Exercise

DrugDrug NameDrug Description
DB06203AlogliptinAlogliptin is a selective, orally-bioavailable inhibitor of enzymatic activity of dipeptidyl peptidase-4 (DPP-4). Chemically, alogliptin is prepared as a benzoate salt and exists predominantly as the R-enantiomer (>99%). It undergoes little or no chiral conversion in vivo to the (S)-enantiomer. FDA approved January 25, 2013.
DB08907CanagliflozinCanagliflozin, also known as _Invokana_, is a sodium-glucose cotransporter 2 (SGLT2) inhibitor used in the management of type 2 diabetes mellitus along with lifestyle changes including diet and exercise [FDA label]. It was initially approved by the FDA in 2013 for the management of diabetes and later approved in 2018 for a second indication of reducing the risk of cardiovascular events in patients diagnosed with type 2 diabetes mellitus [L5897], [FDA label]. Canagliflozin is the first oral antidiabetic drug approved for the prevention of cardiovascular events in patients with type 2 diabetes [L5897]. Cardiovascular disease is the most common cause of death in these patients [A177083].
DB06292DapagliflozinDapagliflozin is a sodium-glucose cotransporter 2 inhibitor indicated for managing diabetes mellitus type 2[A6757]. When combined with diet and exercise in adults, dapagliflozin helps to improve glycemic control by inhibiting glucose resorption in the proximal tubule of the nephron and causing glycosuria[A6757]. Dapagliflozin was approved by the FDA on Jan 08, 2014[L6034].
DB09038EmpagliflozinEmpagliflozin is a sodium glucose co-transporter-2 (SGLT-2) inhibitor indicated as an adjunct to diet and exercise to improve glycemic control in adult patients with type 2 diabetes. SGLT2 co-transporters are responsible for reabsorption of glucose from the glomerular filtrate in the kidney. The glucuretic effect resulting from SGLT2 inhibition reduces renal absorption and lowers the renal threshold for glucose, therefore resulting in increased glucose excretion. Additionally, it contributes to reduced hyperglycaemia and also assists weight loss and blood pressure reduction.
DB11827ErtugliflozinErtugliflozin belongs to the class of potent and selective inhibitors of the sodium-dependent glucose cotransporters (SGLT), more specifically the type 2 which is responsible for about 90% of the glucose reabsorption from glomerulus.[A31581] This drug was developed under the collaboration of Merck and Pfizer. It was FDA approved as monotherapy and in combination with sitagliptin or metformin hydrochloride on December 22, 2017.[L1132]
DB00222GlimepirideFirst introduced in 1995, glimepiride is a member of the second-generation sulfonylurea (SU) drug class used for the management of type 2 diabetes mellitus (T2DM) to improve glycemic control. Type 2 diabetes is a metabolic disorder with increasing prevalences worldwide; it is characterized by insulin resistance in accordance with progressive β cell failure and long-term microvascular and macrovascular complications that lead to co-morbidities and mortalities. Sulfonylureas are one of the insulin secretagogues widely used for the management of type 2 diabetes to lower blood glucose levels. The main effect of SUs is thought to be effective when residual pancreatic β-cells are present [A177715], as they work by stimulating the release of insulin from the pancreatic beta cells and they are also thought to exert extra-pancreatic effects, such as increasing the insulin-mediated peripheral glucose uptake [A177709]. Glimepiride works by stimulating the secretion of insulin granules from pancreatic islet beta cells by blocking ATP-sensitive potassium channels (KATP channels) and causing depolarization of the beta cells. Compared to [glipizide], another second SU drug, glimepiride has a longer duration of action. It is sometimes classified as a third-generation SU because it has larger substitutions than other second-generation SUs [A177703]. Compared to other SUs, glimepiride was associated with a lower risk of developing hypoglycemia and weight gain in clinical trials [A177709] as well as fewer cardiovascular effects than other SUs due to minimal effects on ischemic preconditioning of cardiac myocytes [A177703]. It is effective in reducing fasting plasma glucose, postprandial glucose, and glycosylated hemoglobin levels and is considered to be a useful, cost-effective treatment option for managing type 2 diabetes mellitus [A177703]. Glimepiride was approved by the Food and Drug Administration (FDA) in the United States in 1995 for the treatment of T2DM. It is commonly marketed under the brand name Amaryl as oral tablets and is typically administered once daily.
