ArticleActa pharmacologica Sinica2026
A novel shark VNAR antibody-based immunotoxin targeting ERα36 disrupts non-genomic estrogen signaling and tumor metabolic reprogramming in breast cancer.
Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Anticancer drug discovery: Embracing the next wave of innovation.Acta pharmacologica Sinica · 2026Article
- Anticancer drug discovery: Embracing the next wave of innovation.Acta pharmacologica Sinica · 2026Article
- Anticancer drug discovery: Embracing the next wave of innovation.Acta pharmacologica Sinica · 2026Article
- Anticancer drug discovery: Embracing the next wave of innovation.Acta pharmacologica Sinica · 2026Article
- Anticancer drug discovery: Embracing the next wave of innovation.Acta pharmacologica Sinica · 2026Article
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Authors and funding
9 authors.
Funding
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Abstract
ERα36, a membrane-associated splice variant of estrogen receptor α, mediates rapid non-genomic estrogen signaling and is frequently overexpressed in aggressive and therapy-resistant breast cancers. Although ERα36 represents a promising therapeutic target, its clinical exploitation remains limited due to the lack of high-affinity and highly specific targeting ligands capable of recognizing its extracellular domain. In this paper, we constructed a shark-derived variable new antigen receptor (VNAR) phage display immune library and isolated two high-affinity VNAR single-domain antibodies (FR6 and TH4) targeting distinct epitopes on ERα36. The TH4 VNAR was further engineered by fusion with a truncated Pseudomonas aeruginosa exotoxin (PE24) to generate a recombinant immunotoxin (TH4-PE24), characterized by (1) high specificity and affinity for ERα36 (K
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