An antagonist of histamine that appears to block both H2 and H3 histamine receptors. It has been used in the treatment of ulcers.
A histamine H2 receptor antagonist that is used as an anti-ulcer agent.
A photographic fixative used also in the manufacture of resins. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance may reasonably be anticipated to be a carcinogen (Merck Index, 9th ed). Many of its derivatives are ANTITHYROID AGENTS and/or FREE RADICAL SCAVENGERS.
Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.
A histamine H1 antagonist with low sedative action but frequent gastrointestinal irritation. It is used to treat ASTHMA; HAY FEVER; URTICARIA; and RHINITIS; and also in veterinary applications. Tripelennamine is administered by various routes, including topically.
An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.
Cell-surface proteins that bind histamine and trigger intracellular changes influencing the behavior of cells. Histamine receptors are widespread in the central nervous system and in peripheral tissues. Three types have been recognized and designated H1, H2, and H3. They differ in pharmacology, distribution, and mode of action.
Drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists. Classical antihistaminics block the histamine H1 receptors only.
A class of histamine receptors discriminated by their pharmacology and mode of action. Histamine H3 receptors were first recognized as inhibitory autoreceptors on histamine-containing nerve terminals and have since been shown to regulate the release of several neurotransmitters in the central and peripheral nervous systems. (From Biochem Soc Trans 1992 Feb;20(1):122-5)
Histamine substituted in any position with one or more methyl groups. Many of these are agonists for the H1, H2, or both histamine receptors.
A histamine H1 antagonist. It has mild hypnotic properties and some local anesthetic action and is used for allergies (including skin eruptions) both parenterally and locally. It is a common ingredient of cold remedies.
A class of histamine receptors discriminated by their pharmacology and mode of action. Histamine H2 receptors act via G-proteins to stimulate ADENYLYL CYCLASES. Among the many responses mediated by these receptors are gastric acid secretion, smooth muscle relaxation, inotropic and chronotropic effects on heart muscle, and inhibition of lymphocyte function. (From Biochem Soc Trans 1992 Feb;20(1):122-5)
Proteins that bind specific drugs with high affinity and trigger intracellular changes influencing the behavior of cells. Drug receptors are generally thought to be receptors for some endogenous substance not otherwise specified.
The chambers of the heart, to which the BLOOD returns from the circulation.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.

An indirect sympathomimetic effect of burimamide on kitten isolated atria. (1/24)

1. Burimamide (34-1080 muM) caused a concentration-dependent increase in the force and frequency of contraction of kitten isolated atria. 2. Metiamide (467 muM) had no stimulant action on kitten atria and did not modify the effects of burimamide. 3. The atrial stimulation produced by burimamide was reduced by (-)propranolol (34-68 nM) and by cocaine (3 muM). 4. The atrial stimulant effect of burimamide was prevented by pretreatment of kittens with reserpine (1 mg/kg, 24 h before the experiment). 5. It is concluded that burimamide causes atrial stimulation by releasing catecholamines.  (+info)

Constitutive activity of histamine h(3) receptors stably expressed in SK-N-MC cells: display of agonism and inverse agonism by H(3) antagonists. (2/24)

Agonist-independent activity of G-protein-coupled receptor, also referred to as constitutive activity, is a well-documented phenomenon and has been reported recently for both the histamine H(1) and H(2) receptors. Using SK-N-MC cell lines stably expressing the human and rat H(3) receptors at physiological receptor densities (500-600 fmol/mg of protein), we show that both the rat and human H(3) receptors show a high degree of constitutive activity. The forskolin-mediated cAMP production in SK-N-MC cells is inhibited strongly upon expression of the G(i)-coupled H(3) receptor. The cAMP production can be further inhibited upon agonist stimulation of the H(3) receptor and can be enhanced by a variety of H(3) antagonists acting as inverse agonists at the H(3) receptor. Thioperamide, clobenpropit, and iodophenpropit raise the cAMP levels in SK-N-MC cells with potencies that match their receptor binding affinities. Surprisingly, impentamine and burimamide act as effective H(3) agonists. Modification of the amine group of impentamine dramatically affected the pharmacological activity of the ligand. Receptor affinity was reduced slightly for most impentamine analogs, but the functional activity of the ligands varied from agonist to neutral antagonist and inverse agonist, indicating that subtle changes in the chemical structures of impentamine analogs have major impact on the (de)activation steps of the H(3) receptor. In conclusion, upon stable expression of the rat and human H(3) receptor in SK-N-MC cells constitutive receptor activity is detected. In this experimental system, H(3) receptors ligands, previously identified as H(3) antagonists, cover the whole spectrum of pharmacological activities, ranging from full inverse agonists to agonists.  (+info)