DB09564Insulin DegludecInsulin degludec is an ultra-long-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin, such as insulin degludec, to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Tresiba, insulin degludec has a duration of action up to 42 hours allowing for once-daily dosing, typically at bedtime. Due to its duration of action, Tresiba is considered "basal insulin" as it provides low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Basal insulin is often combined with short-acting "bolus insulin" such as [DB00046], [DB01309], or [DB01306] to provide higher doses of insulin required following meals. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Compared to endogenous insulin, insulin degludec has an added hexadecanedioic acid on lysine at the B29 position which allows for the formation of multi-hexamers. When injected subcutaneously, these multi-hexamers form a drug depot store from which monomers are slowly and continuously absorbed into the circulation. As a result, Insulin Degludec has a protracted time action profile due to the delayed absorption from subcutaneous tissue depots into the systemic circulation. Compared to available long-acting analogues such as [DB00047] and [DB01307], which have a duration of action of 20-24 hours, insulin degludec provides a consistent level of basal insulin over 42 hours with a low peak:trough ratio. Limitations of shorter acting analogues include more frequent dosing and less stable pharmacokinetics, which may negatively impact patient adherence and glucose control, particularly nocturnal control. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. Insulin Degludec was approved by the FDA in September 2015 as the product Tresiba, for use in providing glycemic control to adults with diabetes mellitus.
DB00047Insulin glargineInsulin glargine is a long-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis. Insulin is an important treatment in the management of Type 1 Diabetes (T1D), which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin, such as insulin glargine, to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Available as the brand name product Lantus, insulin glargine has a duration of action up to 24 hours allowing for once-daily dosing, typically at bedtime. Due to its duration of action, Lantus is considered "basal insulin" as it provides low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Basal insulin is often combined with short-acting "bolus insulin" such as [DB00046], [DB01309], and [DB01306] to provide higher doses of insulin that are required following meals. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Insulin glargine is also available as the biosimilar, or "follow-on" product, Basaglar in the US and as Abasaglar in the EU. As of 2015, insulin glargine was reformulated by Sanofi as the product Toujeo in an extra-concentrated form containing 300IU/mL (compared to 100IU/mL contained in Lantus). Use of the higher concentrated Toujeo as compared to Lantus results in slightly different pharmacokinetics, with a later onset (up to 6 hours) and duration of action (up to 30 hours). Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12) as the production organism. Insulin glargine differs from endogenous human insulin by the replacement of an asparagine residue at position A21 of the A-chain with glycine and addition of two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4 allowing for the slow release of small amounts of insulin glargine, giving the drug a long duration of action and no pronounced peak concentration. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy.
DB08882LinagliptinLinagliptin is a DPP-4 inhibitor developed by Boehringer Ingelheim for the treatment of type II diabetes [FDA Label]. Linagliptin differs from other DPP-4 inhibitors in that it has a non-linear pharmacokinetic profile, is not primarily eliminated by the renal system, and obeys concentration dependant protein binding[A37050]. Linagliptin was approved by the FDA on May 2, 2011[FDA Label].
DB06655LiraglutideVictoza contains liraglutide, a synthetic analog of human glucagon-like peptide-1(GLP-1) and acts as a GLP-1 receptor agonist[Label,A6932]. Liraglutide is 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34[A6932]. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor[A6932]. Liraglutide was granted FDA approval on Januray 25, 2010[L6070].
