Browsing Pathways
Showing 124111 -
124120 of 605359 pathways
SMPDB ID | Pathway Name and Description | Pathway Class | Chemical Compounds | Proteins |
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SMP0175134View Pathway |
Chlorpheniramine H1-Antihistamine Immune Response Action PathwayChlorpheniramine is a histamine-H1 receptor antagonist indicated for the management of symptoms associated with upper respiratory allergies. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles.
H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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SMP0175151View Pathway |
Chlorpromazine H1-Antihistamine Immune Response Action PathwayChlorpromazine is an H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles.
H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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SMP0175153View Pathway |
Zuclopenthixol H1-Antihistamine Immune Response Action PathwayZuclopenthixol is a weak H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles.
H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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SMP0175127View Pathway |
Olopatadine H1-Antihistamine Immune Response Action PathwayOlopatadine is a histamine H1 antagonist used to treat allergic conjunctivitis and rhinitis. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles.
H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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SMP0175139View Pathway |
GSK-1004723 H1-Antihistamine Immune Response Action PathwayGSK-1004723 is an H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles.
H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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SMP0126475View Pathway |
Mercaptopurine Action Pathway (New)Mercaptopurine is an antimetabolic antineoplastic agent used in the treatment and maintenance therapy of acute lymphatic leukemia (ALL), acute promyelocytic leukemia, autoimmune hepatitis, Crohn's disease (CD), lymphoblastic lymphoma, and ulcerative colitis. This drug is a purine analogue, so it acts by interfering with the nucleic acid biosynthesis in cells. More specifically, this molecule is an analogue of the adenine and hypoxanthine bases. By being an analogue of those, mercaptopurine competes with them for the hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) enzyme and is itself converted to thioinosinic acid (TIMP). It is this metabolite that inhibits many reactions: among others, the conversion of inosinic acid to xanthylic acid and the conversion of IMP to adenylic acid (via the adenylosuccinate). There are 3 ways that this drug causes immunosuppression 1) One of the metabolites (thiodeoxyguanosine-5'-triphosphate) can be incorporated into DNA creating false information that cannot be used for replication or RNA transcription and translation, 2) Thioguanosine 5'-triphosphate (not deoxy form metabolite) causes inhibition of ras-related c3 botulinum toxin substrate 1, a small GTPase protein on the cell membranes. This protein regulates many events like replication, cell-to-cell adhesion, epithelial differentiation, apoptosis, and more. Most importantly, it helps the regulation of the apoptosis of T and B lymphocytes so when this substrate is inhibited, T and B cells undergo apoptosis since there is no regulation lowering the immune system. 3) the 6-methyl thiopurine 5'-monophosphate ribonucleotide/6-methylthioisonate, a mercaptopurine metabolite, inhibits amidophosphoribosyltransferase (glutamine-5-phosphoribosylpyrophosphate aminotransferase) which is a key enzyme in the purine de novo synthesis pathway. Amidophosphoribosyltransferase catalyzes the conversion of phosphoribosyl pyrophosphate into 5-phosphoribosylamine, the first committed step to the biosynthesis of purines. By inhibiting this step, adenine, adenosine, guanine, and guanosine cannot be produced. Because T and B lymphocytes are reliant on the purine de novo pathway to obtain purines, inhibition causes them to die since they cannot proliferate quickly. Other cells can obtain purines from other sources, but T and B cells cannot. An overdose of this drug would result in anorexia, nausea, vomiting, myelosuppression, liver dysfunction, and gastroenteritis. Mercaptopurine is administered as an oral suspension or tablet.
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SMP0126605View Pathway |
Domperidone Mechanism of Action Action PathwayDomperidone is known as a prokinetic dopamine antagonist. It acts as a gastrointestinal emptying (delayed) adjunct and peristaltic stimulant. The gastroprokinetic properties of domperidone are related to its peripheral dopamine receptor blocking properties. Domperidone facilitates gastric emptying and decreases small bowel transit time by increasing esophageal and gastric peristalsis and by lowering esophageal sphincter pressure. Antiemetic: The antiemetic properties of domperidone are related to its dopamine receptor blocking activity at both the chemoreceptor trigger zone and at the gastric level. It has strong affinities for the D2 and D3 dopamine receptors, which are found in the chemoreceptor trigger zone, located just outside the blood brain barrier, which - among others - regulates nausea and vomiting
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SMP0126619View Pathway |
Methamphetamine Serotonin Reuptake Inhibitor Action PathwayMethamphetamine (metamfetamine) is a psychostimulant and sympathomimetic drug. It is mainly taken recreationally but can be taken for ADHD and exogenous obesity in the form of a drug called Desoxyn. Methamphetamine induces effects of euphoria and affects heart rate, body temperature, blood pressure, appetite, attention, mood, and responses associated with alertness or alarm conditions. The drug triggers mainly a fight or flight response in the body and brain.