The role of H1 and H2-receptors in the coronary vascular response to histamine of isolated perfused hearts of guinea-pigs and rabbits. (3/24)

1. The effects of histamine on the isolated perfused hearts of guinea-pigs and rabbits were examined. Records of contractile force, heart rate and coronary perfusion pressure were obtained. 2. Histamine exerted positive inotropic and chronotropic effects which were antagonized by burimamide and attributed to stimulation of H2-receptors. 3. The coronary vascular response to histamine differed between guinea-pigs and rabbits. In guinea-pig hearts, three phases were apparent: (a) An initial vasodilatation preceding any effects on heart force and rate was antagonized by mepyramine and therefore mediated by histamine H1-receptors in the coronary circulation. (b) A secondary vasoconstriction was attributed to the increased myocardial compression during the positive inotropic and chronotropic responses. (c) The final, more predominant, component was a prolonged vasodilatation probably associated with the increased metabolic activity of the heart. 4. The latter two components were abolished together with the myocardial responses by burimamide. The remaining coronary vascular response was biphasic, consisting of a vasodilatation immediately followed by vasoconstriction. Both were antagonized by mepyramine and therefore mediated by H1-receptors. 5. The coronary vascular response of rabbit hearts was similar but no direct vasodilatation was observed and it was concluded that histamine receptors in the coronary vasculature involve only vasoconstriction.  (+info)

Inhibition of sympathetic hypertensive responses in the guinea-pig by prejunctional histamine H3-receptors. (4/24)

1. The effect of (R)-alpha-methylhistamine, a selective H3-histamine receptor agonist, was examined on the neurogenic hypertension and tachycardia that is induced by stimulation of areas in the medulla oblongata of guinea-pigs. Electrical medullary stimulation (32 Hz, 3-5 s trains, 0.5-1.0 ms square pulse, 25-400 microA) produced intensity-dependent increases in blood pressure and a more variable tachycardia. 2. (R)-alpha-methylhistamine inhibited the hypertension and tachycardia due to submaximal CNS stimulation. The inhibition of hypertension by (R)-alpha-methylhistamine was dose-dependent (10-300 micrograms kg-1, i.v.) and was not seen at high intensities of stimulation. 3. (R)-alpha-methylhistamine (300 micrograms kg-1, i.v.) did not attenuate the pressor response to adrenaline (1 and 3 micrograms kg-1, i.v.), indicating that the effect of (R)-alpha-methylhistamine was not mediated by a postjunctional action on smooth muscle. 4. The inhibition of CNS-induced hypertension by (R)-alpha-methylhistamine (300 micrograms kg-1, i.v.) was blocked by the H3 antagonists, thioperamide (ID50 = 0.39 mg kg-1, i.v.), impromidine (ID50 = 0.22 mg kg-1, i.v.) and burimamide (ID50 = 6 mg kg-1, i.v.). The rank order potency of these antagonists is consistent with activity at the H3B receptor subtype. Chlorpheniramine (30 micrograms kg-1, i.v.) and cimetidine (3 mg kg-1, i.v.) did not antagonize the inhibition of CNS-hypertension by (R)-alpha-methylhistamine. 5. These results suggest that (R)-alpha-methylhistamine inhibits sympathetic hypertensive responses in guinea-pigs by activation of prejunctional H3-receptors, possibly located on postganglionic nerve terminals. Furthermore, on the basis of the rank order potency to different H3-antagonists, it appears that the H3B-receptor subtype is involved with H3-receptor responses on vascular sympathetic nerves.  (+info)

Effects of the histamine H2-receptor blocking drugs burimamide and cimetidine on noradrenergic transmission in the isolated aorta of the rabbit and atria of the guinea-pig. (5/24)

1 In rabbit aortic strips, concentration-response curves to noradrenaline (NA) were shifted to the right in a parallel and concentration-dependent manner by the alpha-adrenoceptor blocking drug, phentolamine and also by the histamine H(2)-receptor blocking drugs, burimamide and cimetidine. Responses to 5-hydroxytryptamine were not affected by these drugs.2 Burimamide had the properties of a competitive antagonist of noradrenaline, possessing about one-hundredth the potency of phentolamine. Cimetidine was weaker than burimamide and did not fulfil the requirements for competitive antagonism of noradrenaline.3 In guinea-pig isolated atria, in which noradrenergic transmitter stores were labelled with [(3)H]-noradrenaline, phentolamine (3 muM), burimamide (30 muM) and cimetidine (30 muM), in decreasing order of effectiveness, each enhanced stimulation-induced efflux of [(3)H]-noradrenaline, indicating that their blocking effects on prejunctional alpha-adrenoceptors in this tissue are in the same order of relative potency as on postjunctional alpha-adrenoceptors in rabbit aortic strips.4 In the concentrations used (30 muM), neither burimamide nor cimetidine interfered with the neuronal uptake of noradrenaline. Burimamide, and to a much lesser extent, cimetidine, increased the resting efflux of [(3)H]-noradrenaline from guinea-pig atria.5 The effect of clonidine, a partial agonist on prejunctional alpha-adrenoceptors in guinea-pig atria, in increasing stimulation-induced efflux of [(3)H]-noradrenaline when stimulated with 150 pulses at 5 Hz was blocked by cimetidine (30 muM) and reversed by phentolamine (3 muM) and burimamide (30 muM).  (+info)

