Brand Name, Class, MOA

Question 1

Capoten

Answer 1

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.

Question 2

Vasotec

Answer 2

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.

Question 3

Zestril, Prinivil

Answer 3

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.

Question 4

Altace

Answer 4

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.

Question 5

Mavik

Answer 5

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.

Question 6

Cozaar

Answer 6

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.

Question 7

Avapro

Answer 7

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.

Question 8

Atacand

Answer 8

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.

Question 9

Benicar

Answer 9

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.

Question 10

Micardis

Answer 10

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.

Question 11

Diovan

Answer 11

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.

Question 12

Tekturna

Answer 12

Aliskiren, Direct Renin Inhibitor, decreases plasma renin activity and inhibits the conversion of angiotensinogen to angiotensin I.

Question 13

Tenormin

Answer 13

Atenolol, Beta Blocker, competitive inhibition of beta-blockers.

Question 14

Zebeta

Answer 14

Bisoprolol, Beta Blocker, competitive inhibition of beta-blockers.

Question 15

Lopressor, Toprol- XL

Answer 15

Metoprolol, Beta Blocker, competitive inhibition of beta-blockers.

Question 16

Inderal (LA)

Answer 16

Propranolol, Beta Blocker, competitive inhibition of beta-blockers.

Question 17

Coreg (CR)

Answer 17

Carvedilol, Beta Blocker, competitive inhibition of beta-blockers.

Question 18

Trandate

Answer 18

Labetalol, Beta Blocker, competitive inhibition of beta-blockers.

Question 19

Microzide

Answer 19

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.

Question 20

Chlorthalidone (generic)

Answer 20

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.

Question 21

Indapamide (generic)

Answer 21

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.

Question 22

Zaroxolyn

Answer 22

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?)

Question 23

Lasix

Answer 23

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.

Question 24

Bumex

Answer 24

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.

Question 25

Demadex

Answer 25

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.

Question 26

Edecrin

Answer 26

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.

Question 27

Amiloride (generic)

Answer 27

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.

Question 28

Dyrenium

Answer 28

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.

Question 29

Norvasc

Answer 29

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.

Question 30

Plendil

Answer 30

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.

Question 31

Cardene SR

Answer 31

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.

Question 32

Adalat, Procardia

Answer 32

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.

Question 33

Cardiazem

Answer 33

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.

Question 34

Verapamil (generic)

Answer 34

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.

Question 35

Cardura

Answer 35

Doxazosin, Alpha 1 blockers, selective alpha1 antagonist that works by blocking the action of adrenaline on smooth muscle of the blood vessel walls.

Question 36

Minipress

Answer 36

Prazosin, Alpha 1 blockers, selective alpha1 antagonist that works by blocking the action of adrenaline on smooth muscle of the blood vessel walls.

Question 37

Hytrin

Answer 37

Terazosin, Alpha 1 blockers, selective alpha1 antagonist that works by blocking the action of adrenaline on smooth muscle of the blood vessel walls.

Question 38

Aldactone

Answer 38

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+.

Question 39

Inspra

Answer 39

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+.

Question 40

Catapres

Answer 40

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.

Question 41

Aldomet

Answer 41

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.

Question 42

Intuniv, Tenex

Answer 42

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.

Question 43

Apresoline

Answer 43

Hydralazine, Vasodilator, direct acting smooth muscle relaxant that acts as a vasodilator primarily in arteries and arterioles.

Question 44

Loniten

Answer 44

Minoxidil, Vasodilator, direct acting smooth muscle relaxant that acts as a vasodilator primarily in arteries and arterioles.

Question 45

Lipitor

Answer 45

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.

Question 46

Lescol

Answer 46

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.

Question 47

Mevacor

Answer 47

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.

Question 48

Altacor

Answer 48

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.

Question 49

Livalo

Answer 49

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.

Question 50

Pravachol

Answer 50

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.

