Testosterone modulates vascular endothelial cell (EC) growth and platelet aggregation through its direct action on endothelial NO production. Testosterone stimulates NO synthesis via its direct action on ECs. Testosterone involves a nongenomic stimulation of NO synthesis, which depends on calcium influx from the extracellular medium and on MAPK and PKC pathways. Testosterone increases EC growth in bovine aortic and in vein ECs. Testosterone stimulates EC migration. Testosterone stimulates VEGF and NOS expression and promotes capillary formation in the cerebral vascular system. In fact, in bovine aortic ECs, Testosterone and DHEA promote EC proliferation, migration, and vascular tube formation, effects dependent on PTX-sensitive G protein and ERK1/2 activation The calculated EC50 value of morning Testosterone corresponding to a 50% increase in the pubertal growth ratio is 3.1 nM (2.4-4.2, r2=0.84) using the dose-response model. Growth velocity increases by 50% from prepubertal growth to PHV at a morning Testosterone level of 3.1 nM (95% confidence interval 2.4-4.2), EC50.
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
|Solubility||52 mg/mL in DMSO|
Long-acting testosterone injections for treatment of testosterone deficiency after brachytherapy for prostate cancer.
Balbontin FG, et al. BJU Int. 2014 Jul;114(1):125-30. PMID: 25101359.
The response to testosterone undecanoate in men with type 2 diabetes is dependent on achieving threshold serum levels (the BLAST study).
Hackett G, et al. Int J Clin Pract. 2014 Feb;68(2):203-15. PMID: 24355040.
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