Exam 4 Drugs Flashcards
(127 cards)
1
Q
heparin
A
- drug class: indirect thrombin inhibitor
- indications: prevent venous thrombosis
- MOA: target - anti-thrombin III
+binds an activates antithrombin (conformational change)
+enhances activity 1000x
+catalyzes rxns without being consumed - tox:
+bleeding, HIT - monitoring: aPTT
- reversal agent: protamine sulfate - highly positively charged and binds heparin and inactivates it
- contraindications: active bleeding, hemophilia, thrombocytopenia, severe hypertension, ICH, infective endocarditis, active TB, GI ulcers, advanced hepatic disease
2
Q
lmw heparin
A
- more specific for factor Xa (less effect on thrombin)
- less effective on coagulation in general
- more predictable plasma levels for monitoring
- examples include: enoxaparin, dalteparin, tinzaparin (-parin drugs)
3
Q
fondaparinux (arixtra)
A
- pentasaccharide molecule of heparin
- synthetic
- not as effective; selective for factor X
- less bleeding risks involved
- indications: anticoagulation for people with HIT
- indirect thrombin inhibitor
4
Q
protamine sulfate
A
* reversal agent for heparin
* highly positively charged; binds heparin and inactivates
* excess protamine is also anticoagulant
* less effect on LMW heparins
* does not affect fondaparinux
5
Q
leprudin (hirudin) or bivalirudin (angiomax)
A
- drug class: direct thrombin inhibitors
- MOA: bind to both active and subtrate recognition sites of thrombin; prevents fibrin clot from forming
- hirudin - leech therapy
6
Q
argatroban, dabigatran (pradaxa)
A
- drug class: direct thrombin inhibtor
- MOA: binds only to thrombin active sites (from biological sources); prevents fibrin clot from forming
7
Q
warfarin
A
- drug class: direct thrombin inhibitor
- MOA: blocks the gamma-carboxylation of several glutamate residues (vitamin k dependent)
- onset: 8-12 hour delay in onset (heparin weaned off to warfarin)
- tox:
+hemorrhagic disorder in the fetus
+birth defects
+cutaneous necrosis - measured with INR (normal 0.8-1.2; target 2-3)
- reversal:
+d/c drug
+vitamin K
+FFP
+factor IX concentrates
8
Q
rivaroxaban (xarelto), apixaban (eliquis)
A
- drug class: factor Xa inhibitors
- MOA: targets factor Xa
- indication: clot prevention
- no reversal agent
- effects: less bleeding issue d/t Xa specificity
- indication: CVA, VTE
9
Q
tissue plasminogen activator (tPA)
A
- drug class: fibrinolytic
- recombinant forms: alteplase
- MOA:
+plasminogen activates to plasmin
+t-PA activates plasminogen that is bound to fibrin
+confines fibrinolysis to the formed thrombus and avoids systemic activation - indication: MI, PE
10
Q
streptokinase
A
- drug class: fibrinolytic
- synthesized by Streptococci
- MOA: binds to plasminogen to activate it to promote fibrinolysis
- indication: MI, PE
11
Q
urokinase
A
- drug class: fibrinolytic
- synthesized by the kidney
- MOA: lyses the thrombus from within
12
Q
ASA
A
- drug class: COX-1 selective antiplatelet drug (effects both COX-1 and COX-2, but more selective for COX-1)
- MOA:
+TXA2 normally causes: PLT shape change, granule release, and aggregation
+ASA inhibits TXA2 synthesis, which will cause antiplatelet activity
+irreversibly binds to COX-1; this means that it inhibits the enzyme activity for the lifetime of the enzyme (8-10 days). - indication: arterial thrombosus
- adverse effects:
+GI upset
+buffering may decrease (d/t irritation of gastric mucosa and inhibition of GI protective PGG)
+increase in GI ulcers
+salicylate poisoning
+reye syndrome: hepatic injury and encephalopathy in children treated with ASA after a viral infection - can be used for colon/breast/prostate CA for anti-inflammatory properties & prevention
ASA toxicity graph:
mild: N/V, dizziness
moderate: N/V, tinnitus, HA, confusion, hyperventilation, tachycardia, fever
severe: delerium, hallucinations, seizures, coma, respiratory arrest
13
Q
clopidogrel (plavix), ticlopidine (ticlid)
A
- drug class: antiplatelet aggregation
- MOA: irreversibly inhibits ADP receptors on PLTs; no effects on PGG metabolism
- can be released from drug-eluting stents with polymer coating
14
Q
abiciximab
A
- drug class: IIb/IIIa receptor blocker
- MOA: antiplatelet aggregation by targeting IIb/IIIa-R complex (this receptor normally gets activated in the final common pathway)
15
Q
vitamin k
A