Question 51

Zocor

Answer 51

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.

Question 52

Crestor

Answer 52

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.

Question 53

Niacin

Answer 53

Vitamin B3, Inhibits the hepatic production of VLDL and consequently its metabolite LDL-C.

Question 54

Zetia

Answer 54

Exetimibe, Cholesterol absorption inhibitor, selective inhibitor of dietary and biliary cholesterol absorption.

Question 55

Questran

Answer 55

Cholestryramine, Bile Acid Sequestrant, Binds bile acids in the intestine, decreasing biliary cholesterol absorption.

Question 56

Welchol

Answer 56

Colesevelam, Bile Acid Sequestrant, Binds bile acids in the intestine, decreasing biliary cholesterol absorption.

Question 57

Tricor

Answer 57

Fenofibrate, Fibrate, peroxisome proliferator-activated receptor alpha activation. Reduced hepatic secretion of VLDL, Induction of lipoprotein lipase- mediated lipolysis and clearance of TG.

Question 58

Lopid

Answer 58

Gemfibrozil, Fibrate, peroxisome proliferator-activated receptor alpha activation. Reduced hepatic secretion of VLDL, Induction of lipoprotein lipase- mediated lipolysis and clearance of TG.

Question 59

Lotensin HTC

Answer 59

Benazepril and HCTZ (ACEI and thaizide)

Question 60

Capozide

Answer 60

Captopril and HCTZ

Question 61

Vaseretic

Answer 61

Enalapril and HCTZ

Question 62

Prinzide, Zestoretic

Answer 62

Lisinopril and HCTZ

Question 63

Uniretic

Answer 63

Moexipril and HCTZ

Question 64

Hyzaar

Answer 64

Losartan and HCTZ

Question 65

Diovan HCT

Answer 65

Valsartan and HCTZ

Question 66

Tenoretic

Answer 66

Atenolol and Chlorthalidone

Question 67

Ziac

Answer 67

Bisoprolol and HCTZ

Question 68

Lopressor HCT

Answer 68

Metoprolol and HCTZ

Question 69

Corzide

Answer 69

Nadolol and Benzoflumethazide

Question 70

Inderide

Answer 70

Timolol and HCTZ

Question 71

Timolide

Answer 71

Timolol and HCTZ

Question 72

Lotrel

Answer 72

Amlodipine and Benazepril

Question 73

Lexxel

Answer 73

Felodipine and Enalapril

Question 74

Tarka

Answer 74

Verapamil and Trandolapril

Question 75

Moduretic

Answer 75

Amlodipine and HCTZ

Question 76

Aldactazide

Answer 76

Spironolactone and HCTZ

Question 77

Maxzide

Answer 77

Triamterene and HCTZ

Question 78

Combipres

Answer 78

Clonidine and Chlorthalidone

Question 79

Apresazide

Answer 79

Hydralazine and HCTZ

Question 80

Aldoril

Answer 80

Methyldopa and HCTZ

Question 81

Minizide

Answer 81

Prazosin and Polythiazide

Question 82

Diabinese

Answer 82

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.

Question 83

Glucotrol

Answer 83

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.

Question 84

Diabeta, Glynase

Answer 84

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.

Question 85

Amaryl

Answer 85

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.

Question 86

Glucophage

Answer 86

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

Question 87

Actos

Answer 87

Pioglitazone, TZD, act on ppar gamma which results in glucose uptake (fat cells) and decreases hepatic glucose output and ultimately increases insulin sensitivity.

Question 88

Avandia

Answer 88

Rosiglitazone, TZD, act on ppar gamma which results in glucose uptake (fat cells) and decreases hepatic glucose output and ultimately increases insulin sensitivity

Question 89

Prandin

Answer 89

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.

Question 90

Starlix

Answer 90

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.

Question 91

Precose

Answer 91

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.

Question 92

Glyset

Answer 92

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.

Question 93

Symlin

Answer 93

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.

