Levonorgestrel (D-Norgestrel) is a Progestin and Progestin-containing Intrauterine Device. The physiologic effect of levonorgestrel is by means of Inhibit Ovum Fertilization.

Levonorgestrel significantly upregulates mRNA expression of the gene encoding luteinizing hormone beta subunit (lhβ) in both male and female cockroaches, while downregulating mRNA expression of the gene encoding follicle-stimulating hormone beta subunit (fshβ). Furthermore, in long-clawed ground squirrels, Levonorgestrel decreases the mRNA expression of ovarian follicle-stimulating hormone receptor, luteinizing hormone receptor, ovarian estrogen receptor β, and progesterone receptor, as well as the mRNA expression of ERα and PR in the uterus.

Levonorgestrel elevates cyclic AMP levels in the veins and inhibits the activation of protein kinase C induced by PMA. It suppresses progesterone secretion in rat luteal cells, which is stimulated by oLH, dibutyryl-cAMP, and pregnenolone. Levonorgestrel also inhibits contractions induced by high potassium (K(+)) solutions or PMA in the presence and absence of extracellular calcium (Ca(2+)), effectuating endothelium-dependent relaxation through hindrance of calcium ion ingress and protein kinase C activation. Moreover, while the inhibitory effects of Levonorgestrel on estrogen-induced pituitary weight gain and hyperprolactinemia are attenuated by mifepristone, flunarizine does not block its effects.