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No published human clinical trial has established a medical use for the compound

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This severe metabolic blockade reduces the transmitter content of individual vesicles by more than 50%, resulting in a dramatic decrease in quantal size and a rapid, dose-independent decay of the sympathomimetic response (Sulzer et al, 1995

Emodin-induced necroptosis in prostate cancer cells via the mitochondrial fission HSP90/MLKL/PGAM pathway

Androgens stimulate periosteal bone formation in both men and male rodents [41, 42] and are known to have a direct effect on bone healing, as it induced callus formation in segmental bone defect mouse models [43], which are in line with our present results that male mice lacking AR (AR -/Y ;Prrx1::Cre) have decreased periosteal cell activity with low levels of collagens and integrins and testosterone can only promote bone fracture repair in AR flox/Y control mice, but not in AR -/Y ;Prrx1::Cre mice

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