Question 94

Byetta

Answer 94

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.

Question 95

Victoza

Answer 95

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.

Question 96

Januvia

Answer 96

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.

Question 97

Onglyza

Answer 97

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.

Question 98

Nesina

Answer 98

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.

Question 99

Tradjenta

Answer 99

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.

Question 100

Invokana

Answer 100

Canaglifozin, sodium glucose transporters, inhibits SGT2 in promixal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose.

Question 101

Whelcol

Answer 101

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.

Question 102

Cycloset, Parlodel

Answer 102

Bromocriptine mesylate, Dopamine agonsit, MOA unknown.

Question 103

Trulicity

Answer 103

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.

Question 104

Farxiga

Answer 104

Dapagliflozin, sodium glucose transporters, inhibits SGT2 in promixal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose.

Question 105

Cladiribine (generic)

Answer 105

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)

Question 106

Clofarabine (generic)

Answer 106

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)

Question 107

Fludarabine (generic)

Answer 107

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)

Question 108

Mercaptopurine (generic)

Answer 108

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)

Question 109

Nelarabine (generic)

Answer 109

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)

Question 110

Pentostatin (generic)

Answer 110

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)

Question 111

Thioguanine (generic)

Answer 111

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)

Question 112

Xeloda

Answer 112

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)

Question 113

ARA-C

Answer 113

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)

Question 114

Floxuridine (gen)

Answer 114

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)

Question 115

5-FU

Answer 115

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)

Question 116

Gemzar

Answer 116

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)

Question 117

Methotrexate (gen)

Answer 117

Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation

Question 118

Alimta

Answer 118

Pemetrexid, Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation

Question 119

Pralatrexate (gen)

Answer 119

Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation

Question 120

Raltitrexed (gen)

Answer 120

Antimetabolite (folate), Inhibit enzymes involved with folate synthesis to aid in DNA formation

Question 121

Vidaza

Answer 121

Azacitidine, antimetabolite (other), DNA methylation inhibitor Direct cellular toxicity at abnormal bone marrow cells

Question 122

Decogen

Answer 122

Decitabine, antimetabolite (other), DNA methylation inhibitor Direct cellular toxicity at abnormal bone marrow cells

Question 123

Adriamycin

Answer 123

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.

Question 124

Doxil

Answer 124

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.

Question 125

Danorubucin (gen)

Answer 125

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.

Question 126

Epirubicin (gen)

Answer 126

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.

Question 127

Idarubicin (gen)

Answer 127

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.

Question 128

Valrubicin (gen)

Answer 128

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.

Question 129

Vincristine (gen)

Answer 129

Microtubule (Vinca Alkaloid), Bind to tubulin, a key factor in the assembly and disassembly of microtubules, arresting cell proliferation

Question 130

Vinblastine (gen)

Answer 130

Microtubule (Vinca Alkaloid), Bind to tubulin, a key factor in the assembly and disassembly of microtubules, arresting cell proliferation

Question 131

Vinorelbine (gen)

Answer 131

Microtubule (Vinca Alkaloid), Bind to tubulin, a key factor in the assembly and disassembly of microtubules, arresting cell proliferation

Question 132

Taxol

Answer 132

Paclitaxel, microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.

Question 133

Taxotere

Answer 133

Docetaxel, microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.

Question 134

Abraxane

Answer 134

Paclitaxel-protein bound, microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.

Question 135

Cabazitaxel (gen)

Answer 135

microtubule (taxane), Promotes assembly, disassembly, and stabilization of microtubule, arresting cell proliferation.

