Brand Name, Class, MOA Flashcards
Capoten
Captopril, ACEI, Prevents conversion of angiotensin I to Angiotensin II (potent vasoconstrictor) by competitive inhibition of ACE. Results in lower BP secondary to lower levels of angiotensin II, increased levels of plasma renin activity, and a reduction in aldosterone secretion.
Vasotec
Enalapril, ACEI, Prevents conversion of angiotensin I to Angiotensin II (potent vasoconstrictor) by competitive inhibition of ACE. Results in lower BP secondary to lower levels of angiotensin II, increased levels of plasma renin activity, and a reduction in aldosterone secretion.
Zestril, Prinivil
Lisinopril, ACEI, Prevents conversion of angiotensin I to Angiotensin II (potent vasoconstrictor) by competitive inhibition of ACE. Results in lower BP secondary to lower levels of angiotensin II, increased levels of plasma renin activity, and a reduction in aldosterone secretion.
Altace
Ramipril, ACEI, Prevents conversion of angiotensin I to Angiotensin II (potent vasoconstrictor) by competitive inhibition of ACE. Results in lower BP secondary to lower levels of angiotensin II, increased levels of plasma renin activity, and a reduction in aldosterone secretion.
Mavik
Trandolapril, ACEI, Prevents conversion of angiotensin I to Angiotensin II (potent vasoconstrictor) by competitive inhibition of ACE. Results in lower BP secondary to lower levels of angiotensin II, increased levels of plasma renin activity, and a reduction in aldosterone secretion.
Cozaar
Losartan, ARB, Selective, competitive angiotensin II receptor type 1 receptor antagonist, reducing the end-organ responses to angiotensin II. Results in a decrease in total peripheral resistance (afterload) and cardiac venous return (prelaod). Reduction in BP occurs independently of the status of the renin-angiotensin system.
Avapro
Irbesartan, ARB, Selective, competitive angiotensin II receptor type 1 receptor antagonist, reducing the end-organ responses to angiotensin II. Results in a decrease in total peripheral resistance (afterload) and cardiac venous return (prelaod). Reduction in BP occurs independently of the status of the renin-angiotensin system.
Atacand
Candesartan, ARB, Selective, competitive angiotensin II receptor type 1 receptor antagonist, reducing the end-organ responses to angiotensin II. Results in a decrease in total peripheral resistance (afterload) and cardiac venous return (prelaod). Reduction in BP occurs independently of the status of the renin-angiotensin system.
Benicar
Olmesartan, ARB, Selective, competitive angiotensin II receptor type 1 receptor antagonist, reducing the end-organ responses to angiotensin II. Results in a decrease in total peripheral resistance (afterload) and cardiac venous return (prelaod). Reduction in BP occurs independently of the status of the renin-angiotensin system.
Micardis
Telmisartan, ARB, Selective, competitive angiotensin II receptor type 1 receptor antagonist, reducing the end-organ responses to angiotensin II. Results in a decrease in total peripheral resistance (afterload) and cardiac venous return (prelaod). Reduction in BP occurs independently of the status of the renin-angiotensin system.
Diovan
Valsartan, ARB, Selective, competitive angiotensin II receptor type 1 receptor antagonist, reducing the end-organ responses to angiotensin II. Results in a decrease in total peripheral resistance (afterload) and cardiac venous return (prelaod). Reduction in BP occurs independently of the status of the renin-angiotensin system.
Tekturna
Aliskiren, Direct Renin Inhibitor, decreases plasma renin activity and inhibits the conversion of angiotensinogen to angiotensin I.
Tenormin
Atenolol, Beta Blocker, competitive inhibition of beta-blockers.
Zebeta
Bisoprolol, Beta Blocker, competitive inhibition of beta-blockers.
Lopressor, Toprol- XL
Metoprolol, Beta Blocker, competitive inhibition of beta-blockers.
Inderal (LA)
Propranolol, Beta Blocker, competitive inhibition of beta-blockers.
Coreg (CR)
Carvedilol, Beta Blocker, competitive inhibition of beta-blockers.
Trandate
Labetalol, Beta Blocker, competitive inhibition of beta-blockers.