drug class: factor replenisher
target: oxidation/reduction
MOA: carboxylation & 2 reductions will activate vitamin k to active form (hydroquinone
+confers activity on prothrombin (II), VII, IX, and X
indications: warfarin OD, vit K deficiency
16
Q
fresh frozen plasma (FFP)
A
drug class: factor replenishment
target: multiple
result: normal clotting cascade
indications: hemophilia
17
Q
desmopressin
A
- increased factor VIII activity
- indications: mild hemophilia A, von-willebrand disease
18
Q
aminocaproic acid
A
drug class: fibrinolytic inhibitor
MOA: competitively inhibits plasminogen activation
result: stablized clot
indication: post-op
19
Q
tranexamic acid (TXA)
A
drug class: fibrinolytic inhibitor
MOA: inhibits plasminogen conversion to plasmin
indication: trauma, heavy menstrual bleeding, postpartum, epistaxis
decreased risk of death in major bleeding
20
Q
lispro, aspart, glulisine
A
rapid acting insulins
bolus insulin
21
Q
novolin, humulin
A
short acting (regular) insulin
acts fast; leaves fast (longer acting than RA)
22
Q
NPH
neutral protamine Hagedorn
A
intermediate acting
23
Q
glargine, detemir
A
long acting insulin
24
Q
metformin
A
- drug class: biguanide (two guanine molecules)
- fist line therapy for NIDDM (type II)
- MOA: **reduces hepatic glucose production **
- 500 mg prandial
- GI toxicities
25
sulfonylurea
| ex) glipizide (2nd gen)
* drug class: insulin secretagogue
* MOA: binds to K+ channel, K+ channel closes causing **depolarization**
* 1st gen vs 2nd gen
+2nd gen requires a **lower dose for same efficacy**
* increased CV mortality
26
thiazolidinediones (TZDs)
* MOA: decrease insulin resistance (PPAR mediated)
+**drug binds to receptors and increases likelihood of cellular responsiveness to insulin**
+increases insulin signal transduction
* **risk of MI**, increased with **insulin and nitrates**
* **Avandia-Rosiglitazone Medicine Access Program** - only certain physicians had access to Rx it
| *PPAR: peroxisome proliferator-activated receptor
27
acarbose
* drug class: alpha-glucosidase inhibitor
* MOA: blocks digestion of complex carbs
* beneficial in pre-diabetics
* SE: GI upset
+**flatulence**
+diarrhea
+bd pain
28
bile acid binding resin
* large cation exchange resins - not absorbed
* also good for dyslipidemia
* **binds bile acids - prevents reabsorption**
+must be taken with food
* GI upset
29
amylin
* amylin is **released by beta cells**
+**suppresses glucagon release**
* decreases circulating glucose
* concomitant with insulin
30
semaglutide (ozempic)
* drug class: GLP-1 agonist//incretin-based therapuetic agent
* GLP-1 agonism:
+stimulates insulin release
+inhibits glucagon release
+both leads to effect of lowering blood glucose
**pancreatic CA risk**
| GLP: gluagon-like peptide
31
sitagliptin (januvia)
* drug class: DPP-4 antagonist
* MOA: **blocks DPP-4, which increases GLP-1 agonism and incretin hormones leading to decreased glucose**
| DPP-4: dipeptidyl peptidase-4
32
gliflozins
| AKA SGLT-2 inhibitors
* MOA: **prevents glucose reaborption** in PCT
* SE: **glucosuria**
+osmotic diuretic - BP reduction
+wt. loss
+dehydration
* ex) Jardiance, Invokana
33
statins
* MOA: HMG-CoA reductase inhibitors
* decreases overall cellular cholesterol synthesis
* increases LDL receptors
+scavenge LDL from blood
+major effect on liver (raises liver enzymes)
* modest decrease in triglycerides
* small increase in HDL
* SE/tox: muscle pain/increased CK
34
niacin
| vitamin B3
* decreases VLDL and LDL (reduces VLDL secretion from liver)
* increases HDL
* incorporated into NAD - ETC glycolysis/energy producing pathway
* dosing 2-6g daily
* **main tox: flushing**
* other tox: pruritic, dry skin, nausea, abd pain, elevation of liver enzymes
35
gemfibrozil
* drug class: fibrate
* MOA: decreases VLDL, moderate decrease in LDL
* tox: GI upset (rare)
* increaes lipolysis in the liver (PPAR mediated)
36
BABR
| bile acid binding resins
* MOA: cationic bile acid binding (positively charged drug binds to negatively charged bile)
* prevents reuptake from the bile
* SE: constipation, bloating, **steatorrhea**, oral drug absorption impairment
37
ezetimibe
* drug class: absorption inhibitors
* MOA: **inhibits cholesterol absorption; NPCL-1 antagonist**
* tox: possible hepatic, ENHANCE trial (reduced LDL, promoted arterial wall thickening?)
