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The Study

Abstract 4569: D3S-003, an orally bioavailable potent and selective dual-state inhibitor targeting both GDP- and GTP-bound KRAS G12D

In simple terms

This study is like testing a new key in a lock inside a lab — it works on a few types of locks in a petri dish and in mice, but we don’t know if it’ll open real doors in people yet.

10%

Analysis score

10/ 90

Maximum 90 for a randomized controlled trial.

Where the score came from

Reporting0
Methodology19
Publication100
Statistical31
Study type (basis of the score)
Randomized Controlled Trial
Level 1b - Individual RCT
What’s the bottom line?

Scientists made a new drug that grabs onto a broken protein (KRAS G12D) that makes cancer grow, and stops it whether it's 'on' or 'off'.

Where does this study sit?

Reviews of RCTs (Meta-analyses)

Max 100

Randomized Trials

Max 90

Reviews of Cohort Studies

Max 85

Cohort Studies

Max 72

Reviews of Case-Control Studies

Max 63

Case-Control Studies

Max 58

Cross-Sectional & Case Series

Max 50

Expert Opinion

Max 5
StrongerWeaker
Randomized Trials
Level 1b
10

10 / 100

Quality score

Participants are randomly assigned to treatment or control groups, minimizing bias. The gold standard for testing whether an intervention causes an effect.

Cannot establish causation

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Key takeaways

Summary

Based on the study abstract and findings.

  1. 1Yes — 70% tumor response in diverse models suggests this could help many patients with KRAS G12D cancers, which are currently hard to treat.
  2. 2The drug worked at very low doses (nanomolar) in cancer cells and shrank tumors in mice: 70% of tumors responded, and some disappeared completely.

Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data

Publication

Journal

Cancer Research

Year

2026

Authors

Jing Zhang, Tienan Wang, Robert A. Mook Jr., Haibo Xie, Shaonan Wang, Zhiqiang Zheng, Xin Xiong, Hui Wang, Zhi Jian Chen

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