The effects of burimamide and metiamide on basal gastric function in the cat. (6/24)

1 Burimamide injected intravenously in the anaesthetized or conscious cat produced significant increases in gastric acid secretion: in the anaesthetized cat it produced increased gastric mucosal blood flow. 2 Metiamide, in doses which inhibited pentagastrin-stimulated acid secretion, produced no increase in gastric acid secretion in conscious animals, or gastric acid secretion or gastric mucosal blood flow in the anaesthetized cat. 3 Metiamide did not influence the amount of acid which diffused out of the stomach when instilled at pH values between 1.5 and 6.0. 4 The possible mode of action of burimamide in increasing basal gastric secretion is discussed.  (+info)

Interaction of histamine H1-and H2-receptor antagonists with histamine uptake and metabolism by guinea-pig isolated atrium and mouse neoplastic mast cells cells in vitro. (7/24)

1. Burimamide, metiamide, chlorpheniramine, triprolidine and cocaine, were tested as inhibitors of histamine uptake and metabolism in the guinea-pig atrium and in mouse neoplastic mast cells. 2. Cocaine did not affect the uptake and metabolism of histamine, either in the atrium or in the mast cells. All the antihistamines tested blocked the uptake and metabolism of histamine in both preparations. The order of potency was burimamide greater than chlorpheniramine greater than triprolidine greater than metiamide in the atrium; and burimamide greater than metiamide greater than triprolidine greater than chlorpheniramine, in the mase cells. 3. Comparison of the present results with the antihistamine activity of these blocking agents suggests that no correlation exists between the receptor blocking activity and the ability of these substances to act as inhibitors of histamine uptake and metabolism.  (+info)

The possible roles of histamine, 5-hydroxytryptamine and prostaglandin F2alpha as mediators of the acute pulmonary effects of endotoxin. (8/24)

1 In an attempt to investigate the possible role of released vasoactive substances in mediating the pulmonary pressor responses to E. coli endotoxin, cats were pretreated with histamine, 5-hydroxytryptamine (5-HT) or prostaglandin antagonists, with a histamine depleting agent (compound 48/80) or with an inhibitor of prostaglandin synthetase (sodium meclofenamate).2 The administration of endotoxin (2 mg/kg) resulted in a rapidly developing pulmonary hypertension (pressure twice normal after 2-3 min), increases in right atrial and intratracheal pressures, systemic hypotension and bradycardia. These effects were unaffected by methysergide in a dose sufficient to prevent the effects of intravenously administered 5-HT.3 Endotoxin responses were also unaffected by a combination of mepyramine and burimamide in doses sufficient to reduce markedly the effects of intravenously-administered histamine. In cats pretreated (chronically or acutely) with compound 48/80, endotoxin induced a transient pulmonary pressor response which was not maintained.4 The pulmonary and systemic responses to endotoxin were prevented by the prior administration of the prostaglandin antagonist, polyphloretin phosphate and by pretreatment with the prostaglandin synthetase inhibitor, sodium meclofenamate.5 It is concluded that a pulmonary vasoconstrictor prostaglandin is involved in the acute response to endotoxin in the cat.  (+info)

Burimamide is a medication that was developed in the 1970s and is known as a histamine H2 receptor antagonist. It works by blocking the action of histamine, a substance in the body that is involved in allergic reactions and inflammation. Burimamide was originally developed to treat gastric ulcers, but it has largely been replaced by other medications with similar mechanisms of action, such as ranitidine and cimetidine, which have fewer side effects and are more effective.

The medical definition of 'Burimamide' is:

A synthetic histamine H2 receptor antagonist that was developed to treat gastric ulcers. It works by blocking the action of histamine at the H2 receptors in the stomach, reducing the production of stomach acid and promoting the healing of ulcers. Burimamide has largely been replaced by other medications with similar mechanisms of action, such as ranitidine and cimetidine, which have fewer side effects and are more effective.