DB09265LixisenatideLixisenatide is a glucagon-like peptide-1 (GLP-1) receptor agonist used in the treatment of type 2 diabetes mellitus (T2DM). It is sold under the brand name Adlyxin by Sanofi-Aventis. Adlyxin recieved FDA approval July 28, 2016 [L763].
DB00331MetforminMetformin is an antihyperglycemic agent of the _biguanide_ class, used for the management of type II diabetes) [FDA label]. Currently, metformin is the first drug of choice for the management of type II diabetes and is prescribed to at least 120 million people worldwide [A176173]. Metformin is considered an antihyperglycemic drug because it lowers blood glucose concentrations in type II diabetes without causing hypoglycemia. Metformin is commonly described as an _insulin sensitizer_ leading to a decrease in insulin resistance and a clinically significant reduction of plasma fasting insulin levels [A176173]. Another well-known benefit of this drug is modest weight loss. Metformin is the drug of choice for obese type II diabetes patients [A36559]. Metformin was first approved in Canada in 1972 [A36552], followed by 1995 in the USA [FDA label]. This drug is available in regular and extended-release forms [FDA label].
DB00912RepaglinideRepaglinide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the meglitinide class of short-acting insulin secretagogues, which act by binding to β cells of the pancreas to stimulate insulin release. Repaglinide induces an early insulin response to meals decreasing postprandial blood glucose levels. It should only be taken with meals and meal-time doses should be skipped with any skipped meal. Approximately one month of therapy is required before a decrease in fasting blood glucose is seen. Meglitnides may have a neutral effect on weight or cause a slight increase in weight. The average weight gain caused by meglitinides appears to be lower than that caused by sulfonylureas and insulin and appears to occur only in those naïve to oral antidiabetic agents. Due to their mechanism of action, meglitinides may cause hypoglycemia although the risk is thought to be lower than that of sulfonylureas since their action is dependent on the presence of glucose. In addition to reducing postprandial and fasting blood glucose, meglitnides have been shown to decrease glycosylated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Meglitinides appear to be more effective at lowering postprandial blood glucose than metformin, sulfonylureas and thiazolidinediones. Repaglinide is extensively metabolized in the liver and excreted in bile. Repaglinide metabolites do not possess appreciable hypoglycemic activity. Approximately 90% of a single orally administered dose is eliminated in feces and 8% in urine.
DB00412RosiglitazoneRosiglitazone is an anti-diabetic drug in the thiazolidinedione class of drugs. It is marketed by the pharmaceutical company GlaxoSmithKline as a stand-alone drug (Avandia) and in combination with metformin (Avandamet) or with glimepiride (Avandaryl). Like other thiazolidinediones, the mechanism of action of rosiglitazone is by activation of the intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), specifically PPARγ. Rosiglitazone is a selective ligand of PPARγ, and has no PPARα-binding action. Apart from its effect on insulin resistance, it appears to have an anti-inflammatory effect: nuclear factor kappa-B (NFκB) levels fall and inhibitor (IκB) levels increase in patients on rosiglitazone. Recent research has suggested that rosiglitazone may also be of benefit to a subset of patients with Alzheimer's disease not expressing the ApoE4 allele. This is the subject of a clinical trial currently underway.
DB06335SaxagliptinSaxagliptin (rINN) is an orally active hypoglycemic (anti-diabetic drug) of the new dipeptidyl peptidase-4 (DPP-4) inhibitor class of drugs. FDA approved on July 31, 2009.