Microzide
HCTZ, Thiazide diuretic, acts on kidneys to reduce Na reabsorption in the distal convoluted tubule. Impairs Na transport in the distal convoluted tubule, natiuresis and concomitant water loss is induced.
Chlorthalidone (generic)
Thiazide diuretic, acts on kidneys to reduce Na reabsorption in the distal convoluted tubule. Impairs Na transport in the distal convoluted tubule, natiuresis and concomitant water loss is induced.
Indapamide (generic)
Thiazide diuretic, acts on kidneys to reduce Na reabsorption in the distal convoluted tubule. Impairs Na transport in the distal convoluted tubule, natiuresis and concomitant water loss is induced.
Zaroxolyn
Metolazone, Thiazide diuretic, acts on kidneys to reduce Na reabsorption in the distal convoluted tubule. Impairs Na transport in the distal convoluted tubule, natiuresis and concomitant water loss is induced. (Not for HTN?)
Lasix
Furosemide, Loop diuretics, reversibly binds to the Na, K, Cl cotransport mechanism on the luminal side of the ascending loop of Henle, thereby inhibiting the active reabsorption of these ions.
Bumex
Bumetanide, Loop diuretics, reversibly binds to the Na, K, Cl cotransport mechanism on the luminal side of the ascending loop of Henle, thereby inhibiting the active reabsorption of these ions.
Demadex
Torsemide, Loop diuretics, reversibly binds to the Na, K, Cl cotransport mechanism on the luminal side of the ascending loop of Henle, thereby inhibiting the active reabsorption of these ions.
Edecrin
Ethacrynic acid, Loop diuretics, reversibly binds to the Na, K, Cl cotransport mechanism on the luminal side of the ascending loop of Henle, thereby inhibiting the active reabsorption of these ions.
Amiloride (generic)
K+ sparing, blocks the epithelial Na channel on the luminal side of the kidney collecting tubule. Na channel blockers directly inhibit the entry of Na in to the Na channels.
Dyrenium
Triamterene, K+ sparing, blocks the epithelial Na channel on the luminal side of the kidney collecting tubule. Na channel blockers directly inhibit the entry of Na in to the Na channels.
Norvasc
Amlodipine, DHP CCB, act by relaxing the smooth muscle in the arterial wall, decreasing total peripheral resistance, and hence reducing BP, in angina they increase bloodflow to the heart.
Plendil
Felodipine, DHP CCB, act by relaxing the smooth muscle in the arterial wall, decreasing total peripheral resistance, and hence reducing BP, in angina they increase bloodflow to the heart.
Cardene SR
Nicardipine, DHP CCB, act by relaxing the smooth muscle in the arterial wall, decreasing total peripheral resistance, and hence reducing BP, in angina they increase bloodflow to the heart.
Adalat, Procardia
Nifedipine, DHP CCB, act by relaxing the smooth muscle in the arterial wall, decreasing total peripheral resistance, and hence reducing BP, in angina they increase bloodflow to the heart.
Cardiazem
Diltiazem, Non-DHP CCB, Act as a potent vasodilator of coronary vessels, increasing bloodflow and decreasing the HR by strong depression of atrioventricular node conduction. Also, acts as a potent vasodilator of peripheral vessels, reducing peripheral resistance and afterload. Has negative ionotropic effects.
Verapamil (generic)
Non-DHP CCB, Act as a potent vasodilator of coronary vessels, increasing bloodflow and decreasing the HR by strong depression of atrioventricular node conduction. Also, acts as a potent vasodilator of peripheral vessels, reducing peripheral resistance and afterload. Has negative ionotropic effects.
Cardura
Doxazosin, Alpha 1 blockers, selective alpha1 antagonist that works by blocking the action of adrenaline on smooth muscle of the blood vessel walls.
Minipress
Prazosin, Alpha 1 blockers, selective alpha1 antagonist that works by blocking the action of adrenaline on smooth muscle of the blood vessel walls.
Hytrin
Terazosin, Alpha 1 blockers, selective alpha1 antagonist that works by blocking the action of adrenaline on smooth muscle of the blood vessel walls.