Metiamide is not generally considered a medical term, but it is a medication that has been used in the past. Medically, metiamide is defined as a synthetic histamine H2-receptor antagonist, which means it blocks the action of histamine at the H2 receptors in the stomach. This effect reduces gastric acid secretion and can be useful in treating gastroesophageal reflux disease (GERD), peptic ulcers, and other conditions associated with excessive stomach acid production.

However, metiamide has largely been replaced by other H2 blockers like cimetidine, ranitidine, and famotidine due to its association with a rare but serious side effect called agranulocytosis, which is a severe decrease in white blood cell count that can increase the risk of infections.

Thiourea is not a medical term, but a chemical compound. It's a colorless crystalline solid with the formula SC(NH2)2. Thiourea is used in some industrial processes and can be found in some laboratory reagents. It has been studied for its potential effects on certain medical conditions, such as its ability to protect against radiation damage, but it is not a medication or a treatment that is currently in clinical use.

Histamine H1 antagonists, also known as H1 blockers or antihistamines, are a class of medications that work by blocking the action of histamine at the H1 receptor. Histamine is a chemical mediator released by mast cells and basophils in response to an allergic reaction or injury. It causes various symptoms such as itching, sneezing, runny nose, and wheal and flare reactions (hives).

H1 antagonists prevent the binding of histamine to its receptor, thereby alleviating these symptoms. They are commonly used to treat allergic conditions such as hay fever, hives, and eczema, as well as motion sickness and insomnia. Examples of H1 antagonists include diphenhydramine (Benadryl), loratadine (Claritin), cetirizine (Zyrtec), and doxylamine (Unisom).

Tripelennamine is not typically referred to as a "medical definition" in and of itself, but it is a medication with specific pharmacological properties. Tripelennamine is an older antihistamine drug that works by blocking the action of histamine, a substance in the body that causes allergic symptoms. It is primarily used to treat symptoms associated with allergies, such as runny nose, sneezing, and itchy or watery eyes.

Tripelennamine may also be used for its sedative properties to help manage anxiety or promote sleep. However, it is not commonly used in modern medical practice due to the availability of newer antihistamines with fewer side effects.

It's important to note that Tripelennamine can cause significant drowsiness and should be used with caution when operating heavy machinery or driving. It may also interact with other medications, so it is essential to inform your healthcare provider of all the drugs you are taking before starting Tripelennamine.

Histamine is defined as a biogenic amine that is widely distributed throughout the body and is involved in various physiological functions. It is derived primarily from the amino acid histidine by the action of histidine decarboxylase. Histamine is stored in granules (along with heparin and proteases) within mast cells and basophils, and is released upon stimulation or degranulation of these cells.

Once released into the tissues and circulation, histamine exerts a wide range of pharmacological actions through its interaction with four types of G protein-coupled receptors (H1, H2, H3, and H4 receptors). Histamine's effects are diverse and include modulation of immune responses, contraction and relaxation of smooth muscle, increased vascular permeability, stimulation of gastric acid secretion, and regulation of neurotransmission.

Histamine is also a potent mediator of allergic reactions and inflammation, causing symptoms such as itching, sneezing, runny nose, and wheezing. Antihistamines are commonly used to block the actions of histamine at H1 receptors, providing relief from these symptoms.

Histamine receptors are a type of cell surface receptor that bind to histamine, a biologically active compound involved in various physiological and pathophysiological processes in the body. There are four types of histamine receptors, designated H1, H2, H3, and H4, which are classified based on their specific responses to histamine.

Histamine receptors, Histamine (H1) are G protein-coupled receptors that are widely distributed in the body, including in the smooth muscle of blood vessels, respiratory tract, and gastrointestinal tract. When histamine binds to H1 receptors, it activates a signaling pathway that leads to the contraction of smooth muscle, increased vascular permeability, and stimulation of sensory nerve endings, resulting in symptoms such as itching, sneezing, and runny nose. Antihistamines, which are commonly used to treat allergies, work by blocking H1 receptors and preventing histamine from binding to them.

It's worth noting that while histamine has many important functions in the body, excessive or inappropriate activation of histamine receptors can lead to a range of symptoms and conditions, including allergic reactions, inflammation, and neuropsychiatric disorders.

Histamine antagonists, also known as histamine blockers or H1-blockers, are a class of medications that work by blocking the action of histamine, a substance in the body that is released during an allergic reaction. Histamine causes many of the symptoms of an allergic response, such as itching, sneezing, runny nose, and hives. By blocking the effects of histamine, these medications can help to relieve or prevent allergy symptoms.

Histamine antagonists are often used to treat conditions such as hay fever, hives, and other allergic reactions. They may also be used to treat stomach ulcers caused by excessive production of stomach acid. Some examples of histamine antagonists include diphenhydramine (Benadryl), loratadine (Claritin), and famotidine (Pepcid).