Question 136

Eribulin (gen)

Answer 136

Microtubule (other), Suppresses microtubule polymerization and inhibits spindle formation

Question 137

Ixabepilone (gen)

Answer 137

Microtubule (other), Suppresses microtubule polymerization and inhibits spindle formation

Question 138

Ado-trastuzumab (gen)

Answer 138

Her-2 antibody conjugate with antimicrotubule inhibitor

Question 139

Emtansine (gen)

Answer 139

Her-2 antibody conjugate with antimicrotubule inhibitor

Question 140

Camptosar

Answer 140

Irinotecan, topo I inhibitor, Inhibits topo I (stabilizing the cleaved DNA strand, preventing re-ligation)

Question 141

Hycamtin

Answer 141

Topotecan, topo I inhibitor, Inhibits topo I (stabilizing the cleaved DNA strand, preventing re-ligation)

Question 142

Anthracycline (gen)

Answer 142

Topo II inhibitor, Inhibits topo II (re-ligation) | Other MOAs too

Question 143

Toposar

Answer 143

Etoposide, Topo II inhibitor, Inhibits topo II (re-ligation) Other MOAs too

Question 144

Teniposide (gen)

Answer 144

Topo II inhibitor, Inhibits topo II (re-ligation) | Other MOAs too

Question 145

Mitoxantrone (gen)

Answer 145

Topo II inhibitor, Inhibits topo II (re-ligation) | Other MOAs too

Question 146

Cytoxan

Answer 146

Cyclophosphamide, Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage

Question 147

Iphosphamide (gen)

Answer 147

Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage

Question 148

Bendamustine (gen)

Answer 148

Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage

Question 149

Chlorambucil (gen)

Answer 149

Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage

Question 150

Mechlorethamine (gen)

Answer 150

Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage

Question 151

Melphalan (gen)

Answer 151

Alkylating agent (nitrogen mustard), Alkylate DNA, causing cross-linking, inducing strand breakage

Question 152

Carmustine (BCNU) (gen)

Answer 152

Alkylating agents (Triazense), Alkylate DNA at the O6, N7 position of guanine, causing cross-linking, inducing strand breakage

Question 153

Lomustine (gen)

Answer 153

Alkylating agents (Triazense), Alkylate DNA at the O6, N7 position of guanine, causing cross-linking, inducing strand breakage

Question 154

Streptozocin (gen)

Answer 154

Alkylating agents (Triazense), Alkylate DNA at the O6, N7 position of guanine, causing cross-linking, inducing strand breakage

Question 155

Matulane

Answer 155

Procarbazine (oral), alkylating agent (other), Inhibits transmethylation of methionine into tRNA; insight strand breakage

Question 156

Carboplatin (gen)

Answer 156

``` Alkylating agents (platinums), Insights cross-linking Violates the double-helix structure Strand breakage ```

Question 157

Cisplatin (gen)

Answer 157

``` Alkylating agents (platinums), Insights cross-linking Violates the double-helix structure Strand breakage ```

Question 158

Eloxitan

Answer 158

Oxaloplatin, Alkylating agents (platinums), Insights cross-linking Violates the double-helix structure Strand breakage

Question 159

Bleomycin (gen)

Answer 159

Antibiotic, Inhibits synthesis of DNA | And causes ROS

Question 160

Hydrea

Answer 160

Hydroxyurea (oral), Miscellaneous, Antimetabolite inhibiting ribonucleoside diphosphate reductase, preventing conversion of ribonucleotides to deoxyribonucleotides  halting cell cycle Increases Hgb F levels

Question 161

Mitomycin-C (gen)

Answer 161

MIsc, Alkylating agent, creates cross-linking with guanine and cytosine pairs.

