 Subscribe to postsNew! 31 New Pathways were released on 19-NOV-2011 Released 19 pathways on 28-OCT-2011 (details here) Released 11 pathways on 08-OCT-2011 (details here) Released 9 pathways on 01 SEPT 2011 (details here) New Pathways release forcast: Next release due on 10-FEB-2012 ( ~# of pathways for release = 6 to 10). see below for the list. Main curation theme is Lysosomal storage diseases and Cancer signaling pathways. We will publish curated pathways on the following diseases:  Lysosomal storage diseases
Metabolic disease pathways
Cancer signaling Pathways
ER Stress and Apoptosis Pathways
Number of pathways/Maps currently being validated for release in near future by iPAVS : 40 Preview: see the slide show of pathway diagrams under validation and scheduled to be released Please write to support _ at _ cidms.org if you have a request for a pathway. We may have one in our curation pipeline and we could reassign the priority so that you can see the pathway you need available on iPAVS immediately in our next release. |
Wish-list
| Pathway Name | Summary | Status | Expected Release |
|---|---|---|---|
| Aromatic_L-Aminoacid_Decarboxylase_Deficiency_Metabolite_pathway | Aromatic L-Aminoacid Decarboxylase Deficiency(Dopa decarboxylase; DDC) is an autosomal recessive disease caused by a mutation in the DDC gene which codes for aromatic-L-aminoacid decarboxylase. | Finished | Newly Released |
| 17-Beta Hydroxysteroid Dehydrogenase III Deficiency metabolite pathway | Defects in 17-beta hydroxysteroid dehydrogenase III (HSD17B3) are the cause of male pseudohermaphrodism with gynecomastia. | Finished | Newly Released |
| Alkaptonuria_metabolite_pathway | Alkaptonuria (Homogentisic acid oxidase deficiency) is an autosomal recessive disease caused by a mutation in the HGD gene which codes for homogentisate 1,2-dioxygenase. | Finished | Newly Released |
| beta3_integrin_mediated_Ub_for_NFkB_activation | beta3 integrin mediated ubiquitination activates surivival signaling during myocardial hypertrophy | Finished | Newly Released |
| beta_AR_stimulation_of_CICR_in_the_heart_involves_cAMP_activation | A endogenous PKA-independent betaAR-signaling pathway through cAMP-dependent Epac activation, Rap, and PLC(epsilon) that enhances intracellular Ca(2+) release in cardiac myocytes. cAMP aciviate Epac. | Finished | Newly Released |
| Regulation_of_BetaAR_turnover_via_desensitization_and_sequestration_mechanisms | Regulation of beta-adrenoceptor turnover via desensitization and sequestration mechanisms. The desensitization and the associated uncoupling or down-regulation of beta-AR relate to their adaptational responses to various forms of stress. | Finished | Newly Released |
| positive_and_negative_inotropic_effects_induced_by_beta2AR_agonists_in_mamalian_right_papillary_muscles | Signaling pathways is involved in positive and negative inotropic effects induced by beta2-adrenoceptor (AR) agonists in guinea pig right papillary muscles. Beta2-adrenoceptor partial agonists induce an unexpected NO-mediated biphasic negative inotropic effect in guinea pig right papillary muscles. | Finished | Newly Released |
| Biotinidase_Deficiency_metabolite_pathway | Biotinidase deficiency (Multiple carboxylase deficiency) is an autosomal recessive disease caused by a mutation in the BTD gene which does for biotinidase. | Finished | Newly Released |
| Canavan_diseaes_metabolite_pathway | Canavan Disease (Canavan-Van Bogaert-Bertrand Disease; Aminoacylase 2 Deficiency; Spongy Degeneration of the Central Nervous System; Aspartoacylase Deficiency; ASP Deficiency; ACY2 Deficiency; ASPA) is a rare autosomal recessive disease caused by a defect in the ASPA gene which codes for aspartoacylase. | Finished | Newly Released |
| Congenital_Erythropoietic_Porphyria_metabolite_pathway | Congenital Erythropoietic Porphyria (CEP) or Gunther Disease is a rare inborn error of porphyrin-heme synthesis inherited that is as an autosomal recessive trait. This disorder of bone marrow heme synthesis is caused by a defect in the UROS gene which codes for uroporphyrinogen-III synthase. | Finished | Newly Released |
| GABA_Transaminase_Deficiency_Metabolite_pathway | GABA-Transaminase Deficiency (Gamma-amino butyric acid transaminase deficiency; GABA-T) is caused by a defect in the gene coding for gamma-aminobutyrate transaminase, which is responsible for catabolism of gamma-aminobutyric acid (GABA), an important, mostly inhibitory neurotransmitter in the central nervous system, into succinic semialdehyde. | Finished | Newly Released |