Aldactone
Spironolactone, Aldosterone Receptor Blockers, inhibit the effect of aldosterone by competing for intracellular aldosterone receptors in the cortical collecting duct. This decreases the reabsorption of Na+ and water while decreasing the secretion of K+.
Inspra
Eplerenone, Aldosterone Receptor Blockers, inhibit the effect of aldosterone by competing for intracellular aldosterone receptors in the cortical collecting duct. This decreases the reabsorption of Na+ and water while decreasing the secretion of K+.
Catapres
Clonidine, Central alpha 2 agonist, stimulates alpha2 receptors in the brain, which decreases sympathetic outflow cardiac output and peripheral vascular resistance, lowering BP and HR.
Aldomet
Methyldopa, Central alpha 2 agonist, stimulates alpha2 receptors in the brain, which decreases sympathetic outflow cardiac output and peripheral vascular resistance, lowering BP and HR.
Intuniv, Tenex
Guanfacine, Central alpha 2 agonist, stimulates alpha2 receptors in the brain, which decreases sympathetic outflow cardiac output and peripheral vascular resistance, lowering BP and HR.
Apresoline
Hydralazine, Vasodilator, direct acting smooth muscle relaxant that acts as a vasodilator primarily in arteries and arterioles.
Loniten
Minoxidil, Vasodilator, direct acting smooth muscle relaxant that acts as a vasodilator primarily in arteries and arterioles.
Lipitor
Atorvastatin, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Lescol
Fluvastatin, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Mevacor
Lovastatin, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Altacor
Lovastatin ER, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Livalo
Pitavastatin, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Pravachol
Pravastatin, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Zocor
Simvastatin, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Crestor
Rosuvastatin, HMG-CoA Reductase Inhibitor,Very similar to HMG-CoA, so they get reduced instead of acutal HMG-CoA. Less HMG-CoA is reduced to mevalonate (rate limiting step in production of cholesterol). Less cholesterol is produced.
Niacin
Vitamin B3, Inhibits the hepatic production of VLDL and consequently its metabolite LDL-C.
Zetia
Exetimibe, Cholesterol absorption inhibitor, selective inhibitor of dietary and biliary cholesterol absorption.
Questran
Cholestryramine, Bile Acid Sequestrant, Binds bile acids in the intestine, decreasing biliary cholesterol absorption.
Welchol
Colesevelam, Bile Acid Sequestrant, Binds bile acids in the intestine, decreasing biliary cholesterol absorption.
Tricor
Fenofibrate, Fibrate, peroxisome proliferator-activated receptor alpha activation. Reduced hepatic secretion of VLDL, Induction of lipoprotein lipase- mediated lipolysis and clearance of TG.
Lopid
Gemfibrozil, Fibrate, peroxisome proliferator-activated receptor alpha activation. Reduced hepatic secretion of VLDL, Induction of lipoprotein lipase- mediated lipolysis and clearance of TG.
Lotensin HTC
Benazepril and HCTZ (ACEI and thaizide)
Capozide
Captopril and HCTZ
Vaseretic
Enalapril and HCTZ
Prinzide, Zestoretic
Lisinopril and HCTZ
Uniretic
Moexipril and HCTZ
Hyzaar
Losartan and HCTZ
Diovan HCT
Valsartan and HCTZ
Tenoretic
Atenolol and Chlorthalidone
Ziac
Bisoprolol and HCTZ
Lopressor HCT
Metoprolol and HCTZ
Corzide
Nadolol and Benzoflumethazide
Inderide
Timolol and HCTZ
Timolide
Timolol and HCTZ
Lotrel
Amlodipine and Benazepril
Lexxel
Felodipine and Enalapril
Tarka
Verapamil and Trandolapril
Moduretic
Amlodipine and HCTZ
Aldactazide
Spironolactone and HCTZ
Maxzide
Triamterene and HCTZ
Combipres
Clonidine and Chlorthalidone
Apresazide
Hydralazine and HCTZ
Aldoril
Methyldopa and HCTZ
Minizide
Prazosin and Polythiazide
Diabinese
Chlorpropamide, sulfonylurea, stimulates insulin secretion in beta cells (secretagogue) 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, stimulates insulin secretion in beta cells (secretagogue) 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, stimulates insulin secretion in beta cells (secretagogue) 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, stimulates insulin secretion in beta cells (secretagogue) 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 beta pancreatic cells in the same manner that the sulfonlureas do (secretagogues), bind to/blocks K cannel > depolarization of cell > opens Ca channel > Ca influx causes release of insulin.