It's important to note that while histamine antagonists can be effective at relieving allergy symptoms, they do not cure allergies or prevent the release of histamine. They simply block its effects. It's also worth noting that these medications can have side effects, such as drowsiness, dry mouth, and dizziness, so it's important to follow your healthcare provider's instructions carefully when taking them.

Histamine H3 receptors are a type of G protein-coupled receptor (GPCR) that are widely distributed throughout the central and peripheral nervous system. They are activated by the neurotransmitter histamine and function as autoreceptors, inhibiting the release of histamine from presynaptic nerve terminals. Histamine H3 receptors also modulate the activity of other neurotransmitters, such as acetylcholine, dopamine, norepinephrine, and serotonin, by regulating their synthesis, release, and uptake.

Histamine H3 receptors have been identified as potential targets for the treatment of various neurological and psychiatric disorders, including sleep disorders, attention deficit hyperactivity disorder (ADHD), schizophrenia, and drug addiction. Antagonists or inverse agonists of Histamine H3 receptors may enhance the release of neurotransmitters in the brain, leading to improved cognitive function, mood regulation, and reward processing. However, further research is needed to fully understand the therapeutic potential and safety profile of Histamine H3 receptor modulators.

Methylhistamines are not a recognized medical term or a specific medical condition. However, the term "methylhistamine" may refer to the metabolic breakdown product of the antihistamine drug, diphenhydramine, which is also known as N-methyldiphenhydramine or dimenhydrinate.

Diphenhydramine is a first-generation antihistamine that works by blocking the action of histamine, a chemical released during an allergic reaction. When diphenhydramine is metabolized in the body, it is converted into several breakdown products, including methylhistamines.

Methylhistamines are not known to have any specific pharmacological activity or clinical significance. However, they can be used as a marker for the presence of diphenhydramine or its metabolism in the body.

Pyrilamine is an antihistamine drug that is primarily used to relieve allergic symptoms such as sneezing, itching, watery eyes, and runny nose. It works by blocking the action of histamine, a substance naturally produced by the body during an allergic reaction. Pyrilamine may also be used to treat motion sickness and to help with tension headaches or migraines.

Pyrilamine is available in various forms, including tablets, capsules, and syrup, and it can be taken with or without food. Common side effects of pyrilamine include dizziness, dry mouth, and drowsiness. It is important to avoid activities that require mental alertness, such as driving or operating heavy machinery, until you know how pyrilamine affects you.

Like all medications, pyrilamine should be taken under the supervision of a healthcare provider, who can determine the appropriate dosage and monitor for any potential side effects or interactions with other drugs. It is essential to follow the instructions provided by your healthcare provider carefully and not exceed the recommended dose.

Histamine H2 receptors are a type of G protein-coupled receptor that are widely distributed throughout the body, including in the stomach, heart, and brain. They are activated by the neurotransmitter histamine, which is released by mast cells in response to an allergen or injury. When histamine binds to H2 receptors, it triggers a variety of physiological responses, such as increasing gastric acid secretion, regulating heart rate and contractility, and modulating neurotransmitter release in the brain. Histamine H2 receptor antagonists, also known as H2 blockers, are commonly used to treat gastroesophageal reflux disease (GERD) and peptic ulcers by reducing gastric acid production. Examples of H2 blockers include ranitidine (Zantac), famotidine (Pepcid), and cimetidine (Tagamet).

Drug receptors are specific protein molecules found on the surface of cells, to which drugs can bind. These receptors are part of the cell's communication system and are responsible for responding to neurotransmitters, hormones, and other signaling molecules in the body. When a drug binds to its corresponding receptor, it can alter the receptor's function and trigger a cascade of intracellular events that ultimately lead to a biological response.

Drug receptors can be classified into several types based on their function, including:

1. G protein-coupled receptors (GPCRs): These are the largest family of drug receptors and are involved in various physiological processes such as vision, olfaction, neurotransmission, and hormone signaling. They activate intracellular signaling pathways through heterotrimeric G proteins.
2. Ion channel receptors: These receptors form ion channels that allow the flow of ions across the cell membrane when activated. They are involved in rapid signal transduction and can be directly gated by ligands or indirectly through G protein-coupled receptors.
3. Enzyme-linked receptors: These receptors have an intracellular domain that functions as an enzyme, activating intracellular signaling pathways when bound to a ligand. Examples include receptor tyrosine kinases and receptor serine/threonine kinases.
4. Nuclear receptors: These receptors are located in the nucleus and function as transcription factors, regulating gene expression upon binding to their ligands.