| Glutaric_aciduria_type3_metabolite_pathway | Glutaric Aciduria Type III is an extremly rare metabolic abnormality of peroxisomal metabolism presumed to be cause by a deficiency in peroxisomal glutaryl-CoA oxidase. | Finished | Newly Released |
| Obesity_Metabolic_Syndrome_metabolite_pathway | In Obesity/Metabolic Syndrome, high plasma fatty acids regulate genes responsible for increase insulin resistance, visceral fat deposits, fatty acid oxidation, and thermogenesis. | Finished | Newly Released |
| Primary_Hyperoxaluria_Type1_Metabolite_pathway | Primary hyperoxaluria type 1 (PH1) is an atypical peroxisomal disorder, as befits a deficiency of alanine:glyoxylate aminotransferase (AGT), which is itself an atypical peroxisomal enzyme. PH1 is characterized by excessive synthesis and excretion of the metabolic end-product oxalate and the progressive accumulation of insoluble calcium oxalate in the kidney and urinary tract. | Finished | Newly Released |
| Pyrimidine salvage reactions | In pyrimidine salvage reactions, nucleosides and free bases generated by DNA and RNA breakdown are converted back to nucleotide monophosphates, allowing them to re-enter the pathways of pyrimidine biosynthesis (interconversion). | Validation | One Month |
| activation of focal adhesion by Tie2 Tek signaling pathway | The TEK signaling pathway appears to be critical for endothelial cell-smooth muscle cell communication in venous morphogenesis | Validation | One Month |
| Refsum_disease_metabolite_pathway | Refsum's disease (hereditary motor sensory neuropathy type IV, heredopathia atactica polyneuritiformis) is an autosomal recessive disorder the clinical features of which include retinitis pigmentosa, blindness, anosmia, deafness, sensory neuropathy, ataxia and accumulation of phytanic acid in plasma- and lipid-containing tissues | Finished | Newly Released |
| AKT PI3K pathway in cardiovasclar tissue | The PI3K/AKT/mTOR pathway is an intracellular signalling pathway important in apoptosis and hence cancer e.g. breast cancer and non-small-cell lung cancer. In heart it has Cardioprotective Effects. | Validation | One Month |
| Obesity_Metabolic_Syndrome_pathway | In Obesity/Metabolic Syndrome, high plasma fatty acids regulate genes responsible for increase insulin resistance, visceral fat deposits, fatty acid oxidation, and thermogenesis. Many of these responses have a role in metabolic syndrome, obesity and diabetes. | Finished | Newly Released |
| Leigh_Syndrome_metabolic_pathway | Leigh’s disease (Encephalopathy), a form of Leigh syndrome, also known as Subacute Necrotizing Encephalomyelopathy (SNEM), is a rare neurometabolic disorder that affects the central nervous system. It is an inherited disorder that usually affects infants between the age of three months and two years, but, in rare cases, teenagers and adults as well. | Finished | Newly Released |
| Galactosemia_Metabolic_pathway | Galactosemia (GALT Deficiency; GALT; Galactose-1-Phosphate Uridylyltransferase Deficiency) is a rare genetic disorder caused by a mutation in the GALT gene which codes for galactose-1-phosphate uridylyltransferase. | Finished | Newly Released |
| Histidinemia_metabolic_pathway | Leigh’s disease (Encephalopathy), a form of Leigh syndrome, also known as Subacute Necrotizing Encephalomyelopathy (SNEM), is a rare neurometabolic disorder that affects the central nervous system. It is an inherited disorder that usually affects infants between the age of three months and two years, but, in rare cases, teenagers and adults as well. | Finished | Newly Released |
| Glycerol_Kinase_Deficiency_metabolic_pathway | _metabolic_pathway Glycerol Kinase Deficiency (Hyperglycerolemia; Glyceroluria; GK Deficiency; GKD) is a rare metabolic disease caused by a deficiency in the GK gene which codes for glycerol kinase. | Finished | Newly Released |
| Richner-Hanhart_syndrome_metabolite_pathway | A defect in this enzyme results in accumulation of tyrosine in both blood and urine; increased excretion of 4-hydroxyphenylpyruvic acid, hydroxyphenyllactic acid, and p-hydroxyphenylacetic acid in urine. Symptoms often begin in early childhood, they include excessive tearing, abnormal sensitivity to light (photophobia), eye pain and redness, and painful skin lesions on the palms and soles. | Finished | Newly Released |