Starlix
Nateglinide, meglitinide, stimulate the release of insulin from the beta pancreatic cells in the same manner that the sulfonlureas do (secretagogues), bind to/blocks K cannel > depolarization of cell > opens Ca channel > Ca influx causes release of insulin.
Precose
Acarbose, alpha-glucosidase inhibitor, compeitively inhibits 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, compeitively inhibits 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.
Symlin
Pramlintide, amylinomimetic, synthetic analog of amylin, a neurohormone co-secreted from the cells with insulin. it suppresses inappropraitely 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-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.
Januvia
Sitagliptin, DPP-4 inhibitor, 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 for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. Significantly reduces 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, DPP-4 inhibitor, 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 for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. Significantly reduces 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, DPP-4 inhibitor, 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 for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. Significantly reduces 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, DPP-4 inhibitor, 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 for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. Significantly reduces 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
Canaglifozin, sodium glucose transporters, inhibits SGT2 in promixal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose.
Whelcol
Colesevelam, bile acid sequestrants, binds bile acid in the intestinal lumen, decreasing the bile acid pool for reabsorption. Lowers plasma glucose levels in the intestinal lumen or a systemic effect due to the intestinal lumen effect or some combination of these two.
Cycloset, Parlodel
Bromocriptine mesylate, Dopamine agonsit, MOA unknown.
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.
Farxiga
Dapagliflozin, sodium glucose transporters, inhibits SGT2 in promixal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose.
Cladiribine (generic)
Anti-metabolite, Trick DNA into thinking it is utilizing a healthy purine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Clofarabine (generic)
Anti-metabolite, Trick DNA into thinking it is utilizing a healthy purine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Fludarabine (generic)
Anti-metabolite, Trick DNA into thinking it is utilizing a healthy purine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Mercaptopurine (generic)
Anti-metabolite, Trick DNA into thinking it is utilizing a healthy purine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Nelarabine (generic)
Anti-metabolite, Trick DNA into thinking it is utilizing a healthy purine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Pentostatin (generic)
Anti-metabolite, Trick DNA into thinking it is utilizing a healthy purine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Thioguanine (generic)
Anti-metabolite (purine), Trick DNA into thinking it is utilizing a healthy purine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Xeloda
Capcitabine (oral) anti-metabolite (pyrimidine), Trick DNA into thinking it is utilizing a healthy pyrimidine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
ARA-C
Citarabine (liposomal), anti-metabolite (pyrimidine), Trick DNA into thinking it is utilizing a healthy pyrimidine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Floxuridine (gen)
anti-metabolite (pyrimidine), Trick DNA into thinking it is utilizing a healthy pyrimidine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
5-FU
Flurouricil, anti-metabolite (pyrimidine), Trick DNA into thinking it is utilizing a healthy pyrimidine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Gemzar
Gemcitabine, anti-metabolite (pyrimidine), Trick DNA into thinking it is utilizing a healthy pyrimidine for DNA synthesis, then halts DNA replication due to malformation (also leads to RNA demise as well)
Methotrexate (gen)
Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation
Alimta
Pemetrexid, Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation
Pralatrexate (gen)
Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation
Raltitrexed (gen)
Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation
Vidaza
Azacitidine, antimetabolite (other), DNA methylation inhibitor
Direct cellular toxicity at abnormal bone marrow cells
Decogen
Decitabine, antimetabolite (other), DNA methylation inhibitor
Direct cellular toxicity at abnormal bone marrow cells
Adriamycin
Doxorubucin, anthraxyxline, -Interchalates DNA
- ROS
- TOPO Isomerase 2 inhibitor ( alleviate tension in both strands in dna during replicaton) so with anthracycline, the cut DNA cannot re-ligate, so apotosis.
