Diabetes brand/generic/class/MOA Flashcards
Clorpropamide (gen)
Sulfonylurea (1st gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output
Glucotrol
Glipizide, Sulfonylurea (2nd gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output
Diabeta, Glynase
Glyburide, Sulfonylurea (2nd gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output
Amaryl
Glimeperide, Sulfonylurea (2nd gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output
Glucophage
Metformin, Biguanide, -enhances insulin sensitivity of both hepatic and muscle tissues (possibly by activating AMPK)
-allows for an increased uptake of glucose into these insulin-sensitive tissues
Actos
Pioglitazone, TZD, act on ppar gamma which results in glucose uptake (fat cells) and decreases hepatic glucose output and ultimately increases insulin sensitivity
Avandia
Rosiglitazone, TZD, act on ppar gamma which results in glucose uptake (fat cells) and decreases hepatic glucose output and ultimately increases insulin sensitivity
Prandin
Repaglinide, Meglitinide, stimulate the release of insulin from the β pancreatic cells in the same manner that the sulfonylureas do: they are also
secretagogues
bind to/blocks K channel > depolarization of cell > opens Ca channel > Ca influx causes relase of insulin
Starlix
Nateglinide, Meglitinide, stimulate the release of insulin from the β pancreatic cells in the same manner that the sulfonylureas do: they are also
secretagogues
bind to/blocks K channel > depolarization of cell > opens Ca channel > Ca influx causes relase of insulin
Precose
Acarbose, Alpha-glucosidase inhibitor, competitively inhibit enzymes (maltase, isomaltase, sucrase, and glucoamylase) in the small intestine, delaying the breakdown of sucrose and complex carbohydrates. results in reduction of the postprandial blood glucose rise
Glyset
Miglitol, Alpha-glucosidase inhibitor, competitively inhibit enzymes (maltase, isomaltase, sucrase, and glucoamylase) in the small intestine, delaying the breakdown of sucrose and complex carbohydrates. results in reduction of the postprandial blood glucose rise
Humalog
Insulin Lispro, rapid acting insulin (onset 15-30 min)
Novolog
Insulin aspart, rapid acting insulin, (onset 15-30 min)
Apidra
Insulin Glulisine, rapid acting insulin, (onset 15-30 min)
Humulin R
Short acting insulin (onset 30 min- 1 hr)
Novolin R
Short acting insulin, (onset 30 min- 1 hr)
Humulin N
NPH Insulin (onset 2-4 hr)
Novolin N
NPH insulin (onset 2-4hr)
Lantus
Insulin Glargine, long acting insulin (22-24 hr)
Levemire
Insulin detemir, long acting insulin (14-24 hr).
Symlin
Pramlintide, amylinomimetic, Pramlintide is a synthetic analog of amylin (amylinomimetic), a neurohormone co-secreted from the cells with insulin. It suppresses inappropriately high postprandial glucagon secretion, increases satiety, which may result in weight loss, and slows gastric emptying so that the rate of glucose appearance into the plasma better matches the glucose disposition
Byetta
Exenatide, GLP-Agonist, GLP-1 analogue, enhances glucose dependent insulin secretion while suppressing inappropriately high postprandial glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production
Victoza
Liraglutide, GLP-1 receptor agonist, enhances glucose-dependent insulin secretion while suppressing inappropriately high glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production
Trulicity
Dulaglutide, GLP-1 receptor agonist, enhances glucose-dependent insulin secretion while suppressing inappropriately high glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production
Tanzeum
Albiglutide, GLP-1 receptor agonist, enhances glucose-dependent insulin secretion while suppressing inappropriately high glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production
Januvia
Sitagliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.
Onglyza
Saxagliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.
Nesina
Alogliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.
Tradjenta
Linagliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.
Invokana
Canagliflozin, Sodium Glucose Transporter, Inhibits SGT2 in proximal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose
Farxiga
Dapagliflozin, Sodium Glucose Transporter, Inhibits SGT2 in proximal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose
Whelcol
Colesevelam, Bile Acid Sequestrant, Binds bile acid in the intestinal lumen, decreasing the bile acid pool for reabsorption. MOA is to lower plasma glucose levels is in the intestinal lumen or a systemic effect due to the intestinal lumen effect or some combination of these two. We don’t know.
Cycloset, Parlodel
Bromocriptine Mesylate, Dopamine agonist, Bromocriptine is thought to act on the circadian neuronal activities in the hypothalamus, to reset an abnormally elevated hypothalamic drive for increased plasma glucose, free fatty acids, and triglycerides in insulin-resistant patients