| Refsum_disease_metabolic_pathway | Adult Refsum Disease (Classic Refsum Disease; Phytanic Acid Oxidase Deficiency; Heredopathia Atactica Polyneurtiformis; Hereditary Motor and Sensory Neuropathy IV; HSMN4; Adult Refsum Disease I; Adult Refsum Disease II), can be caused by mutations in the PHYH (or PAHX) gene, which encodes Phytanoyl-CoA hydroxylase (, the first enzyme in the Phytanic Acid Peroxisomal Oxidation pathway) on chromosome 10 (adult Refsum disease I), and by mutation of the PEX7 gene. | Finished | Newly Released |
| Sialuria_or_French_Type_Sialuria_Metabolic_pathway | Sialuria is caused by mutation in the gene encoding uridinediphosphate-N-acetylglucosamine 2-epimerase (UDP-GlcNAc 2-epimerase, which causes an excessive synthesis of sialic acid (N-acetylneuraminic acid, NeuAc).This causes accumulation of sialic acid in the urine. Symptoms of sialuria include hepatosplenomegaly, hypotonia, frequent upper respiratory infections, gastroenteritis and seizures. | Finished | Newly Released |
| Electron Transport Chain | An electron transport chain (ETC) couples electron transfer between an electron donor (such as NADH) and an electron acceptor (such as O2) with the transfer of H+ ions (protons) across a membrane. The resulting electrochemical proton gradient is used to generate chemical energy in the form of adenosine triphosphate (ATP). Electron transport chains are the cellular mechanisms used for extracting energy from sunlight in photosynthesis and also from redox reactions, such as the oxidation of sugars (respiration). | Validation | One Month |
| Maple_Syrup_Urine_Disease_Metabolite_pathway | Maple syrup urine disease is an inherited disorder in which the body is unable to process certain protein building blocks (amino acids) properly. The condition gets its name from the distinctive sweet odor of affected infants' urine. Beginning in early infancy, this condition is characterized by poor feeding, vomiting, lack of energy (lethargy), and developmental delay. If untreated, maple syrup urine disease can lead to seizures, coma, and death. | Finished | Newly Released |
| Methionine_Adenosyltransferase_Deficiency_metabolite_pathway | Methionine adenosyltransferase deficiency is an inborn error of metabolism resulting in isolated hypermethioninemia. Most patients have no clinical abnormalities, although some neurologic abnormalities have been reported in rare cases with severe loss of enzyme activity (Mudd et al., 2003|PubMed: 7573050). | Finished | Newly Released |
| Malonic aciduria metabolic pathway | Malonic Aciduria, is an autosomal recessive metabolic disorder caused by a genetic mutation which disrupts the activity of Malonyl-Coa decarboxylase. | Finished | Newly Released |
| Saccharopinuria(Hyperlysinemia) II metabolic pathway | Saccharopinuria (an excess of saccharopine in the urine), also called saccharopinemia or saccharopine dehydrogenase deficiency, or alpha-aminoadipic semialdehyde synthase deficiency, is a variant form of hyperlysinemia caused by a partial deficiency of the enzyme aminoadipic semialdehyde synthase (AASS), which has lysine ketoglutarate reductase (LKR) and saccharopine dehydrogenase (SDH) activity | Finished | Newly Released |
| Tyrosinemia Type3 metabolic pathway | Tyrosinemia type 3, one of the 3 types of tyrosinemia, is caused by a defect in the HPD gene which codes for 4-hydroxyphenylpyruvate dioxygenase. | Finished | Newly Released |
| Prostaglandin Metabolic Pathway | prostaglandins were first detected in human seminal fluid. prostaglandins are found throughout the animal kingdom, even in species as lowly as insects, shellfish and corals.Prostaglandins are a subset of a larger family of substances called eicosanoids. Other subgroups include thromboxanes, leukotrienes and lipoxins. Eicosanoids are localized tissue hormones that seem to be the fundamental regulating molecules in most forms of life. They do not travel in the blood like hormones, but are created in the cells to serve as catalysts for a large number of processes including the movement of calcium and other substances into and out of cells, dilation and contraction, inhibition and promotion of clotting, regulation of secretions including digestive juices and hormones, and control of fertility, cell division and growth | Finished | Newly Released |
| Lidocaine Local Anaesthetic Pathway | Lidocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. | Finished | Newly Released |
| ABCIXIMAB Drug Pathway | Abciximab (previously known as c7E3 Fab), is a glycoprotein IIb/IIIa receptor antagonist manufactured by Centocor and distributed by Eli Lilly under the trade name ReoPro, is a platelet aggregation inhibitor mainly used during and after coronary artery procedures like angioplasty to prevent platelets from sticking together and causing thrombus (blood clot) formation within the coronary artery. It is a glycoprotein IIb/IIIa inhibitor. | Finished | Newly Released |