Doxil
Liposomal doxorubucin, anthraxyxline, -Interchalates DNA
- ROS
- TOPO Isomerase 2 inhibitor ( alleviate tension in both strands in dna during replicaton) so with anthracycline, the cut DNA cannot re-ligate, so apotosis.
Danorubucin (gen)
anthraxyxline, -Interchalates DNA
- ROS
- TOPO Isomerase 2 inhibitor ( alleviate tension in both strands in dna during replicaton) so with anthracycline, the cut DNA cannot re-ligate, so apotosis.
Epirubicin (gen)
anthraxyxline, -Interchalates DNA
- ROS
- TOPO Isomerase 2 inhibitor ( alleviate tension in both strands in dna during replicaton) so with anthracycline, the cut DNA cannot re-ligate, so apotosis.
Idarubicin (gen)
anthraxyxline, -Interchalates DNA
- ROS
- TOPO Isomerase 2 inhibitor ( alleviate tension in both strands in dna during replicaton) so with anthracycline, the cut DNA cannot re-ligate, so apotosis.
Valrubicin (gen)
anthraxyxline, -Interchalates DNA
- ROS
- TOPO Isomerase 2 inhibitor ( alleviate tension in both strands in dna during replicaton) so with anthracycline, the cut DNA cannot re-ligate, so apotosis.
Vincristine (gen)
Microtubule (Vinca Alkaloid), Bind to tubulin, a key factor in the assembly and disassembly of microtubules, arresting cell proliferation
Vinblastine (gen)
Microtubule (Vinca Alkaloid), Bind to tubulin, a key factor in the assembly and disassembly of microtubules, arresting cell proliferation
Vinorelbine (gen)
Microtubule (Vinca Alkaloid), Bind to tubulin, a key factor in the assembly and disassembly of microtubules, arresting cell proliferation
Taxol
Paclitaxel, microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.
Taxotere
Docetaxel, microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.
Abraxane
Paclitaxel-protein bound, microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.
Cabazitaxel (gen)
microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.
Eribulin (gen)
Microtubule (other), Suppresses microtubule polymerization and inhibits spindle formation
Ixabepilone (gen)
Microtubule (other), Suppresses microtubule polymerization and inhibits spindle formation
Ado-trastuzumab (gen)
Her-2 antibody conjugate with antimicrotubule inhibitor
Emtansine (gen)
Her-2 antibody conjugate with antimicrotubule inhibitor
Camptosar
Irinotecan, topo I inhibitor, Inhibits topo I (stabilizing the cleaved DNA strand, preventing re-ligation)
Hycamtin
Topotecan, topo I inhibitor, Inhibits topo I (stabilizing the cleaved DNA strand, preventing re-ligation)
Anthracycline (gen)
Topo II inhibitor, Inhibits topo II (re-ligation)
Other MOAs too
Toposar
Etoposide, Topo II inhibitor, Inhibits topo II (re-ligation)
Other MOAs too
Teniposide (gen)
Topo II inhibitor, Inhibits topo II (re-ligation)
Other MOAs too
Mitoxantrone (gen)
Topo II inhibitor, Inhibits topo II (re-ligation)
Other MOAs too
Cytoxan
Cyclophosphamide, Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage
Iphosphamide (gen)
Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage
Bendamustine (gen)
Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage
Chlorambucil (gen)
Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage
Mechlorethamine (gen)
Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage
Melphalan (gen)
Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage
Carmustine (BCNU) (gen)
Alkylating agents (Triazense), Alkylate DNA at the O6, N7 position of guanine, causing cross-linking, inducing strand breakage
Lomustine (gen)
Alkylating agents (Triazense), Alkylate DNA at the O6, N7 position of guanine, causing cross-linking, inducing strand breakage
Streptozocin (gen)
Alkylating agents (Triazense), Alkylate DNA at the O6, N7 position of guanine, causing cross-linking, inducing strand breakage
Matulane
Procarbazine (oral), alkylating agent (other), Inhibits transmethylation of methionine into tRNA; insight strand breakage
Carboplatin (gen)
Alkylating agents (platinums), Insights cross-linking Violates the double-helix structure Strand breakage
Cisplatin (gen)
Alkylating agents (platinums), Insights cross-linking Violates the double-helix structure Strand breakage
Eloxitan
Oxaloplatin, Alkylating agents (platinums), Insights cross-linking
Violates the double-helix structure
Strand breakage
Bleomycin (gen)
Antibiotic, Inhibits synthesis of DNA
And causes ROS
Hydrea
Hydroxyurea (oral), Miscellaneous, Antimetabolite inhibiting ribonucleoside diphosphate reductase, preventing conversion of ribonucleotides to deoxyribonucleotides halting cell cycle
Increases Hgb F levels
Mitomycin-C (gen)
MIsc, Alkylating agent, creates cross-linking with guanine and cytosine pairs.