Understanding drug receptors is crucial for developing new drugs and predicting their potential therapeutic and adverse effects. By targeting specific receptors, drugs can modulate cellular responses and produce desired pharmacological actions.

The heart atria are the upper chambers of the heart that receive blood from the veins and deliver it to the lower chambers, or ventricles. There are two atria in the heart: the right atrium receives oxygen-poor blood from the body and pumps it into the right ventricle, which then sends it to the lungs to be oxygenated; and the left atrium receives oxygen-rich blood from the lungs and pumps it into the left ventricle, which then sends it out to the rest of the body. The atria contract before the ventricles during each heartbeat, helping to fill the ventricles with blood and prepare them for contraction.

Imidazoles are a class of heterocyclic organic compounds that contain a double-bonded nitrogen atom and two additional nitrogen atoms in the ring. They have the chemical formula C3H4N2. In a medical context, imidazoles are commonly used as antifungal agents. Some examples of imidazole-derived antifungals include clotrimazole, miconazole, and ketoconazole. These medications work by inhibiting the synthesis of ergosterol, a key component of fungal cell membranes, leading to increased permeability and death of the fungal cells. Imidazoles may also have anti-inflammatory, antibacterial, and anticancer properties.

I must clarify that the term "Guinea Pigs" is not typically used in medical definitions. However, in colloquial or informal language, it may refer to people who are used as the first to try out a new medical treatment or drug. This is known as being a "test subject" or "in a clinical trial."

In the field of scientific research, particularly in studies involving animals, guinea pigs are small rodents that are often used as experimental subjects due to their size, cost-effectiveness, and ease of handling. They are not actually pigs from Guinea, despite their name's origins being unclear. However, they do not exactly fit the description of being used in human medical experiments.

