Pathways

Anileridine is an opioid analgesic that is most commonly used to treat pain varying from moderate to severe in intensity. Mainly in practice, it is to alleviate pain from narcotic substances as it acts upon the central nervous system to relieve pain one might experience from withdrawal. Anileridine is an analog of pethidine (another synthetic opioid pain medication that is a part of the class of phenylpiperidine). The mechanism of action is elicited by the binding of Anileridine with mu-opioid receptors that are coupled with Gi protein-coupled receptors. This causes the hydrolysis of GTP to GDP of the G protein leading to the downstream cascade of decreasing adenylate cyclase activity in turn decreasing available cAMP concentration. cAMP levels decreasing inhibits the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and norepinephrine, not only this but inhibiting the release of hormones such as vasopressin, somatostatin, insulin, and glucagon. Anileridine continues to elicit its inhibitory effects by causing hyperpolarization leading to reduced neuronal excitability by closing N-type voltage calcium channels and opening calcium-dependent inwardly rectifying potassium channels. These effects facilitate relaxation, reduces spasms of the larynx, and when using in conjunction with meperidine can reduce the amount of anesthetic needed to administer to supply patients with sufficient anesthesia. Administration of Anileridine is not limited to any one form it can be administered via intravenous, subcutaneous, inhalation, and so forth. It is metabolized by the hepatic system, any overexposure to Anileridine can result in dizziness, perspiration, dry mouth. difficulty with visual field, itching, euphoria, restlessness, nervousness, excitement, and experiencing a feeling of warmth.

Anileridine (also known as Leritine) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of anileridine will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.

Anileridineb is a synthetic opioid analgesic medication. It is a narcotic pain reliever used to treat severe pain. It can be taken intramuscularly, intravenously, subcutaneously, or orally. Anileridineb binds to mu opioid receptors, stimulating the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA is inhibited. Opioids close N-type voltage-operated calcium channels and open calcium-dependent inwardly rectifying potassium channels. This results in hyperpolarization and reduced neuronal excitability. Morphine acts at A delta and C pain fibres in the dorsal horn of the spinal cord. By decreasing neurotransmitter action there is less pain transmittance into the spinal cord. This leads to less pain perception.

Anisindione is a synthetic vitamin K antagonist derived from indanedione that is used only if coumarin-derived anticoagulants such as warfarin or coumadin cannot be taken, due to its side effects. It is also marketed as Miradon or Unidone. Anisindione works as other vitamin K antagonists, by reducing the stores of reduced vitamin K, by inhibiting the vitamin K gamma reductase complex, and preventing the recycling of the vitamin K within the cell. This in turn prevents coagulation factors VIII, IX, X as well as prothrombin, factor II, from activating, which in turn prevents fibrin clots from being formed and stabilized. Anisindione is administered orally and is absorbed in the intestine and enters the liver. There, it inhibits the vitamin K epoxide reductase complex, preventing vitamin K1 2,3-epoxide from being recycled into reduced vitamin K. This leads to less reduced vitamin K to be present in order to react with the precursors of coagulation factors II, VII, IX and X through the vitamin K dependent gamma-carboxylase, and prevents those coagulation factors from being produced. Normally, coagulation factor IX is activated by factor XIa, which then, with the addition of coagulation factor VIII, forms the tenase complex that activates coagulation factor X. Activated coagulation factor Xa then joins with coagulation factor V to form the prothrombinase complex which forms thrombin from prothrombin. Thrombin is then necessary to convert fibrinogen to loose fibrin within the blood plasma, as well as converting coagulation factor XIII into its activated form. The fibrin then is able to polymerizes, and is stabilized into a water insoluble clot by coagulation factor XIIIa. The presence of anisindione and the absence of reduced vitamin K prevents this coagulation cascade from occurring as much due to lack of substrates, and thus helps to prevent blood clotting.

Metabolites of Anisindione are predicted with biotransformer.

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

Anisotropine methylbromide is a quaternary ammonium compound. Its use as treatment adjunct in peptic ulcer has been replaced by the use of more effective agents. Depending on the dose, anisotropine methylbromide may reduce the motility and secretory activity of the gastrointestinal system, and the tone of the ureter and urinary bladder and may have a slight relaxant action on the bile ducts and gallbladder. In general, smaller doses of anisotropine methylbromide inhibit salivary and bronchial secretions, sweating, and accommodation; cause dilatation of the pupil; and increase the heart rate. Larger doses are required to decrease motility of the gastrointestinal and urinary tracts and to inhibit gastric acid secretion. Quaternary ammonium compounds such as anisotropine methylbromide inhibit the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves as well as on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These postganglionic receptor sites are present in the autonomic effector cells of the smooth muscle, cardiac muscle, sinoatrial and atrioventricular nodes, and exocrine glands. By being an antagonist of the M2 receptor on the smooth muscle of the GI tract, this drug inhibits the Gi signalling pathway leading to decreased intracellular calcium levels and muscle relaxation, therefore decreasing the motility of the GI tract. Possible side effects of using anisotropine methylbromide may include constipation, dry mouth, urinary retention, and headache.