"LUTALYSE® Injection (dinoprost injection)". www.zoetisus.com. Retrieved 2021-04-06. "Hormonal Control of Estrus in Cattle - ...
"Dinoprost tromethamine Injection Advanced Patient Information". Truvn Health Analytics Inc. 2016. Retrieved November 2, 2017.. ... This article is about the pharmaceutical agent 'dinoprost'. For the drug 'dinoprostone', see Prostaglandin E2. ...
Dinoprost: also known as PGF 2α, is a naturally occurring prostaglandin which causes contraction via PG F receptors. Dinoprost ...
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... , as a lipophilic ester, easily penetrates the cornea and is then activated to the carboxylic acid, tafluprost acid. Onset of action is 2 to 4 hours after application, the maximal effect is reached after 12 hours, and ocular pressure remains lowered for at least 24 hours.[2][3] Tafluprost acid is inactivated by beta oxidation to 1,2-dinortafluprost acid, 1,2,3,4-tetranortafluprost acid, and its lactone, which are subsequently glucuronidated or hydroxylated. The cytochrome P450 liver enzymes play no role in the metabolism.[3] An analogous pathway (at least up to the tetranor-metabolites) has been found for latanoprost and travoprost. ...
It is believed that the vasoconstriction caused by thromboxanes plays a role in Prinzmetal's angina. Omega-3 fatty acids are metabolized to produce higher levels of TxA,3 which is relatively less potent than TxA2 and PGI3; therefore, there is a balance shift toward inhibition of vasoconstriction and platelet aggregation. It is believed that this shift in balance lowers the incidence of myocardial infarction (heart attack) and stroke. Vasoconstriction and, perhaps, various proinflammatory effects exerted by TxA on tissue microvasculature, is probable reason why the TxA is pathogenic in various diseases, such as ischemia-reperfusion injury.,[2] hepatic inflammatory processes,[3] acute hepatotoxicity [4] etc. TxB2, a stable degradation product of TxA2, plays a role in acute hepatoxicity induced by acetaminophen.[5][6] ...
The US National Institute of Health's MedlinePlus lists medical conditions for which EPA (alone or in concert with other ω-3 sources) is known or thought to be an effective treatment.[18] Most of these involve its ability to lower inflammation. Intake of large doses (2.0 to 4.0 g/day) of long-chain omega-3 fatty acids as prescription drugs or dietary supplements are generally required to achieve significant (, 15%) lowering of triglycerides, and at those doses the effects can be significant (from 20% to 35% and even up to 45% in individuals with levels greater that 500 mg/dL). It appears that both EPA and DHA lower triglycerides; however, DHA appears to raise low-density lipoprotein (the variant which drives atherosclerosis, sometimes inaccurately called "bad cholesterol") and LDL-C values (always only a calculated estimate; not measured by labs from person's blood sample for technical and cost reasons), while EPA does not. EPA and DHA ethyl esters (all forms) may be absorbed less well, thus ...
Leukotriene B4 (i.e. LTB4) is an arachidonic acid metabolite made by the 5-lipoxygenase enzyme pathway. It activates cells through both its high affinity (Dissociation constant [Kd] of 0.5-1.5 nM) Leukotriene B4 receptor 1 (BLT1 receptor) and its low affinity BLT2 receptor (Kd=23 nM); both receptors are G protein coupled receptors that, when ligand-bound, activate cells by releasing the Gq alpha subunit and pertussis toxin-sensitive Gi alpha subunit from Heterotrimeric G proteins.[19][20] BLT1 receptor has a high degree of ligand-binding specificity: among a series of hydroxylated eicosanoid metabolites of arachidonic acid, it binds only LTB4, 20-hydroxy-LTB4, and 12-epi-LTB4; among this same series, BLT2 receptor has far less specificity in that it binds not only LTB4, 20-hydroxy-LTB4, and 12-epi-LTB4 but also 12(R)-HETE and 12(S)-HETE (i.e. the two stereoisomers of 12-Hydroxyeicosatetraenoic acid) and 15(S)-HpETE and 15(S)-HETE (i.e. the two stereoisomers of 15-Hydroxyicosatetraenoic ...
The drug is clear with a pH of 10.[7] Its production is inhibited indirectly by NSAIDs, which inhibit the cyclooxygenase enzymes COX1 and COX2. These convert arachidonic acid to prostaglandin H2 (PGH2), the immediate precursor of prostacyclin. Since thromboxane (an eicosanoid stimulator of platelet aggregation) is also downstream of COX enzymes, one might think that the effect of NSAIDs would act to balance. However, prostacyclin concentrations recover much faster than thromboxane levels, so aspirin administration initially has little to no effect but eventually prevents platelet aggregation (the effect of prostaglandins predominates as they are regenerated). This is explained by understanding the cells that produce each molecule, TXA2 and PGI2. Since PGI2 is primarily produced in a nucleated endothelial cell, the COX inhibition by NSAID can be overcome with time by increased COX gene activation and subsequent production of more COX enzymes to catalyze the formation of PGI2. In contrast, TXA2 is ...
