biological targets critical to the cell cycle, DNA-damage repair, or metabolic pathways, aiming to modulate them to address underlying diseases while minimizing effects on normal cellular processes. This approach enables us to develop drugs with transformative potential for conditions including cancer, inflammation, and metabolic disorders
Founder and CEO
Senior Director, Discovery Biology
Director, Medicinal Chemistry
Satyas Scientific Advisory Board comprises seasoned and accomplished scientists, with preclinical and clinical expertise in oncology.
Advisor, Science And Strategy
Scientific Advisor
Satya’s Pipeline comprises First-In-Class and Best-In-Class
Targets focused on DDR pathway and Oncogenes.
| Target | MOA / Indication | Bio Marker | Rights | Early Discovery | Lead Optimization | Pre - Clinical | IND |
|---|---|---|---|---|---|---|---|
| RAD51:BRCA2 Disruptor | DDR; PARPi-Resistant Ovarian and Breast Cancers | RAD51 | Global | ||||
| SOS1 | Oncogene; NSCLC, CRC | EGFR Mutation & Pan RAS Mutation | Global | ||||
| PKMYT1 | DDR / Cell Cycle | CCNE1 Amplification | Partnered | ||||
| First-in-class biology (Platform) | Oncology/ Inflammation | Undisclosed | Partnered | ||||
| PARG (Covalent Inhibitor) | DDR; Breast and Ovarian Cancers | HRD | Global | ||||
| Metabolic pathways | Obesity & complementary care | Undisclosed | Global | ||||
RAD51 is the central recombinase involved in homologous recombination-mediated DNA double strand break repair.
SOS1 is a guanine nucleotide exchange factor for RAS proteins involved in activating RAS. Inhibition of SOS1 results in lowering the RAS-GTP activated state, inhibiting the RAS-MEK-ERK pathway and lowering proliferation, in both WT and the various mutant Ras isoforms.
PARG inhibition disrupts DNA damage repair cycle and leads to cell death. PARG depleted/ inhibited cells show increased sensitivity to DNA damage agents.
PKMYT1 kinase functions as negative regulator of CDK1. Inhibiting its function leads to unscheduled activation of CDK1 selectively in CCNE1-overexpressing cells, promoting early mitosis in cells undergoing DNA synthesis.
Recent highlights on our programs, News, Events and Leadership
