Pathways

Sesquiterpenoids have 15 carbons and three isoprene units. They are derived from farnesyl diphosphate. They may contain rings or be acyclic, depending on the bonds formed by the loss of the diphosphate group. First, the terpenoid backbone is synthesized, producing farnesyl pyrophosphate. Two molecules of farnesyl pyrophosphate then join together to form presqualene diphosphate, catalyzed by squalene synthase 1. Then, the same enzyme removes the pyrophosphate group and replaces it with a hydrogen ion, forming squalene. Squalene then undergoes oxidation of one of its bonds via squlene monooxygenase 1, to form (S)-2,3-epoxysqualene. This may then proceed to the steroid biosynthesis pathway or may react with an isomerase or lyase to form a chair-chair-chair-boat triterpenoid. Similarly, squalene may interact with an isomerase or lyase to form a chair-chair-chair-chair triterpenoid. After the backbone is complete, farnesyl pyrophosphate can have its pyrophosphate removed by different enzymes, leading to different conformations of sesquiterpenoids. If it interacts with (Z)-gamma-bisabolene synthase, it forms gamma-bisabolene. If it interacts wtih (+)-alpha-barbatene synthase, it forms (+)-alpha-barbatene, if it interacts wtih beta-chamigrene synthase it forms (+)-beta-chamigrene, and finally if it interacts with thujopsene synthase it forms (+)-thujopsene.

Sevelamer is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Sevelamer passes through the liver and is then excreted from the body mainly through the kidney.

Sevoflurane is an inhalation anaesthetic agent used for induction and maintenance of general anesthesia during surgical procedures. It can be found under the brand names Sevorane, Sojourn, and Ultane. It is a volatile, non-flammable compound with a low solubility profile and blood/gas partition coefficient. Sevoflurane was patented in 1972, was approved for clinical use in Japan in 1990, and approved by the FDA in 1996. Sevoflurane is three times more potent than desflurane, but has lower potency compared to halothane and isoflurane. Unlike other volatile anesthetics, sevoflurane has a pleasant odor and does not irritate the airway. The hemodynamic and respiratory depressive effects of sevoflurane are well tolerated, and most patients receiving this anesthetic agent present little toxicity. Therefore, it can be used for inhalational induction in adults and children for a wide variety of anesthetic procedures. The precise mechanism of action of sevoflurane has not been fully elucidated. Like other halogenated inhalational anesthetics, sevoflurane induces anesthesia by binding to ligand-gated ion channels and blocking CNS neurotransmission. It has been suggested that inhaled anesthetics enhance inhibitory postsynaptic channel activity by binding GABAA receptors. This ability to modulate ion channel activity can also regulate cardiac excitability and contractility. Sevoflurane acts as a positive allosteric modulator of the GABAA receptor in electrophysiology studies of neurons and recombinant receptors. Some side effects of using sevoflurane may include blurred vision, chest pain, choking, and dizziness. Sevoflurane is expected to exert its action via a majority of mechanisms, including GABA(A) agonism, glycine agonism, glutamate antagonism, inhibiting calcium transporting ATPases, and activating potassium channels. It is administered via respiratory inhalation.

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