... supplementation in daily doses of 1,000-1,500 mg for 50 days has been well tolerated during several clinical studies, with no significant side effects reported. All common markers of health, including kidney and liver function,[35] serum lipids,[39] immunity,[40] and platelet aggregation[34] appear to be unaffected with this level and duration of use. Furthermore, higher concentrations of ARA in muscle tissue may be correlated with improved insulin sensitivity.[41] Arachidonic acid supplementation of the diets of healthy adults appears to offer no toxicity or significant safety risk. While studies looking at arachidonic acid supplementation in sedentary subjects have failed to find changes in resting inflammatory markers in doses up to 1,500 mg daily, strength-trained subjects may respond differently. One study reported a significant reduction in resting inflammation (via marker IL-6) in young men supplementing 1,000 mg/day of arachidonic acid for 50 days in combination with ...
Alprostadil is sold in the United States as urethral suppositories and in injectable form. The suppositories are sold under the brand name Muse.[6] The injectable forms are Edex[7] and Caverject.[8] Muse delivers alprostadil as a penile suppository, inserted into the urethra, at least ten minutes before the erection is needed. Caverject and Edex are similarly fast-acting, but instead are injected by syringe directly into the corpus cavernosum of the penis. Alprostadil is also available as a generic. The major cost is that it must be mixed by a compounding pharmacy and supplies may be difficult to obtain. The different formulations, including Bimix and Trimix, may include papaverine and/or phentolamine. A typical mix might be 30 mg of papaverine, 2 mg of phentolamine, and 20 μg alprostadil. As a generic, it is much less expensive than the packaged injectables. It is premixed and must be kept refrigerated and the user must load a syringe with the quantity needed. Most recently, the compound has ...
Both COX1 and COX2 (also termed prostaglandin-endoperoxide synthase-1 (PTGS1) and PTGS2, respectively) metabolize arachidonic acid by adding molecular O2 between carbons 9 and 11 to form an endoperoxide bridge between these two carbons, adding molecular O2 to carbon 15 to yield a 15-hydroperoxy product, creating a carbon-carbon bond between carbons 8 and 12 to create a cyclopentane ring in the middle of the fatty acid, and in the process making PGG2, a product that has two fewer double bonds than arachidonic acid. The 15-hydroperoxy residue of PGG2 is then reduced to a 15-hydroxyl residue thereby forming PGH2. PGH2 is the parent prostanoid to all other prostanoids. It is metabolized by (see diagram in Prostanoids: a) the Prostaglandin E synthase pathway in which any one of three isozymes, PTGES, PTGES2, or PTGES3, convert PGH2 to PGE2 (subsequent products of this pathway include PGA2 and PGB2 (see Prostanoid#Biosynthesis); b) PGF synthase which converts PGH2 to PGF2α; c) Prostaglandin D2 ...
Prostaglandin F2α (PGF2α u prostanoidnoj nomenklaturi), farmaceutski naziv dinoprost (INN), prirodni prostaglandin koji se ...
F2α (Dinoprost): Bimatoprost · Karboprost · Latanoprost · Tafluprost · Travoprost · Unoproston. I. I2 (Prostaciklin/ ...
F2α (Dinoprost): Bimatoprost · Karboprost · Latanoprost · Tafluprost · Travoprost · Unoproston. I. I2 (Prostaciklin/ ...
F2α (Dinoprost): Bimatoprost • Karboprost • Latanoprost • Tafluprost • Travoprost • Unoproston. I. I2 (Prostaciklin/ ...
F2α (Dinoprost): Bimatoprost • Karboprost • Latanoprost • Tafluprost • Travoprost • Unoproston. I. I2 (Prostaciklin/ ...
F2α (Dinoprost): Bimatoprost • Karboprost • Latanoprost • Tafluprost • Travoprost • Unoproston. I. I2 (Prostaciklin/ ...
വിവരങ്ങൾ ക്രിയേറ്റീവ് കോമൺസ് ആട്രിബ്യൂഷൻ-ഷെയർഎലൈക്ക് അനുമതിപത്ര പ്രകാരം ലഭ്യമാണ്; മേൽ നിബന്ധനകൾ ഉണ്ടായേക്കാം. കൂടുതൽ വിവരങ്ങൾക്ക് ഉപയോഗനിബന്ധനകൾ കാണുക ...