Tarceda
Elotinib (oral), Anti-EGFR ORAL, EGFR selective TKI
Tykerb
Lapatinib (oral), Anti-Her2 new agent ORAL, EGFR and HER 2 TKI
Gleevac
IMatinib (oral), BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML
Dasatinib (gen)
BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML
Nilotinib (gen)
BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML
Bosutinib (gen)
BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML
Iclusig
Ponatinib (oral), BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML
Sutent
Sunitinib (oral), Kinase inhibitor, Inhibit multiple receptor TKs
Nexavar
Soratenib (oral), Kinase inhibitor, Inhibit multiple receptor TKs
Pazopanib (gen)
Kinase inhibitor, Inhibit multiple receptor TKs
Azitinib (oral) (gen)
Kinase inhibitor, Inhibit multiple receptor TKs
Rforafenib (gen)
Kinase inhibitor, Inhibit multiple receptor TKs
Vandetanib (gen)
Kinase inhibitor, Inhibit multiple receptor TKs
Valcade
Bortezomib, proteosome inhibitor, Inhibits proteasomes, critical for protein homeostasis, inducing apoptosis
Kyprolis
Carfilzomib, proteosome inhibitor, Inhibits proteasomes, critical for protein homeostasis, inducing apoptosis
Xalkori
Cicotinib (oral), misc oral, ALK inhibition, ALK is a down-stream mutation causing constant “on” of proliferation; used in NSCLC
Zykadia
Ceritinib (oral), ALK inhibition, ALK is a down-stream mutation causing constant “on” of proliferation; used in NSCLC
Jakafi
Ruxolitinib, misc oral, JAK1, JAK2 inhibition of the JAK-STAT signaling pathway. Used in myeloproliferative disorders with JAK2 mutations
Rituxan
Rituximab, Anti-CD 20, Binds to CD20 on B cells, induces ADCC
Azerra
Ofatumumab, Anti-CD 20, Binds to CD20 on B cells, induces ADCC
Campath
Alemtuxumab, Anti-CD 52, Binds to CD 52 on B and T cells, inhibits interaction with other immune system functions, induces ADCC
Adcetris
Brentuzimab Vedotin, Anti-CD 30, Binds to CD 30 and introduces Vedotin (microtubule poison)
Erbitux
Cetuximab, EGFR, Bind to and inhibit extracellular EGFR, induces apoptosis
Panitumumbab (gen)
EGFR, Bind to and inhibit extracellular EGFR, induces apoptosis
Herceptin
Trastuzumab, HER 2, Binds to HER2 at different points on the receptor, induces ADCC
Perjeta
Pertuzumab, HER 2, Binds to HER2 at different points on the receptor, induces ADCC
Ado-Trastuzumab (gen)
HER 2, Binds to HER2 at different points on the receptor, induces ADCC
Ematansine (gen)
HER 2, Binds to HER2 at different points on the receptor, induces ADCC
Avastin
Bevacizumab, VEGF, Binds to circulating VEGF, inhibits the formation for vasculature, required for tumor growth
Yervoy
Ipilimumab, CTLA-4, Binds to cytotoxic T-lymphocyte associated antigen 4 (CTLA-4), enhancing T-cell activation
IL-2 (aldesleukin) (gen)
Interferon, Cytokine, promoting B and T cell proliferation, anti-cancer therapy based on tumor susceptibility to lymphokine-activated killer cells and tumor-infiltrating lymphocytes