Methamphetamine acts on the serotonin pathway both in the brain and in the gastrointestinal tract. More than 90% of serotonin is produced in gut cells. It is synthesized from Tryptophan which synthesizes 5-Hydroxy-L-tryptophan which synthesizes serotonin or 5-hydroxytryptamine. The mechanisms in which methamphetamine acts on serotonin are very similar to that of dopamine and norepinephrine in the presynaptic neuron. Methamphetamine inhibits Amine oxidase [flavin-containing] A which when uninhibited metabolizes serotonin into 5-Hydroxyindoleacetic acid. The inhibition of this causes serotonin to accumulate in the cytosol. Like norepinephrine the methods are less tested than for dopamine. The high concentration of serotonin in the synapse activates 5-hydroxytryptamine receptor 2A, 3A, and 3B on the postsynaptic neuron membrane. Activation of 5-hydroxytryptamine receptors in the gut causes the smooth muscles around intestines to contract which causes food to pass through the intestine more quickly. The faster food passes through, the less nutrients absorbed into the blood stream which would help with exogenous obesity. In the brain, the mechanisms of 5-hydroxytryptamine receptor activation is not well understood, but it has been found that there is an effect on mood, perception, cognition, which can possibly help with ADHD.
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SMP0126617View Pathway |
Amitriptyline Serotonin Antagonist Action PathwayAmitriptyline is a tricyclic antidepressant indicated in the treatment of depressive illness, either endogenous or psychotic, and to relieve depression associated anxiety. The non-FDA-approved indications are anxiety, post-traumatic stress disorder, insomnia, chronic pain (diabetic neuropathy, fibromyalgia), irritable bowel syndrome, interstitial cystitis (bladder pain syndrome), migraine prophylaxis, postherpetic neuralgia, and sialorrhea. The three-ring central structure, along with a side chain, is the basic structure of tricyclic antidepressants.
The monoamine hypothesis in depression, one of the oldest hypotheses, postulates that deficiencies of serotonin (5-HT) and/or norepinephrine (NE) neurotransmission in the brain lead to depressive effects. Amitriptyline by blocking the reuptake of both serotonin and norepinephrine neurotransmitters. In serotonergic neurons, serotonin is synthesized from tryptophan and stored in synaptic vesicles. Once an action potential arrives at the nerve terminal, calcium channels open, causing the influx of calcium in the cytosol. Calcium then triggers the release of neurotransmitters stored in synaptic vesicles via exocytosis. The serotonin is released into the synapse and acts on 5HT2A and 5HT2C receptors which are responsible for mood improvements. The serotonin in the synapse is rapidly taken up by the serotonin reuptake transporter on the presynaptic neuron, and is recycled. Amitriptyline inhibits these reuptake transporters on serotonergic neurons, thereby increasing serotonin concentration in the synapse. This allows more stimulation of 5HT2A and 5HT2C receptors needed to improve depressive moods.
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SMP0126597View Pathway |
Paliperidone Serotonin Antagonist Action PathwayPaliperidone is the primary active metabolite of risperidone. The two antipsychotics are also metabolized differently, as risperidone is metabolized in the liver mainly by the polymorphic cytochrome P450 2D6 (CYP2D6) to its active metabolite 9-hydroxyrisperidone (paliperidone). Paliperidone, by contrast, is predominantly excreted unchanged in the urine The mechanism of action of paliperidone is unknown but it is likely to act via a similar pathway to risperidone as second generation antipsychotics. It has been proposed that the drug's therapeutic activity in schizophrenia is mediated through a combination of central dopamine Type 2 (D2) and serotonin Type 2 (5HT2A) receptor antagonism. Paliperidone is also active as an antagonist at alpha 1 and alpha 2 adrenergic receptors and H1 histaminergic receptors, which may explain some of the other effects of the drug. It is available as an extended-release tablet, a once-monthly intramuscular injection, an every-three-month intramuscular injection, and a twice-yearly gluteal injection.
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Showing 124111 -
124120 of 142613 pathways