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Article

Dual targeting of SLC25A51 and succinate dehydrogenase selectively depletes mitochondrial NAD+ to eradicate KRAS-driven AML.

Cell metabolism - 2 Jun 2026

Jia Ang, Zhang Xiaowen, Zhou Ji-Hao, Ma Yongcan, Wang Jing, Gong Yongbo, Song Wenjie, Hu Hangcheng, Yu Yufei, Yang Haixia, Lu Youli, Huang Linzhang, Du Xingrong, Chang Chunmei, Pei Shanshan, Li Peng, Jordan Craig T, Zhao Tong-Jin, Ye Haobin

Abstract excerpt

Acute myeloid leukemia (AML) arises from diverse mutations, yet its most aggressive drivers remain elusive. Here, we show that Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations drive hyperproliferative and therapy-/glucose stress-resistant AML, whereas existing inhibitors lack sufficient cytotoxicity. Dual physiological/glucose-deprived screening identified compound 615 selectively eliminating...

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Share to Cell Line, Tumor
Share to Leukemia, Myeloid, Acute

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Proto-Oncogene Proteins p21(ras)

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Source

Identifiers

PMID: 41616775
DOI: 10.1016/j.cmet.2026.01.001

Genes

KRAS
SLC25A51

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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