DB13928SemaglutideSemaglutide is a once-daily glucagon-like peptide-1 analog that differs to others by the presence of an acyl group with a steric diacid at Lys26 and a large synthetic spacer and modified by the presence of a α-aminobutyric acid in position 8 which gives stability against the dipeptidylpeptidase-4.[A31421] The stability of semaglutide by the acylation permits a high-affinity albumin binding and gives it a long plasma half-life which allows the once-daily dosage. It was developed by the Danish pharmaceutical company Novo Nordisk and FDA approved on December 5, 2017.[L1067]
DB00641SimvastatinSimvastatin, also known as the brand name product Zocor, is a lipid-lowering drug derived synthetically from a fermentation product of _Aspergillus terreus_. It belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage abnormal lipid levels by inhibiting the endogenous production of cholesterol in the liver. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase,[A181421] which catalyzes the conversion of HMG-CoA to mevalonic acid and is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as "bad cholesterol"), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America.[A181087, A181406] Simvastatin and other drugs from the statin class of medications including [atorvastatin], [pravastatin], [rosuvastatin], [fluvastatin], and [lovastatin] are considered first-line options for the treatment of dyslipidemia.[A181087, A181406] Increasing use of the statin class of drugs is largely due to the fact that cardiovascular disease (CVD), which includes heart attack, atherosclerosis, angina, peripheral artery disease, and stroke, has become a leading cause of death in high-income countries and a major cause of morbidity around the world.[A181084] Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.[A181087,A181553] Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality.[A181090,A181093,A181096,A181427,A181475,A181538] Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack.[A181087, A181406] Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.[A181397, A181403] While all statin medications are considered equally effective from a clinical standpoint, [rosuvastatin] is considered the most potent; doses of 10 to 40mg [rosuvastatin] per day were found in clinical studies to result in a 45.8% to 54.6% decrease in LDL cholesterol levels, while simvastatin has been found to have an average decrease in LDL-C of ~35%.[A181409,A181535,A181538,A1793] Potency is thought to correlate to tissue permeability as the more lipophilic statins such as simvastatin are thought to enter endothelial cells by passive diffusion, as opposed to hydrophilic statins such as [pravastatin] and [rosuvastatin] which are taken up into hepatocytes through OATP1B1 (organic anion transporter protein 1B1)-mediated transport.[A181424,A181460] Despite these differences in potency, several trials have demonstrated only minimal differences in terms of clinical outcomes between statins.[A181438, A181427]
DrugDrug NameTargetType
DB06203AlogliptinDipeptidyl peptidase 4target
DB06203AlogliptinCytochrome P450 3A4enzyme
DB06203AlogliptinCytochrome P450 2D6enzyme
DB08907CanagliflozinUDP-glucuronosyltransferase 1-9enzyme
DB08907CanagliflozinUDP-glucuronosyltransferase 2B4enzyme
DB08907CanagliflozinCytochrome P450 3A4enzyme
DB08907CanagliflozinSodium/glucose cotransporter 2target
DB08907CanagliflozinMultidrug resistance protein 1transporter
DB08907CanagliflozinCanalicular multispecific organic anion transporter 1transporter
