Background:

Estrogen receptor α (ERα) and ERβ are ligand-activated transcription factors that mediate the actions of estrogen. Activation of ERα, but not ERβ, is required for the cardioprotective effects of estradiol. Propylpyrazole triol (PPT) is an ERα selective agonist with a 410-fold relative binding affinity for ERα (49%) versus ERβ (0.12%) and therefore activates gene transcription only through ERα.[1],[2] In an in vivo rabbit model of ischemia-reperfusion injury, treatment with estradiol and PPT, but not diarylpropinitrile (a selective agonist of ERβ) significantly decreased the infarct size compared with vehicle.[3]
Reference:
[1]. Stauffer, S.R., Coletta, C.J., Tedesco, R., et al. Pyrazole ligands: Structure-affinity/activity relationships and estrogen receptor-α-selective agonists. Journal of Medicinal Chemistry 43, 4934-4947 (2000).
[2]. Meyers, M.J., Sun, J., Carlson, K.E., et al. Estrogen receptors-β potency-selective ligands: Structure-activity relationship studies of diarylpropionitriles and their acetylene and polar analogus. Journal of Medicinal Chemistry 44, 4230-4251 (2001).
[3]. Booth, E.A., Obeid, N.R., and Lucchesi, B.R. Activation of estrogen receptor-α protects the in vivo rabbit heart from ischemia-reperfusion injury. American Journal of Physiology 289, H2039-H2047 (2005).