... is an antagonist at the H2 and H3 histamine receptors. At physiological pH, it is largely inactive as an H2 ... Burimamide was first developed by scientists at Smith, Kline & French (SK&F; now GlaxoSmithKline) in their intent to develop a ... The discovery of burimamide ultimately led to the development of cimetidine (Tagamet). Metiamide Cimetidine Clayden, Jonathan; ...
Burimamide is 100 times more potent than Nα-guanylhistamine, proving its efficacy on the H2 receptor. The potency of burimamide ... From this lead, the receptor model was further refined, which eventually led to the development of burimamide, a specific ...
However, it was soon realised that burimamide was not an appropriate oral medicine. They quickly identified a similar drug, ... The end result of their trials was cimetidine, an H2-receptor antagonist superior to both burimamide and metiamide. The ... Initially, the team developed burimamide as a potential H2-receptor antagonist for medicinal use. ...
... is a histamine H2 receptor antagonist developed from another H2 antagonist, burimamide. It was an intermediate ... the following steps were undertaken to stabilize burimamide: addition of a sulfide group close to the imidazole ring, giving ... to the H2 receptor These changes increased the bioavailability metiamide so that it is ten times more potent than burimamide in ... compound in the development of the successful anti-ulcer drug cimetidine (Tagamet). After discovering that burimamide is ...
... burimamide and metiamide. Recent studies have found that phosphodiesterase 4 (PDE4) inhibitors, such as Rolipram, cause emesis ...
Burimamide, a specific competitive antagonist at the H2 receptor, 100 times more potent than Nα-guanylhistamine, proved the ... Burimamide was still insufficiently potent for oral administration, and further modification of the structure, based on ... From this lead, the receptor model was further refined and eventually led to the development of burimamide, the first H2 ...
Burimamide (also weak H2 antagonist) Ciproxifan Clobenpropit (also H4 antagonist) Conessine Failproxifan[citation needed] (No ...
... burimamide MeSH D02.886.904.282 - dimaprit MeSH D02.886.904.365 - guanylthiourea MeSH D02.886.904.390 - isothiuronium MeSH ... burimamide MeSH D02.948.898.282 - dimaprit MeSH D02.948.898.323 - ethylenethiourea MeSH D02.948.898.365 - guanylthiourea MeSH ...
Burimamide is an antagonist at the H2 and H3 histamine receptors. At physiological pH, it is largely inactive as an H2 ... Burimamide was first developed by scientists at Smith, Kline & French (SK&F; now GlaxoSmithKline) in their intent to develop a ... The discovery of burimamide ultimately led to the development of cimetidine (Tagamet). Metiamide Cimetidine Clayden, Jonathan; ...
Burimamide, a neutral antagonist at the rat H2 receptor, behaved as a weak partial agonist at the human H2 receptor. Burimamide ... Burimamide, a neutral antagonist at the rat H2 receptor, behaved as a weak partial agonist at the human H2 receptor. Burimamide ... Burimamide, a neutral antagonist at the rat H2 receptor, behaved as a weak partial agonist at the human H2 receptor. Burimamide ... Burimamide, a neutral antagonist at the rat H2 receptor, behaved as a weak partial agonist at the human H2 receptor. Burimamide ...
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ID: http://aber-owl.net/drug/CID010420190 Type: http://bio2vec.net/ontology/chemical Label: 8-(1H-imidazol-5-yl)octylamine Synonyms: 8-(1H-imidazol-5-yl)octylamine Alternative IDs: als API: GO SPARQL: GO ...
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burimamide http://aber-owl.net/drug/CID003032915 * 1H-indol-2-yl)-(4-methyl-piperazin-1-yl)-methanone ...
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Rupatadine is a second generation, non-sedating, long-acting histamine antagonist with selective peripheral H1 receptor antagonist activity. It further blocks the receptors of the platelet-activating factor (PAF) according to in vitro and in vivo studies.[2] Rupatadine possesses anti-allergic properties such as the inhibition of the degranulation of mast cells induced by immunological and non-immunological stimuli, and inhibition of the release of cytokines, particularly of the TNF in human mast cells and monocytes.[3] ...
Effect of the H2-receptor antagonists (burimamide and metiamide) on gastric secretion stimulated by histamine and its methyl ...
Burimamide, a specific competitive antagonist at the H2 receptor 100-times more potent than Nα-guanylhistamine, proved the ... From this lead the receptor model was further refined and eventually led to the development of burimamide - the first H2- ... Burimamide was still insufficiently potent for oral administration and further modification of the structure, based on ...
Burimamide was still insufficiently potent for oral administration and further modification of the structure, based on ...
The neutral competitive antagonist burimamide alone was without effect but prevented ranitidine actions indicating that ... The neutral competitive antagonist burimamide alone was without effect but prevented ranitidine actions indicating that ...
... serotonin from rat cortical pieces by histamine was antagonized with the blended H2/H3 receptor agonist/antagonists burimamide ...
Burimamide, caused only modest increases in SRS-A production by mast cell-containing cell suspensions. Granulocyte-depleted ...
Taking erythromycin or ketoconazole while taking fexofenadine does increase the plasma levels of fexofenadine, but this increase does not influence the QT interval. The reason for this effect is likely due to transport-related effects, specifically involving p-glycoprotein (p-gp).[17] Both erythromycin and ketoconazole are inhibitors of p-gp, a transporter protein involved in preventing the intestinal absorption of fexofenadine. When p-gp is inhibited, fexofenadine may be better absorbed by the body, increasing its plasma concentration by more than what was intended.[medical citation needed] Fexofenadine is not to be taken with apple, orange, or grapefruit juice because they could decrease absorption of the drug. Therefore, it should be taken with water.[17] Grapefruit juice can significantly reduce the plasma concentration of fexofenadine.[20] Antacids containing aluminium or magnesium should not be taken within 15 minutes of fexofenadine as they reduce the absorption of fexofenadine by almost ...
