Casting new light with bold science.

Our Science Our Team

Skiaphos Hematology is driven by a simple mission: to cast new light on cancer and give patients better options when current treatments fall short. The company is advancing targeted medicines designed to address the underlying biology of cancer, beginning with acute myeloid leukemia (AML), where significant unmet need remains. Its lead program, SKP-001, is an IND-ready dual ENL-AF9 and FLT3 inhibitor that has demonstrated compelling activity across multiple preclinical AML models, with the potential to improve upon current standards of care.

Built by an experienced team of biotech leaders and backed by SKIA, Skiaphos is translating bold science into targeted therapies with the potential to change what is possible for people living with cancer.

About SKIA

The Challenge in AML

Acute myeloid leukemia (AML) is an aggressive and often life-threatening blood cancer where patients urgently need better treatment options. Despite advances in understanding the molecular drivers of AML and the emergence of targeted therapies, many patients continue to face intensive treatment, significant toxicity, relapse and poor long-term outcomes. The biological complexity of AML can enable disease to survive treatment and develop resistance, and therapeutic options remain limited. There is an urgent need for new approaches that can target AML more precisely, overcome mechanisms of resistance, and deliver deeper, more durable responses. Addressing these challenges requires moving beyond single-pathway approaches toward therapies that can simultaneously disrupt complementary vulnerabilities underlying leukemia initiation, survival and persistence.

Our Science

Our IND-ready lead program is SKP-001, a first-in-class dual inhibitor designed to target two critical drivers of acute myeloid leukemia (AML): ENL-AF9 (MLLT1/3) and FLT3 kinase.

ENL and AF9 are chromatin proteins that sustain leukemogenesis in ~ 40% of newly diagnosed adult AML patients, while FLT3 drives leukemia-cell growth and survival and is mutated in ~ 30% of cases. By targeting both pathways in a single molecule, SKP-001 is designed to address complementary vulnerabilities across AML, potentially reach more than half of patients, overcome resistance and more effectively eliminate leukemia cells that can drive disease persistence and relapse. Preclinical studies have demonstrated compelling activity across multiple AML models, supporting its potential to improve upon current treatment approaches.

Preclinical studies have demonstrated compelling activity across multiple AML models, supporting its potential to improve upon current treatment approaches.

Our Lead Program — SKP-001

A First-in-Class Dual Inhibitor Targeting ENL-AF9 (MLLT1/3) and FLT3 Kinase

Current AML therapies generally target a single node — menin or FLT3. SKP-001 is designed to target two complementary dependencies at once: FLT3, a key oncongenic kinase, and ENL-AF9 (MLLT1/3), two chromatin “reader” proteins that bind acetylated histones and regulate oncogenic gene expression. By simultaneously disrupting FLT3 signaling and the chromatin machinery that supports leukemic cell survival and stemness, SKP-001 is designed to address AML through a differentiated dual mechanism.

SKP-001 Blocks Two Important Oncogenic Pathways in AML

Publications

ENLIGHT-AML: A Phase 1 Study of GB3226, a Novel Dual Inhibitor of ENL-YEATS and FLT3, in Patients with Relapsed / Refractory Acute Myeloid Leukemia
2025 ASH Annual Meeting, Poster 1652

GB3226, a Novel, Orally Active, First-in-Class, Small Molecule Dual Inhibitor of ENL-YEATS and FLT3 Kinase for the Treatment of Relapsed/Refractory Acute Myeloid Leukemia
2025 ASH Annual Meeting, Poster 6106

Lead Optimization of Small Molecule ENL YEATS Inhibitors to Enable In Vivo Studies: Discovery of TDI-11055
ACS Med. Chem. Lett., 2024, 15, 4, 524–532

Small-Molecule Inhibition of the Acyl-Lysine Reader ENL as a Strategy against Acute Myeloid Leukemia
Nature Cancer, 2022 Jan; 3(1):43-59

ENL links histone acetylation to oncogenic gene expression in AML
Nature, 2017 Mar 9; 543(7644):265-269

Our Team

Leadership

Shane Kovacs, MBA  CEO

Shane is an experienced biotech executive and enterprise builder with more than 20 years of leadership experience. His successful track record includes senior roles at Olema Oncology, Bluerock Therapeutics and PTC Therapeutics. He has built and scaled organizations, executed clinical development, raised significant capital and led the negotiation of multiple value generating business development transactions.

Brian Jacoby MD, MBA  CMO

Brian is an experienced clinical development leader having held senior medical roles at Novo Nordisk, Roche, UCB, LEO Pharma, Orphazyme, and Galecto. His responsibilities and experience span both clinical development and global medical affairs. For the past eight years, he has advised numerous biotech companies on medical strategy, clinical development, and medical communication.

Lou Renzetti, PhD  CSO

Lou has more than 30 years of experience in the pharmaceutical industry, encompassing all aspects of drug discovery and early development. He served as CSO for Bridge Medicines where he led the discovery and preclinical development of SKP-001, a novel ENL/FLT3 inhibitor for AML. He spent a significant portion of his drug discovery career at Roche, as leader of the RNA Therapeutics division and Biology Head for Inflammation.

Board of Directors

Carl Goldfischer, MD  SKIA Chief Investment Officer & Co-Founder, Skiaphos Chairman

Managing Director at Bay City Capital since 2000. Over 30 years of healthcare investment experience.

Jayson Dallas, MD, MBA  SKIA Chief Executive Officer & Co-Founder, Skiaphos Director

25 years of global biopharma leadership. Former CEO of Aimmune and Rivus; CCO at Ultragenyx. Previously director at Arena, Galecto, Antag and Faeth.

Stuart Weisbrod, PhD  SKIA Co-Founder, Skiaphos Director

TBD

About SKIA

Turning Overlooked Biology into Medicines the World Remembers


A strategy built on complex situations is only as good as the people executing it, and this is where SKIA is most grounded. The hub — SKIA itself — sources and acquires overlooked assets, funds the initial work to establish a strategy, and then seeds a new portfolio company or strengthens an existing one. Each portfolio company carries a single therapeutic-area focus and is either founded by SKIA around a foundational asset or brought into the fold through recapitalization or acquisition. Our partners have collectively generated more than $25 billion in value, raised over $5 billion in capital, completed more than 180 M&A transactions, and worked across more than 15 therapeutic areas. Each partner brings decades of investment, strategic, and operational experience. Importantly, they have all done this work before: the company-builds, the exits, the turnarounds, and the deals on which this model depends.


Visit skia.bio for more information.