| Oxaprozin Drug Pathway | Oxaprozin is a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. | Finished | Newly Released |
| Mefenamic Acid Drug Pathway | Mefanamic Acid Pathway Most NSAIDs, including mefanamic acid, are non-selective prostaglandin G/H synthase (better known as cyclooxygenase or COX) inhibitors that act on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). | Finished | Newly Released |
| Von Gierke disease-metabolite pathway | Glycogen storage disease type 1A (GSD1A), or von Gierke disease, is caused by a defect in the G6PC gene which codes for Glucose-6-phosphatase. Glucose-6-phosphatase hydrolyzes glucose-6-phosphate to glucose and is responsible for the regulation of blood glucose level. A defect in this enzyme results in accumulation of glycogen in affected tissues, like liver and kidney; decreased glucose level; and accumulation of lactate. | Finished | Newly Released |
| Androgen and Estrogen Metabolic Pathway | This pathway describes the inactivation and catabolism of male (androgen) and female (estrogen) hormones. Many steroid hormones are transformed by sulfatases, dehydrogenases and glucuronide transferases to enhance their solubility and to facilitate their elimination. Inactivation refers to the metabolic conversion of a biologically active compound into an inactive one. Peripheral inactivation (e.g. by liver enzymes) is required to ensure steady-state levels of plasma androgens and estrogens. | Finished | Newly Released |
| Benzocaine Local Anaesthetic Pathway | Benzocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Benzocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore benzocaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Bupivacaine Local Anaesthetic Pathway | Bupivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Bupivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore bupivacaine preferentially inhibits neurons that are actively firing | Finished | Newly Released |
| Chloroprocaine Local Anaesthetic Pathway | Chloroprocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Chloroprocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore chloroprocaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Cocaine Local Anaesthetic Pathway | Cocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Cocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore cocaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Dibucaine Local Anaesthetic Pathway | Dibucaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Dibucaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore dibucaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Diclofenac Drug Pathway | Diclofenac is an acetic acid nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. Diclofenac is used to treat pain, dysmenorrhea, ocular inflammation, osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and actinic keratosis. The antiinflammatory effects of diclofenac are believed to be due to inhibition of both leukocyte migration and the enzyme cylooxygenase (COX-1 and COX-2 or prostaglandin G/H synthase 1 and 2), leading to the peripheral inhibition of prostaglandin synthesis. | Finished | Newly Released |
| Diflunisal Drug Pathway | Diflunisal is a non-selective prostaglandin G/H synthase (better known as cyclooxygenase or COX) inhibitor that acts on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). COX catalyzes the conversion of arachidonic acid to a number of prostaglandins involved in fever, pain, swelling, inflammation, and platelet aggregation. Diflunisal antagonizes COX by binding to the upper portion of the active site and preventing its substrate, arachidonic acid, from entering the active site. The analgesic, antipyretic and anti-inflammatory effects of diflunisal occur as a result of decreased prostaglandin synthesis. Diflunisal also inhibits the migration of leukocytes into sites of inflammation and prevents the production of thromboxane A2, an aggregating agent, by platelets. | Finished | Newly Released |