DB08907CanagliflozinAlpha-1-acid glycoprotein 1carrier
DB08907CanagliflozinATP-binding cassette sub-family G member 2transporter
DB06292DapagliflozinSodium/glucose cotransporter 2target
DB06292DapagliflozinCytochrome P450 1A1enzyme
DB06292DapagliflozinCytochrome P450 1A2enzyme
DB06292DapagliflozinCytochrome P450 2A6enzyme
DB06292DapagliflozinCytochrome P450 2C9enzyme
DB06292DapagliflozinCytochrome P450 2D6enzyme
DB06292DapagliflozinCytochrome P450 3A4enzyme
DB06292DapagliflozinUDP-glucuronosyltransferase 1-9enzyme
DB06292DapagliflozinUDP-glucuronosyltransferase 2B4enzyme
DB06292DapagliflozinUDP-glucuronosyltransferase 2B7enzyme
DB06292DapagliflozinMultidrug resistance protein 1transporter
DB09038EmpagliflozinSodium/glucose cotransporter 2target
DB11827ErtugliflozinUDP-glucuronosyltransferase 1-9enzyme
DB11827ErtugliflozinUDP-glucuronosyltransferase 2B7enzyme
DB11827ErtugliflozinSodium/glucose cotransporter 2target
DB11827ErtugliflozinMultidrug resistance protein 1transporter
DB11827ErtugliflozinATP-binding cassette sub-family G member 2transporter
DB11827ErtugliflozinSerum albumincarrier
DB11827ErtugliflozinUDP-glucuronosyltransferase 1-1enzyme
DB11827ErtugliflozinUDP-glucuronosyltransferase 1-4enzyme
DB00222GlimepirideATP-sensitive inward rectifier potassium channel 1target
DB00222GlimepirideATP-sensitive inward rectifier potassium channel 11target
DB00222GlimepirideCytochrome P450 2C9enzyme
DB00222GlimepirideATP-binding cassette sub-family C member 8target
DB00222GlimepirideBile salt export pumptransporter
DB09564Insulin DegludecInsulin receptortarget
DB09564Insulin DegludecInsulin-like growth factor 1 receptortarget
DB09564Insulin DegludecSerum albumincarrier
DB09564Insulin DegludecCytochrome P450 1A2enzyme
DB00047Insulin glargineInsulin receptortarget
DB00047Insulin glargineInsulin-like growth factor 1 receptortarget
DB00047Insulin glargineCytochrome P450 1A2enzyme
DB08882LinagliptinDipeptidyl peptidase 4target
DB08882LinagliptinCytochrome P450 3A4enzyme
DB08882LinagliptinMultidrug resistance protein 1transporter
DB08882LinagliptinSolute carrier family 22 member 1transporter
DB08882LinagliptinSolute carrier family 22 member 2transporter
DB08882LinagliptinSolute carrier family 22 member 3transporter
DB06655LiraglutideGlucagon-like peptide 1 receptortarget
DB06655LiraglutideDipeptidyl peptidase 4enzyme
DB06655LiraglutideNeprilysinenzyme
DB06655LiraglutideSerum albumincarrier
DB09265LixisenatideGlucagon-like peptide 1 receptortarget
DB00331Metformin5'-AMP-activated protein kinase subunit beta-1target
DB00331MetforminSolute carrier family 22 member 2transporter
DB00331MetforminSolute carrier family 22 member 1transporter
DB00331MetforminMultidrug and toxin extrusion protein 1transporter
DB00331MetforminEquilibrative nucleoside transporter 4transporter
DB00331MetforminSolute carrier family 22 member 3transporter
DB00331MetforminMultidrug and toxin extrusion protein 2transporter
DB00331MetforminMitochondrial complex Itarget
DB00331MetforminGlycerol-3-phosphate dehydrogenase [NAD(+)], cytoplasmictarget
DB00912RepaglinideATP-binding cassette sub-family C member 8target
DB00912RepaglinideCytochrome P450 2C8enzyme
DB00912RepaglinidePeroxisome proliferator-activated receptor gammatarget
DB00912RepaglinideCytochrome P450 3A4enzyme
DB00912RepaglinideSerum albumincarrier
DB00912RepaglinideSolute carrier organic anion transporter family member 1B1transporter
DB00912RepaglinideBile salt export pumptransporter
DB00412RosiglitazonePeroxisome proliferator-activated receptor gammatarget