Question 162

Tarceda

Answer 162

Elotinib (oral), Anti-EGFR ORAL, EGFR selective TKI

Question 163

Tykerb

Answer 163

Lapatinib (oral), Anti-Her2 new agent ORAL, EGFR and HER 2 TKI

Question 164

Gleevac

Answer 164

IMatinib (oral), BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML

Question 165

Dasatinib (gen)

Answer 165

BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML

Question 166

Nilotinib (gen)

Answer 166

BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML

Question 167

Bosutinib (gen)

Answer 167

BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML

Question 168

Iclusig

Answer 168

Ponatinib (oral), BCR-ABL, Inhibits TK activity of BCR-ABL Philadelphia chromosome in CML

Question 169

Sutent

Answer 169

Sunitinib (oral), Kinase inhibitor, Inhibit multiple receptor TKs

Question 170

Nexavar

Answer 170

Soratenib (oral), Kinase inhibitor, Inhibit multiple receptor TKs

Question 171

Pazopanib (gen)

Answer 171

Kinase inhibitor, Inhibit multiple receptor TKs

Question 172

Azitinib (oral) (gen)

Answer 172

Kinase inhibitor, Inhibit multiple receptor TKs

Question 173

Rforafenib (gen)

Answer 173

Kinase inhibitor, Inhibit multiple receptor TKs

Question 174

Vandetanib (gen)

Answer 174

Kinase inhibitor, Inhibit multiple receptor TKs

Question 175

Valcade

Answer 175

Bortezomib, proteosome inhibitor, Inhibits proteasomes, critical for protein homeostasis, inducing apoptosis

Question 176

Kyprolis

Answer 176

Carfilzomib, proteosome inhibitor, Inhibits proteasomes, critical for protein homeostasis, inducing apoptosis

Question 177

Xalkori

Answer 177

Cicotinib (oral), misc oral, ALK inhibition, ALK is a down-stream mutation causing constant “on” of proliferation; used in NSCLC

Question 178

Zykadia

Answer 178

Ceritinib (oral), ALK inhibition, ALK is a down-stream mutation causing constant “on” of proliferation; used in NSCLC

Question 179

Jakafi

Answer 179

Ruxolitinib, misc oral, JAK1, JAK2 inhibition of the JAK-STAT signaling pathway. Used in myeloproliferative disorders with JAK2 mutations

Question 180

Rituxan

Answer 180

Rituximab, Anti-CD 20, Binds to CD20 on B cells, induces ADCC

Question 181

Azerra

Answer 181

Ofatumumab, Anti-CD 20, Binds to CD20 on B cells, induces ADCC

Question 182

Campath

Answer 182

Alemtuxumab, Anti-CD 52, Binds to CD 52 on B and T cells, inhibits interaction with other immune system functions, induces ADCC

Question 183

Adcetris

Answer 183

Brentuzimab Vedotin, Anti-CD 30, Binds to CD 30 and introduces Vedotin (microtubule poison)

Question 184

Erbitux

Answer 184

Cetuximab, EGFR, Bind to and inhibit extracellular EGFR, induces apoptosis

Question 185

Panitumumbab (gen)

Answer 185

EGFR, Bind to and inhibit extracellular EGFR, induces apoptosis

Question 186

Herceptin

Answer 186

Trastuzumab, HER 2, Binds to HER2 at different points on the receptor, induces ADCC

Question 187

Perjeta

Answer 187

Pertuzumab, HER 2, Binds to HER2 at different points on the receptor, induces ADCC

Question 188

Ado-Trastuzumab (gen)

Answer 188

HER 2, Binds to HER2 at different points on the receptor, induces ADCC

Question 189

Ematansine (gen)

Answer 189

HER 2, Binds to HER2 at different points on the receptor, induces ADCC

Question 190

Avastin

Answer 190

Bevacizumab, VEGF, Binds to circulating VEGF, inhibits the formation for vasculature, required for tumor growth

Question 191

Yervoy

Answer 191

Ipilimumab, CTLA-4, Binds to cytotoxic T-lymphocyte associated antigen 4 (CTLA-4), enhancing T-cell activation

Question 192

IL-2 (aldesleukin) (gen)

Answer 192

Interferon, Cytokine, promoting B and T cell proliferation, anti-cancer therapy based on tumor susceptibility to lymphokine-activated killer cells and tumor-infiltrating lymphocytes