| Ibuprofen Drug Pathway | Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) used for its analgesic, antipyretic and anti-inflammatory properties. Like most NSAIDs, ibuprofen is a non-selective inhibitor of prostaglandin G/H synthase 1 and 2, better known as cyclooxygenase 1 and 2 or simply COX-1 and -2. COX catalyzes the conversion of arachidonic acid to a number of prostaglandins involved in fever, pain, swelling, inflammation, and platelet aggregation. Ibuprofen antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. The analgesic, antipyretic and anti-inflammatory effects of ibuprofen occurs as a result of decreased prostaglandin synthesis. Ibuprofen is slightly more potent than aspirin and produces analgesic effects at lower doses than aspirin. Unlike aspirin, ibuprofen is a reversible COX inhibitor and thus it is not used as an antiplatelet agent. | Finished | Newly Released |
| Indomethacin Drug Pathway | Indomethacin, an NSAID, is a prostaglandin G/H synthase (a.k.a. cyclooxygenase or COX) inhibitor that acts on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). Prostaglandin G/H synthase catalyzes the conversion of arachidonic acid to a number of prostaglandins involved in fever, pain, swelling, inflammation, and platelet aggregation. Indomethacin antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. Indomethacin, unlike other NSAIDs, also inhibits phospholipase A2, the enzyme responsible for releasing arachidonic acid from phospholipids. Indomethacin is more selective for COX-1 than COX-2, which accounts for its increased adverse gastric effects relative to other NSAIDs. COX-1 is required for maintaining the protective gastric mucosal layer. The analgesic, antipyretic and anti-inflammatory effects of indomethacin occur as a result of decreased prostaglandin synthesis. | Finished | Newly Released |
| Ketoprofen Drug Pathway | Ketoprofen is a nonsteroidal antiinflammatory drug (NSAID) with analgesic and antipyretic properties. Ketoprofen has pharmacologic actions similar to those of other prototypical NSAIDs, that is thought to be associated with the inhibition of prostaglandin synthesis. Ketoprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and to alleviate moderate pain. Its anti-inflammatory effects are believed to be due to inhibition of both prostglandin G/H synthase 1 and 2 (better known as cylooxygenase-1 (COX-1) and cylooxygenase-2 (COX-2)), which leads to the inhibition of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. | Finished | Newly Released |
| Levobupivacaine Local Anaesthetic Pathway | Levobupivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Levobupivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore levobupivacaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Mepivacaine Local Anaesthetic Pathway | Mepivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Mepivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore mepivacaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Nabumetone Drug Pathway | Most NSAIDs, including Nabumetone, are non-selective prostaglandin G/H synthase (better known as cyclooxygenase or COX) inhibitors that act on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). Prostaglandin G/H synthase catalyzes the conversion of arachidonic acid to prostaglandin G2 and prostaglandin G2 to prostaglandin H2. Prostglandin H2 is the precursor to a number of prostaglandins involved in fever, pain, swelling and inflammation (e.g. PGE2). Mefanamic acid antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. The analgesic, antipyretic and anti-inflammatory effects of mefanamic acid occur as a result of decreased prostaglandin synthesis. | Finished | Newly Released |
| Oxybuprocaine Local Anaesthetic Pathway | Oxybuprocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Oxybuprocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. | Finished | Newly Released |
| Prilocaine Local Anaesthetic Pathway | Prilocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Prilocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore prilocaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Procaine Local Anaesthetic Pathway | Procaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Procaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore procaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Proparacaine Local Anaesthetic Pathway | Proparacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Proparacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore proparacaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
| Ropivacaine Local Anaesthetic Pathway | Ropivacaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Ropivacaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore ropivacaine preferentially inhibits neurons that are actively firing. | Finished | Newly Released |
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