DB00412RosiglitazoneCytochrome P450 2C8enzyme
DB00412RosiglitazoneCytochrome P450 2C9enzyme
DB00412RosiglitazoneLong-chain-fatty-acid--CoA ligase 4target
DB00412RosiglitazoneSolute carrier organic anion transporter family member 1B1transporter
DB00412RosiglitazoneProstaglandin G/H synthase 1enzyme
DB00412RosiglitazoneCytochrome P450 1A2enzyme
DB00412RosiglitazoneCytochrome P450 2A6enzyme
DB00412RosiglitazoneCytochrome P450 2D6enzyme
DB00412RosiglitazoneSerum albumincarrier
DB00412RosiglitazonePeroxisome proliferator-activated receptor alphatarget
DB00412RosiglitazonePeroxisome proliferator-activated receptor deltatarget
DB00412RosiglitazoneRetinoic acid receptor RXR-alphatarget
DB00412RosiglitazoneRetinoic acid receptor RXR-betatarget
DB00412RosiglitazoneRetinoic acid receptor RXR-gammatarget
DB00412RosiglitazoneCytochrome P450 3A4enzyme
DB00412RosiglitazoneBile salt export pumptransporter
DB06335SaxagliptinDipeptidyl peptidase 4target
DB06335SaxagliptinCytochrome P450 3A4enzyme
DB06335SaxagliptinCytochrome P450 3A5enzyme
DB06335SaxagliptinMultidrug resistance-associated protein 1transporter
DB06335SaxagliptinSolute carrier organic anion transporter family member 4C1transporter
DB06335SaxagliptinSolute carrier family 22 member 8transporter
DB13928SemaglutideSerum albumincarrier
DB13928SemaglutideDipeptidyl peptidase 4enzyme
DB13928SemaglutideNeprilysinenzyme
DB13928SemaglutideGlucagon-like peptide 1 receptortarget
DB13928SemaglutideSolute carrier organic anion transporter family member 1B1transporter
DB13928SemaglutideSolute carrier organic anion transporter family member 1B3transporter
DB13928SemaglutideLipoprotein lipaseenzyme
DB13928SemaglutideAlpha-amylase 1enzyme
DB00641Simvastatin3-hydroxy-3-methylglutaryl-coenzyme A reductasetarget
DB00641SimvastatinCytochrome P450 3A4enzyme
DB00641SimvastatinCytochrome P450 2C8enzyme
DB00641SimvastatinCytochrome P450 2C9enzyme
DB00641SimvastatinCytochrome P450 3A5enzyme
DB00641SimvastatinMultidrug resistance protein 1transporter
DB00641SimvastatinSolute carrier organic anion transporter family member 1A2transporter
DB00641SimvastatinSolute carrier organic anion transporter family member 1B1transporter
DB00641SimvastatinCytochrome P450 2B6enzyme
DB00641SimvastatinCytochrome P450 2D6enzyme
DB00641SimvastatinUDP-glucuronosyltransferase 1-1enzyme
DB00641SimvastatinUDP-glucuronosyltransferase 1-3enzyme
DB00641SimvastatinUDP-glucuronosyltransferase 2B7enzyme
DB00641SimvastatinCanalicular multispecific organic anion transporter 1transporter
DB00641SimvastatinIntegrin alpha-Ltarget
DB00641SimvastatinBile salt export pumptransporter
DB00641SimvastatinCytochrome P450 2C19enzyme
DB00641SimvastatinSolute carrier organic anion transporter family member 2B1transporter
DB00641SimvastatinSolute carrier organic anion transporter family member 1B3transporter
DB00641SimvastatinHistone deacetylase 2target
DrugDrug NamePhaseStatusCount
DB14297Arnica montana1Completed1
DB00335Atenolol4Completed1
DB01117Atovaquone4Recruiting1
DB01222Budesonide4Recruiting1
DB01016Glyburide4Unknown Status1
DB00331Metformin4Unknown Status1
DB01131Proguanil4Recruiting1
DB11172Sesame oil4Completed1
DB00624Testosterone4Completed1
DB01409Tiotropium4Completed1
DB04876Vildagliptin4Unknown Status1
DB00584EnalaprilNot AvailableRecruiting1
DB09337Medical airNot AvailableCompleted1
DB09152NitrogenNot AvailableCompleted1
DB09140OxygenNot AvailableCompleted1
DB00203SildenafilNot AvailableCompleted1
DB00624TestosteroneNot AvailableActive Not Recruiting1
DB00193TramadolNot AvailableCompleted1