SLU-PP-332 is a small-molecule compound described in scientific literature as an estrogen-related receptor (ERR) agonist with reported activity primarily at ERRα and ERRγ in experimental systems. Published work discusses SLU-PP-332 within non-clinical research contexts, including laboratory studies evaluating receptor engagement, mitochondrial-associated markers, and metabolic signaling readouts in cellular assays and animal models.

All descriptions of SLU-PP-332 are limited to research observations from controlled in-vitro and non-clinical in-vivo model systems and do not extend beyond laboratory investigation.

Source: PubChem

Chemical Formula: C₁₈H₁₄N₂O₂
Molecular Weight: 290.3 g/mol
PubChem CID: 5338394
CAS No.: 303760-60-3
Synonyms: 4-Hydroxy-N’-(naphthalen-2-ylmethylene) benzohydrazide

Biochemical descriptions of SLU-PP-332 in the scientific literature focus on reported receptor-target engagement and downstream molecular markers observed under defined laboratory conditions. Any referenced biochemical behavior is restricted to research contexts and is not presented as indicating outcomes beyond experimental systems.

In the scientific literature, SLU-PP-332 has been discussed in non-clinical research settings involving cell-based assays and animal model studies where molecular endpoints related to energy metabolism and mitochondrial-associated pathways were examined.

Reported research contexts include examination of:

• ERRα/ERRγ-associated transcriptional signatures
• Mitochondrial bioenergetic markers measured in experimental systems
• Oxidative metabolism–associated molecular readouts
• Exercise-response pathway markers observed under laboratory conditions
• Metabolic syndrome–related biomarkers evaluated in animal models

All reported applications remain confined to descriptive investigation within controlled laboratory research environments.

Mechanistic discussions in preclinical publications describe SLU-PP-332 in relation to estrogen-related receptor (ERR) signaling and downstream gene-expression programs associated with oxidative metabolism and mitochondrial function in experimental models.

All pathway-related descriptions are limited to molecular and biochemical observations reported in controlled research systems and do not imply functional outcomes outside of laboratory study conditions.

Preclinical publications describe observations involving SLU-PP-332 in cellular and animal model systems, including measurement of metabolic markers, mitochondrial-associated endpoints, and gene-expression changes recorded under defined experimental protocols.

All reported findings are restricted to the experimental systems employed and do not extend beyond laboratory research contexts.

SLU-PP-332 is supplied as a research-grade material. Identity and composition are typically characterized using analytical techniques commonly applied to laboratory research compounds, including chromatographic and mass spectrometric methods.

Handling, storage, and analytical verification parameters are determined by individual laboratories in accordance with internal research protocols.

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9. P.-M. Badin et al., “Exercise-like effects by Estrogen-related receptor-gamma in muscle do not prevent insulin resistance in db/db mice,” Sci Rep, vol. 6, no. 1, p. 26442, May 2016, doi: 10.1038/srep26442.
10. W. Xu et al., “Novel pan-ERR agonists ameliorate heart failure through enhancing cardiac fatty acid metabolism and mitochondrial function,” Circulation, vol. 149, no. 3, pp. 227–250, Jan. 2024, doi: 10.1161/CIRCULATIONAHA.123.066542.
11. M. Losby et al., “The Estrogen Receptor-Related Orphan Receptors Regulate Autophagy through TFEB,” Mol Pharmacol, vol. 106, no. 4, pp. 164–172, Sep. 2024, doi: 10.1124/molpharm.124.000889.
12. X. X. Wang et al., “Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney,” Am J Pathol, vol. 193, no. 12, pp. 1969–1987, Dec. 2023, doi: 10.1016/j.ajpath.2023.07.008.
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14. E. Schoepke et al., “A Selective ERRα/γ Inverse Agonist, SLU-PP-1072, Inhibits the Warburg Effect and Induces Apoptosis in Prostate Cancer Cells,” ACS Chem Biol, vol. 15, no. 9, pp. 2338–2345, Sep. 2020, doi: 10.1021/acschembio.0c00670.
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