Atosiban 6.75 Mg

Its core mechanism of action lies in its ability to competitively bind to nobitocins receptors on the membrane of uterine smooth muscle cells. Nobitocins is a hormone synthesized by the hypothalamus and released by the neuropituitary gland. It plays a crucial role during childbirth by binding to nobitocins receptors on uterine smooth muscle, activating a series of signaling pathways, and ultimately leading to uterine contractions. It has a similar structure to nobitocins and can bind to nobitocins receptors first, occupying the binding site of the receptor, thereby preventing the normal binding of nobitocins to the receptor. This competitive combination prevents nobitocins from exerting its function of inducing womb contractions.

Thereby inhibiting uterine contractions and achieving the effect of protecting the fetus.
Related studies have shown that in the treatment of premature birth, when pregnant women experience regular contractions and other premature birth symptoms, the level of nobitocins in the body increases. Through competitive binding to nobitocins receptors, it effectively reduces the frequency and tension of uterine contractions. For example, in clinical trials, for pregnant women who experience regular womb contractions between 24-33 weeks of pregnancy, the frequency of uterine contractions is significantly reduced after use, which provides valuable time for the further development of the fetus in the mother's body.

After binding to receptors, nobitocins initiates a series of complex signaling processes within the cell, with a key step being the stimulation of increased production of inositol triphosphate (IP3). As a second messenger, IP3 can bind to the IP3 receptor on the endoplasmic reticulum, promoting the release of calcium ions stored in the endoplasmic reticulum into the cytoplasm. Meanwhile, extracellular calcium ions can also enter the cell through voltage-gated calcium channels, leading to a significant increase in intracellular calcium ion concentration.

Calcium ions are key signaling molecules that trigger womb muscle contraction, and an increase in their concentration activates myosin light chain kinase (MLCK), phosphorylating myosin light chain and triggering womb smooth muscle contraction.

Atoxiban competitively binds to nobitocins receptors, preventing the aforementioned signaling process triggered by nobitocins. Specifically, it inhibits the generation of IP3, thereby reducing the release of calcium ions from the endoplasmic reticulum and preventing the opening of voltage-gated calcium channels, reducing the influx of extracellular calcium ions.

In this way, the intracellular calcium ion concentration cannot increase to a level sufficient to trigger womb contractions, and the womb smooth muscle remains in a relaxed state. Animal experiments have provided strong evidence for this mechanism of action. After intravenous administration of atosiban to rats and guinea pigs, binding to nobitocins receptors can reduce womb contraction frequency and tension, inhibit womb contractions, and have no effect on cardiovascular function. This indicates that it can specifically interfere with calcium signaling in uterine smooth muscle cells without affecting the normal function of other systems.

In assisted reproductive technology, especially in the process of embryo transfer, it also plays an important role, and its mechanism of action is mainly related to improving endometrial receptivity. Endometrial receptivity refers to the ability of the endometrium to accept embryos, and good endometrial receptivity is one of the key factors for successful embryo implantation.
Controlled ovarian hyperstimulation is a commonly used method in assisted reproductive technology, but this method can lead to a significant increase in estrogen levels in the body, which in turn induces the local production of more nobitocins receptors in the uterus.

Resulting in a pre transplant womb contraction activity that is about 6 times higher than before natural cycle ovulation.

This high-frequency womb contractions not only affect the blood flow perfusion of the endometrium, reducing its ability to accept embryos, but may also physically expel embryos transplanted into the womb cavity. Research has shown that less than 50% of embryos can remain stable in the womb cavity one hour after embryo transfer.

As a nobitocins receptor antagonist, it can inhibit womb contractions, reduce peristaltic waves in the endometrium, improve blood flow perfusion in the endometrium, and enhance the endometrium's ability to accept embryos. In addition, atosiban 6.75 mg may also promote the decidualization process of the endometrium by regulating the gene expression and cytokine secretion of endometrial cells, creating a more favorable microenvironment for embryo implantation. Some retrospective studies show that for sisters who have transferred high-quality embryos for many times but are still pregnant, abnormal womb contraction is an important consideration after excluding embryonic factors, endometrial organic diseases and other reasons. After use, the pregnancy rate of some patients has been improved.