... dinoprost (INN) dinoprostone (INN) dinsed (INN) diodone (INN) Dionosil Aqueous diosmin (INN) Diovan dioxadilol (INN) dioxadrol ...
... dinoprost MeSH D10.251.355.255.550.400.350 - 6-ketoprostaglandin f1 alpha MeSH D10.251.355.255.550.550 - prostaglandins i MeSH ... dinoprost MeSH D10.251.355.255.100.637.400.350 - 6-ketoprostaglandin f1 alpha MeSH D10.251.355.255.100.637.550 - prostaglandins ...
... combinations G02AC01 Methylergometrine and oxytocin QG02AC90 Ergometrine and oxytocin G02AD01 Dinoprost G02AD02 Dinoprostone ...
... dinoprost MeSH D23.469.050.175.725.790.450 - 6-ketoprostaglandin f1 alpha MeSH D23.469.050.175.725.895 - prostaglandins i MeSH ...
InChI=1S/C26H32N4O4S/c1-20(2)30(16-10-11-17-34-19-24(31)29-35(3,32)33)23-18-27-25(21-12-6-4-7-13-21)26(28-23)22-14-8-5-9-15-22/h4-9,12-15,18,20H,10-11,16-17,19H2,1-3H3,(H,29,31) ...
In the US, ketorolac is the only widely available intravenous NSAID. An IV form of paracetamol, which is not an NSAID, became available in Europe in 2009 and then in the US.[13] The Syntex company, of Palo Alto, California developed the ophthalmic solution Acular[25] around 2006, which is currently licensed by Allergan, Inc.[26][27] In 2007, there were concerns about the high incidence of reported side effects. This led to restriction in its dosage and maximum duration of use. In the UK, treatment was initiated only in a hospital, although this was not designed to exclude its use in prehospital care and mountain rescue settings.[1] Dosing guidelines were published at that time.[28] Concerns over the high incidence of reported side effects with ketorolac trometamol led to its withdrawal (apart from the ophthalmic formulation) in several countries, while in others its permitted dosage and maximum duration of treatment have been reduced. From 1990 to 1993, 97 reactions with a fatal outcome were ...
... , also known as mesalamine or 5-aminosalicylic acid (5-ASA), is a medication used to treat inflammatory bowel disease, including ulcerative colitis and Crohn's disease.[2] It is generally used for mildly to moderately severe disease.[2] It is taken by mouth or rectally.[2] The formulations which are taken by mouth appear to be similarly effective.[3] Common side effects include headache, nausea, abdominal pain, and fever.[2] Serious side effects may include pericarditis, liver problems, and kidney problems.[2][3] Use in pregnancy and breastfeeding appears safe.[3] In people with a sulfa allergy certain formulations may result in problems.[2] Mesalazine is an aminosalicylate and anti-inflammatory.[2][3] It works by direct contact with the intestines.[2] Mesalazine was approved for medical use in the United States in 1987.[2][4] It is available as a generic medication and sold under many brand names worldwide.[5][2] A month supply in the United Kingdom costs the NHS about £43 as of ...
... is an organic compound, which, especially in its ester form, is called fenamate.[1]:458 serves as a parent structure for several nonsteroidal anti-inflammatory drugs (NSAIDs), including mefenamic acid, tolfenamic acid, flufenamic acid, and meclofenamic acid. These drugs are commonly referred to as "anthranilic acid derivatives" or "fenamates" because fenamic acid is a derivative of anthranilic acid.[2]:235[3]:17[2] ...
... (INN), or benorylate, is an ester-linked codrug of aspirin with paracetamol. It is used as an anti-inflammatory and antipyretic medication. In the treatment of childhood fever, it has been shown to be inferior to paracetamol and aspirin taken separately. In addition, because it is converted to aspirin, benorylate is not recommended in children due to concerns about Reye syndrome.[1] ...
The VIGOR (Vioxx GI Outcomes Research) study, conducted by Bombardier, et al., which compared the efficacy and adverse effect profiles of rofecoxib and naproxen, had indicated a significant 4-fold increased risk of acute myocardial infarction (heart attack) in rofecoxib patients when compared with naproxen patients (0.4% vs 0.1%, RR 0.25) over the 12-month span of the study. The elevated risk began during the second month on rofecoxib. There was no significant difference in the mortality from cardiovascular events between the two groups, nor was there any significant difference in the rate of myocardial infarction between the rofecoxib and naproxen treatment groups in patients without high cardiovascular risk. The difference in overall risk was by the patients at higher risk of heart attack, i.e. those meeting the criteria for low-dose aspirin prophylaxis of secondary cardiovascular events (previous myocardial infarction, angina, cerebrovascular accident, transient ischemic attack, or coronary ...