About

Stuart L. Schreiber is the Morris Loeb Professor of Chemistry and Chemical Biology, Emeritus, and an Investigator at the Howard Hughes Medical Institute. His research group studies the science of therapeutics, focusing on human biology to identify validated therapeutic targets and discovering small molecules that modulate these targets to provide relief or protection from disease. His work has led to discoveries related to signaling by the phosphatase calcineurin and kinase mTOR, demonstrating that drugs can target protein kinases and phosphatases; gene regulation by chromatin-modifying histone deacetylases; small-molecule dimerizers that activate cellular processes; and small-molecule probes for challenging targets such as transcription factors, oncogenes, and protein interactions relevant to human disease. His contributions have advanced principles underlying information transfer and storage in cells, diversity-oriented synthesis, and discovery-based small-molecule screening in an open data-sharing environment. Currently, his lab investigates mechanisms of cancer resistance to therapies, exploring vulnerabilities in cell states, and studies mechanisms by which the brain maintains health, along with therapeutic agents that support brain health. His research involves discovering small-molecule binders that alter protein functions by changing their interactomes and lifetimes, utilizing modern asymmetric synthesis methods to produce candidate binders with DNA barcodes. Outside academia, Professor Schreiber serves on multiple boards and advisory committees, including Jnana Therapeutics, Forma Therapeutics, Decibel Therapeutics, and others, and holds roles on scientific advisory boards for several pharmaceutical and biotech companies. He is actively involved in conflict of interest management policies and may receive honoraria and reimbursements for speaking engagements.

Research topics

• Biology
• Computational biology
• Cell biology
• Biochemistry
• Literature
• Chemistry
• Genetics

Selected publications

• Discovery of molecular glues that bind FKBP12 and structurally distinct targets using DNA-encoded libraries

  Nature Communications · 2026-04-22

  articleOpen access

  Molecular glues are small molecules that engage their target and presenter proteins cooperatively. FKBP12 molecular glues (FK506 and rapamycin) were discovered several decades ago and have been used clinically, but our understanding of the breadth of FKBP12 molecular glues and targets has yet to be fully revealed. To expand the target classes of FKBP12 molecular glues, we construct and screen a multi-million-member non-macrocyclic FKBP12-ligand DNA-encoded library using 25 structurally distinct proteins. Synthesis and validation of select hits in biophysical and cell-based assays confirm FKBP12-dependent molecular-glue recruitment to bromodomain-containing protein 9 (BRD9) and quinoid dihydropteridine reductase (QDPR). One glue shows no measurable binding to QDPR alone but has appreciable binding in the presence of FKBP12 using either purified proteins or intact cells. The sites of recruitment are characterized with mutational analysis, competition-based methods and X-ray crystallography. The results of this study confirm that FKBP12-binding DELs can yield molecular glues generating highly selective FKBP12-target protein interactions. In this study, authors screen a 3.2 million member FKBP scaffold-directed DNA-encoded library and identify FKBP12-binding molecular glues for both bromodomain-containing protein 9 (BRD9) and quinoid dihydropteridine reductase (QDPR).

  PublisherOA PDFDOI

• Suppl. Figure S2 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>S2: HPLC analysis of STO13881 and nNeocuproine showed overlapping profiles and confirmed STO13881 to be neocuproine (purchased from Sigma-Aldrich, Switzerland). High-performance liquid chromatography (HPLC) analysis was performed using the Zuürich functional genomic center.</p>

  PublisherDOI

• Suppl. Figure S12 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>S12: Analysis of CyTof data from fresh melanoma tissue</p>

  PublisherDOI

• Table ST2 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>Table ST2: Summary of the clinical data corresponding to the primary cell cultures used in this publication</p>

  PublisherDOI

• Suppl. Figure S7 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>S7: Pathway enrichment (metabolomics)</p>

  PublisherDOI

• Suppl.Figure S16 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>S16: scRNA-sequencing analysis of xenograft tumors M130227</p>

  PublisherDOI

• Table ST5 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>Table ST5: Table of the 15 most informative proteins upregulated in MEK inhibitor-resistant cell culture (ranked by log2 fold-change).</p>

  PublisherDOI

• Table ST4 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>Table ST4: Table of the 15 most informative proteins upregulated in MEK inhibitor-sensitive cell culture (ranked by log2 fold-change).</p>

  PublisherDOI

• Table ST3 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>Table ST3: Differential expressed RNA transcripts between MEKi-sensitive and -resistant melanoma cell cultures.</p>

  PublisherDOI

• Table ST8 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma

  2025-11-24

  articleOpen access

  <p>Table ST8: Data output of the CCLE cell line screening provided by Prof. Schreiber at Broad Institute.</p>

  PublisherDOI

Recent grants

• NIH Grant R01GM038627

  NIH · $11.3M · 2018

• NIH Grant U01CA176152

  NIH · $4.4M · 2018

• Studies of Materials with Physiological Properties

  NIH · $3.2M · 2018–2023

• NIH Grant RC2CA148399

  NIH · $5.2M · 2013

• NIH Grant R01GM030738

  NIH · $948k · 1990

Frequent coauthors

• James E. Bradner

  Novartis (United States)

  290 shared

• Michelle Palmer

  251 shared

• Paul A. Clemons

  227 shared

• Benito Muñoz

  221 shared

• Nathan West

  207 shared

• Sivaraman Dandapani

  NKT Therapeutics (United States)

  205 shared

• Robert M. Williams

  192 shared

• Albert A. Bowers

  UNC Lineberger Comprehensive Cancer Center

  192 shared

Labs

• Schreiber GroupPI

Education

• B.A., Chemistry

  Harvard University

  1986

• Ph.D., Chemistry

  Harvard University

  1991

Awards & honors

• Novartis Faculty Scholar