38
evolocumab
* drug class: PCSK9 inhibitor
* MOA:
+inhibits protein PCSK9 (this protein normally binds to LDL + LDL receptors on the liver and promotes their degradation)
+by PCSK9 binding to PCSK9, LDL can bind to LDL-Rs & the number of LDL receptors are increased and available to clear cholesterol from the blood, therefore, lowering LDL levels
* **these drugs are not usually given by themselves - they're usually given with statins**
* statins upregulate serum PCSK9 levels
39
celecoxib
* drug class: COX-2 selective inhibitor
* less effects on "housekeeping" COX-1
+**fewer GI effects, **no impact on PLT aggregation, absorption increased by food
* indication: arthritis
* effects: **analgesia, antipyretic, anti-inflammatory**
* adverse effects: CV BB warning (*inhibition of PGI2 production - pro clot!)*
* **is a sulfonamide - allergy warning**
| (COX-2 >>>>>>> COX-1)
40
meloxicam
* drug class: COX-2 inhibitor >> COX-1
* not as selective as other COXIBs
* fewer GI effects
* tox effects similar to other NSAIDs
41
diclofenac (voltaren)
* drug class: non-selective COX inhibitor
* anti-inflammatory, analgesic, antipyretic
* 20% of pts have adverse GI effects (decreased with misoprostol AKA cytotec)
* also comes as a topical gel
42
ibuprofen
* drug class: NSAID (non-selective COX inhibitor)
* less GI upset than ASA (equal in efficacy as an anti-inflammatory/analgesic drug)
* OTC
* PO, cream, gel, IV
* adverse effects: like all other NSAIDs
+agranulocytosis and aplastic anemia is rare
43
indomethacin
* potent COX inhibitor (inhibits COX and LOX synthesis)
* MOA: may also inhibit PLA/PLC
* reduces PMN migration
* decrease T&B cell proliferation
* indications: rheumatism, gout, patent ductus arteriosus - open duct that allows arterial/venous blood to mix between the aorta/PA
44
ketorolac (toradol)
* drug class: NSAID (COX1=COX2 inhibition)
* indication: post-op pain, ER/sports medicine (IV/PO/IM/IN)
* short-term use
* NSAID but primarily used for pain
* can be used in conjunction with opioids
* typically use 25-50% lower dose of opioids
45
acetaminophen
* drug class: NOT AN NSAID//selective COX-2 inhibitor in the CNS
* weak PG inhibitor in peripheral tissues
* PO or PR (newer IV formulation)
* metabolized by hepatic enzymes (toxic to both kidneys/liver)
* it does not affect inflammation
* while it is an analgesic and an antipyretic, it doesn't inhibit the COX enzymes in peripheral tissues to the same extent as NSAIDs, which limits its anti-inflammatory effects
* adverse effects:
+mild increase in hepatic enzymes
+larger doses: **dizziness, excitement, disorientation**
+**FATAL:** **15 grams,** hepatotoxicity, acute renal tubular necrosis
46
glucocorticoids
* bind to glucocorticoid response elements (which increase gene expression that **decreases inflammation**)
* annexin-1 (lipocortin-1) is increased
+this suppresses PLA-2; also inhibits leukocyte response
* SLPI is increased (secretory luekoprotease inhibitor)
* IL-10 is increased (decreases WBCs rushing to area)
* INh-NFK B is decreased (this is pro-inflammatory, so inhibiting this makes it anti-inflammatory)
47
morphine
* phenanthrene structure
* **strong opioid**
48
dilaudid
* phenanthrene structure
* **5x more potent than morphine**
* strong opioid
49
codeine
* phenanthrene structure
* 1/10th as potent as morphine
* moderate agonist
50
oxycodone
* phenanthrene structure
* more effective as a combination med
* 2x more potent than morphine
* moderate agonist
51
percadan/percocet
* oxy + tylenol = percocet
* oxy + ASA = percodan
* moderate agonists
52
methadone
* phenylheptylamine structure
* 10x more potent than morphine
* strong opioid agonist
* indications: chronic pain (with morphine tolerance)
* "less problematic drug" - typically used for people with drug abuse
* duration of analgesia: 4-6 hours
* long half-life (25-50 hrs)
* CYP3A4 metabolism
53
fentanyl
* phenylpiperidine structure
* strong opioid agonist
* **100x more potent than morphine**
* *carfentanil: 10,000x more potent* (drugs laced with this can be fatal)
54
meperidine (demerol)
* phenylpiperidine structure
* strong opioid agonist
* **antimuscarinic effects: tachycardia**
* negative inotrope
* can potentiate seizures to someone who is already predisposed
