Evidence map›Paper›PMID 41806828›Full record

ArticleCell chemical biology2026

A small molecule PTER-selective inhibitor reduces food intake and body weight.

Sipei Fu, Lushun Wang, Veronica L Li, Xuchao Lyu, Wei Wei, Xu Shi, Shuliang Deng, Jacob L Barber, Usman A Tahir, Charleen Adams and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell chemical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors.

Sipei FuDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA; Department of Biology, Stanford University, Stanford, CA, USA.
Lushun WangSarafan ChEM-H, Stanford University, Stanford, CA, USA; Department of Chemical and Systems Biology, Stanford University, Stanford, CA, USA.
Veronica L LiDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA; Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
Xuchao LyuDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA; Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
Wei WeiDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA; Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
Xu ShiDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Shuliang DengDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Jacob L BarberDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Usman A TahirDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Charleen AdamsDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
April CarsonDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
Bertha HidalgoDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
Laura M RaffieldDepartment of Genetics, University of North Carolina, Chapel Hill, NC, USA.
James G WilsonDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Hlib RazumkovDepartment of Chemical and Systems Biology, Stanford University, Stanford, CA, USA; Department of Chemistry, Stanford School of Humanities and Sciences, Stanford University, Stanford, CA 94305, USA.
Shuke XiaoDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
Jan SpaasDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
Daniel FernandezSarafan ChEM-H, Stanford University, Stanford, CA, USA.
Tinghu ZhangSarafan ChEM-H, Stanford University, Stanford, CA, USA; Department of Chemical and Systems Biology, Stanford University, Stanford, CA, USA.
Robert E GersztenDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Mark D BensonDivision of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Nathanael S GraySarafan ChEM-H, Stanford University, Stanford, CA, USA; Department of Chemical and Systems Biology, Stanford University, Stanford, CA, USA.
Stephen M HinshawSarafan ChEM-H, Stanford University, Stanford, CA, USA; Department of Chemical and Systems Biology, Stanford University, Stanford, CA, USA.
Jonathan Z LongDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA; Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA; The Phil & Penny Knight Initiative for Brain Resilience at the Wu Tsai Neurosciences Institute, Stanford University, Stanford, CA, USA. Electronic address: jzlong@stanford.edu.

Funding

Role of a lactate-derived signaling metabolite in tissue crosstalk and energy balanceR01DK136526 · NIDDK · STANFORD UNIVERSITY · PI Jonathan Z Long · 2023 to 2026
$2.0M
Chemical control of energy metabolism by N-acyl amino acidsR01DK124265 · NIDDK · STANFORD UNIVERSITY · PI LONG, JONATHAN Z · 2020 to 2024
$2.0M
Role of the BHB shunt in energy balanceR01DK146315 · NIDDK · STANFORD UNIVERSITY · PI Jonathan Z Long · 2026 to 2026
$796k
NIDDK NIH HHS R01 DK124265NIDDK NIH HHS R01 DK136526NIDDK NIH HHS R01 DK146315
6 · The paper itself

Abstract

PTER (phosphotriesterase-related) is an amidohydrolase that mediates catabolism of the anorexigenic metabolite N-acetyltaurine. However, the structural basis of PTER ligand binding and catalysis remains unknown, limiting our ability to harness this pathway therapeutically. Here, we solve crystal structures of a eukaryotic PTER in apo and product-bound forms. These structures uncover an unexpected pocket homology between PTER and histone deacetylase (HDAC) enzymes. We exploit this similarity to engineer a substrate-competitive PTER inhibitor called PTERi with nanomolar potency and >100-fold selectivity for PTER over HDACs in vitro. The administration of PTERi to diet-induced obese mice reduces feeding, enhances glucagon-like peptide 1 receptor agonist (GLP1-RA)-induced weight loss, and prevents weight regain after GLP1-RA discontinuation. The structure of PTER connects histone and metabolite deacetylation into a parallel conceptual framework and enables proof-of-concept data for the pharmacological inhibition of PTER in obesity.

Indexed as

Body WeightEatingEnzyme InhibitorsSmall Molecule LibrariesAnimalsCrystallography, X-RayHistone DeacetylasesHumansMaleMiceMice, Inbred C57BLModels, MolecularObesityEnzyme InhibitorsHistone DeacetylasesSmall Molecule Librariesacetatebody mass indexenzymeHDACinhibitorobesitytaurine

Identifiers

PMID41806828
PMCPMC12981338

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.