Unlocking CellULAR EpigeneticS to Transform Disease Treatment
Despite remarkable advances in biology and technology, small-molecule drug development—the cornerstone of modern therapeutics—remains slow, costly, and inefficient. We believe this inefficiency stems from outdated paradigms and an incomplete understanding of disease biology. Conventional “one-drug, one-target” strategies—such as those aimed at receptors or kinases—frequently fail to deliver durable benefit due to resistance, toxicity, and limited durability.
As Einstein noted, “We cannot solve our problems with the same level of thinking that created them.” Guided by this principle, Parkside Scientific Inc., based in New York City, is reimagining drug discovery. Rather than focusing on isolated molecular defects, Parkside pursues a systems-level strategy that reprograms the epigenome and transcriptome, addressing the root causes of disease and moving beyond reductionist, signal-centric models.
Rethinking the Root of Disease
Cell behavior is fundamentally governed by gene expression, orchestrated through dynamic epigenomic regulation. While genetic mutations or aberrant signaling may initiate disease, it is often widespread dysregulation of epigenomic and transcriptomic control across diverse cell types that drives disease progression.
This insight defines a new therapeutic paradigm: restoring coordinated gene expression to reset diseased cells toward health.
Among the most promising target classes are bromodomain (BrD) proteins—epigenetic histone readers that interpret acetylation marks to regulate transcription. When dysregulated, these proteins enforce aberrant gene-expression programs underlying cancer, inflammation, and neurodegeneration.
Parkside’s Breakthrough
The BET family of BrD proteins—particularly BRD4—has emerged as a clinically validated drug target. However, first-generation BET inhibitors such as Pelabresib[1](Novartis), developed under a single-target paradigm, have shown limited mono-therapy success due to dose-limiting toxicity and short-lived efficacy .
Parkside’s proprietary STAMP™ (Systems-Targeted Acetylation Modulation Platform) redefines epigenetic drug discovery by modulating transcriptional network rather than inhibiting a single target. Instead of suppressing one bromodomain protein, STAMP™ molecules rewire interconnected acetylation-mediated regulatory circuits, delivered improved therapeutic index, enhanced durability, and broader impact.
Our lead candidate, PS1132, with data from Phase 1 clinical trials for hematologic malignancies, has demonstrated favorable safety and pharmacokinetics, with early clinical efficacy signals in refractory T- and B-cell lymphomas resistant to chemotherapy, immunotherapy, and targeted agents (e.g., JAK1, PI3Kδ, BTK inhibitors). PS1132 represents both meaningful patient impact and a differentiated partnering opportunity.
A Platform with Broad Potential
The STAMP™ platform extends beyond hematologic cancers to encompass solid tumors (prostate, breast) and chronic inflammatory and neurodegenerative diseases, including inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis, and Alzheimer’s disease. This breadth reflects a unifying mechanism—resetting pathogenic gene-expression programs to restore healthy cellular function.
Join the Epigenomic Revolution
Parkside Scientific is transforming therapeutic innovation by harnessing the power of epigenetic reprogramming to develop next-generation, durable therapies.
For investment and partnership opportunities, please contact info@pksci.com.
02/2026
[1] Novartis is seeking EMA and FDA approval for Pelabresib + Ruxolitinib combination for myelofibrosis.