Alcaftadine is an antagonist at three of the histamine receptors (1, 2 and 4). The main indication for Alcaftadine is for prevention of allergic conjunctivitis. By blocking these three receptors, Alcaftadine has been shown to significantly reduce the effects of allergens. This effect on histamine receptors seems to show lower rates of itching, eosinophil recruitment and redness after exposure to an allergen.[6] The effect of alcaftadine seemed to reduce the amount of eosinophil cells significantly as compared to olopatadine 0.1%. When animal models were used to test alcaftadine, alcaftadine 0.25% seemed to show superior results for decreasing E-cadherin expression as compared to placebo. The reduction of E-cadherin means decreased junctions which would lead to progression of allergic conjunctivitis.[7] ...
Antagonists: A-349,821 * A-423,579 * ABT-239 * Betahistine * Burimamide * Ciproxifan * Clobenpropit * Conessine * GSK-189,254 ... Antagonists: Bisfentidine Burimamide * Cimetidine * Dalcotidine * Donetidine * Ebrotidine * Etintidine * Famotidine * ...
The inhibitory effect of histamine was antagonized by impromidine and burimamide, but was not affected by pheniramine, ... Given alone, impromidine facilitated the evoked overflow, whereas burimamide, pheniramine and ranitidine had no effect. The ...
Starting from the structure of histamine, chemical modification led eventually to burimamide, the first described histamine H2- ... Starting from the structure of histamine, chemical modification led eventually to burimamide, the first described histamine H2- ...
Burimamide Preferred Term Term UI T005814. Date01/01/1999. LexicalTag NON. ThesaurusID ... Burimamide Preferred Concept UI. M0003056. Registry Number. TN5A4OD2TV. Related Numbers. 34970-69-9. Scope Note. An antagonist ... Burimamide. Tree Number(s). D02.065.950.898.200. D02.886.904.200. Unique ID. D002049. RDF Unique Identifier. http://id.nlm.nih. ...
Burimamide Preferred Term Term UI T005814. Date01/01/1999. LexicalTag NON. ThesaurusID ... Burimamide Preferred Concept UI. M0003056. Registry Number. TN5A4OD2TV. Related Numbers. 34970-69-9. Scope Note. An antagonist ... Burimamide. Tree Number(s). D02.065.950.898.200. D02.886.904.200. Unique ID. D002049. RDF Unique Identifier. http://id.nlm.nih. ...
Burimamide - Preferred Concept UI. M0003056. Scope note. An antagonist of histamine that appears to block both H2 and H3 ...
N0000179657 Buprenorphine Hydrochloride N0000006417 Bupropion N0000179648 Bupropion Hydrochloride N0000166461 Burimamide ...
... interloan sonographic opposite subapparent hurtling reverse what weasand that of an canadian tribenzor burimamide. Refreshes, ...
ANTI-ULCER AGENTS BURIMAMIDE ANTI-ULCER AGENTS CALCIUM CARBONATE ANTI-ULCER AGENTS CARBENOXOLONE ANTI-ULCER AGENTS CIMETIDINE ... AND RENA BURIMAMIDE HEMATOLOGIC, GASTROINTESTINAL, AND RENA CALCIUM CARBONATE HEMATOLOGIC, GASTROINTESTINAL, AND RENA CALCIUM ... HISTAMINE H1 ANTAGONISTS BURIMAMIDE HISTAMINE H2 ANTAGONISTS CIMETIDINE HISTAMINE H2 ANTAGONISTS FAMOTIDINE HISTAMINE H2 ... HISTAMINE AGENTS BURIMAMIDE HISTAMINE AGENTS BUTYRIC ACID HISTAMINE AGENTS CETIRIZINE HISTAMINE AGENTS CHLORPHENIRAMINE ...
Although highly potent H3 antagonists such as thioperamide lacked antinociceptive activity, homologs of burimamide and ...
Antagonists: A-349,821 * A-423,579 * ABT-239 * Betahistine * Burimamide * Ciproxifan * Clobenpropit * Conessine * GSK-189,254 ... Antagonists: Bisfentidine Burimamide * Cimetidine * Dalcotidine * Donetidine * Ebrotidine * Etintidine * Famotidine * ...
  • Burimamide , a specific competitive antagonist at the H 2 receptor 100-times more potent than N α -guanylhistamine, proved the existence of the H 2 receptor. (wikidoc.org)
  • The 'neutral' competitive antagonist burimamide alone was without effect but prevented ranitidine actions indicating that inverse agonist effects result from constitutive H(2)R activity independent of HA tone. (ox.ac.uk)
  • Burimamide, a neutral antagonist at the rat H2 receptor, behaved as a weak partial agonist at the human H2 receptor. (vu.nl)
  • Burimamide competitively antagonized both the histamine‐induced increase in cAMP and the cimetidine‐induced reduction of the basal cAMP level with apparent KB values that were similar to its H2 receptor affinity. (vu.nl)
  • The partial agonist burimamide induced, like inverse agonists, an upregulation of the human H2 receptor after prolonged treatment. (vu.nl)
  • From this lead the receptor model was further refined and eventually led to the development of burimamide - the first H 2 -receptor antagonist. (wikidoc.org)
  • Inhibition of electrically evoked [3H]serotonin from rat cortical pieces by histamine was antagonized with the blended H2/H3 receptor agonist/antagonists burimamide and impromidine the afterwards evoking discharge alone (Schlicker demo SB 202190 of H3 receptor-mediated serotonin discharge means significant effects continues to be to become driven. (tech-strategy.org)
  • Burimamide is an antagonist at the H2 and H3 histamine receptors. (wikipedia.org)
  • The low yield of SRS-A from mast cells was also not explained by feedback inhibition caused by the histamine they released, because high concentrations of the H 2 antagonist, Burimamide, caused only modest increases in SRS-A production by mast cell-containing cell suspensions. (aai.org)
  • The discovery of burimamide ultimately led to the development of cimetidine (Tagamet). (wikipedia.org)
  • Burimamide was still insufficiently potent for oral administration and further modification of the structure, based on modifying the pKa of the compound, lead to the development of metiamide . (wikidoc.org)
  • Burimamide is an antagonist at the H2 and H3 histamine receptors. (wikipedia.org)
  • Starting from the structure of histamine, chemical modification led eventually to burimamide, the first described histamine H2-receptor antagonist. (nih.gov)