Yakob Togar1
,
Aditya Rahman1,
Muhammad A Wicaksono1,
Sandra N Mahendra1,
Dede Dwi Putra1,
Yosef DC Salan1,
Iwan Darma Putra1,
Hardyan Sauqi1,
Eko Suhartono2
For correspondence:- Yakob Togar Email: vincentharlingcute@gmail.com
Received: 24 March 2026 Accepted: 15 July 2026 Published: 31 July 2026
Citation: Togar Y, Rahman A, Wicaksono MA, Mahendra SN, Putra DD, Salan YD, et al. Targeting endometriosis, preserving receptivity: Molecular insights into glycitein's selective action. Trop J Pharm Res 2026; 25(7):1007-1015 doi: https://dx.doi.org/10.4314/tjpr.v25i7.14
© 2026 The authors.
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Purpose: To investigate the efficacy of glycitein a plant-derived isoflavone aglycone, in inhibiting endometriosis without interfering with endometrial receptivity. Methods: Molecular docking studies were conducted to determine the interaction between glycitein and specific receptors associated with the pathogenesis of endometriosis, such as estrogen receptor-α (ERα), estrogen receptor-β (ERβ), tumour necrosis factor-α (TNF-α), nuclear factor-κB (NF-κB), Prostaglandin EP3, and apoptosis proteins such as survivin, B-cell lymphoma 2 (BCL2), B-cell lymphoma-extra-large (BCL-XL), and Fas ligand (FASL). Binding properties of glycitein were compared with those of dienogest. Results: Glycitein showed superior binding affinity to NF-κB receptor (-6.4 kcal/mol) and stronger interaction with prostaglandin EP3 receptor (-9.2 kcal/mol) compared to dienogest. In contrast, glycitein showed weaker binding affinity to apoptosis-regulating proteins, including survivin (-4.5 kcal/mol), BCL2 (-6.4 kcal/mol), BCL-XL (-6.7 kcal/mol), and FASL (-5.6 kcal/mol), compared to dienogest (-5.7, -7.6, 8.3, and -6.9 kcal/mol, respectively). Conclusion: The computational study has shown that glycitein exerted potent anti-inflammatory activity by inhibiting the NF-κB pathway and prostaglandin EP3 receptor, but had minimal effects on endometrial apoptotic mediators. Such selectivity indicated that glycitein is likely to prevent endometriosis development without negatively affecting endometrial receptivity.