* indications: **post-op shivering**
+**increased kappa opioid receptor agonism; some serotinergic effects**
55
tramadol
* phenylpiperidine structure
* moderate agonist
* also has SNRI activity
* racemic mixture
* *safer alternative
56
buprenorphine (buprenex)
* indication: **opioid abuse/dependency**
* partial agonist
57
butorphanol (stadol)
* partial agonist
* indication: post-op shivering
58
dextromethorphan
* indication: cough
* effect: antisussive
59
naloxone
* derivative of morphine
* opioid reversal agent (1-3 mins)
* short duration; effects may return
* **little effect in absence of agonist**
60
naltrexone
* derivative of morphine
* indication: opioid & ETOH abuse
61
naloxegol
* derivative of morphine
* **indication: treatment of opioid induced constipation**
* **only goes into enteric nervous system**
* suppresses enteric response
62
PCN, ampicillin, amoxicillin
* beta-lactam abx
* MOA: **inhibition of cell wall synthesis**
+beta lactam ring attaches to enzymes that cross link peptidoglycans and prevent cell wall synthesis
+these abx **inhibit cell wall synthesis** of bacterial cell walls by binding to and inactivating PCN binding proteins (PBPs)
+this prevents the cross-linking of petidoglycan chains, **leading to cell lysis and death**
* **PCN is a 5 ring structure**
* effective against **gram (+)** bacteria and *some gram (-) cocci*
* indications: strep throat, syphillis, meningitis
* **adverse effects**: allergic reactions (rash to anaphylaxis), GI upset, neurotoxicity (rare)
| prototype: PCN G
63
cephalosporin
* beta-lactam abx
* **inhibits cell wall synthesis** by binding to and inactivating PCBs
* prevents cross-linking of peptidoglycan chains
* cell lysis/death
* **more resistant to beta-lactamase**
* **broader spectrum than PCNs** and is used for respiratory tract infections, skin infections, & UTIs
* **first generation: better gram (+) activity**
* **adverse effects**: allergic rxns (cross-reactivity with PCNs), GI upset, and potential nephrotoxicity
| prototype: cephalexin
64
vancomycin
* **MOA: inhibits cell wall synthesis**
* * glycopeptide
* useful for **gram (+) bacteria**
* **resistant to beta-lactamase**
* alternative to PCN resistant bacteria (MRSA)
* *drug of last resort*
* adverse reactions: 10%
+irritant to tissues
+ototoxicity
+nephrotoxicity
+chills/fever
+"red neck" syndrome
65
polymyxin
* polypeptide antibiotic
* MOA: disruption of cell membrane function
+binds to phospholipids to cause cell death
+**effective against gram-negative bacteria, which have an outer membrane**
66
daptomycin
* MOA: disruption of cell membrane function
+binds to phospholipids to cause cell death
* **better against gram (+) bacteria**
* indications: skin infections, bacteremia
67
tetracyclines
* **MOA: inhibits protein synthesis**
* bacteriostatic
* pharmacoK: readily absorbed, widely distributed
* **have the widest spectrum of activity on any abx**
* *destroys normal intestinal microbiota, and often produce severe GI disorders (bone deposition disorder)*
* can lead to c. diff
* adverse reactions:
+GI (N/V/D), bone, neurotoxicity, allergies, neprho/ototox
68
erythromycin
* drug class: macrolide
* spectrum: gram + and -
* this is the **prototype drug**
* **MOA: inhibits protein synthesis**
69
azithromycin (zithromax)
* drug class: macrolide
* **MOA: inhibits protein synthesis**
* semi-synthetic derivative
70
neomycin
* MOA: inhibition of protein synthesis
* can be topical
71
rifamycin
* **MOA: DNA/RNA synthesis**
* binds to a bacterial **RNA polymerase**
72
ciprofloxacin (cipro)
* drug class: floroquinolone
* MOA: **targets DNA/RNA synthesis**
+inhibits DNA gyrase (bacterial)
+this is an enzyme crucial for DNA synthesis
* **excellent gram (-) activity**
* **also good for gram (+)**
* routes: PO, IV, opthalmic injections,
* indications: respiratory, inhaled anthrax, tuberculosis, GI/abd infections, prostatitis, UTIs, STDs (chlamydia), bone/soft tissue/joint infections
73
sulfonamide
* MOA: inhibition of **folic acid synthesis**
**structurally similar to PABA (precursor to folic acid production)**
+competitively binds to block synthesis of folic acid
* indications: pneumocystis, taxoplasmosis
* often combined with trimethoprim to enhance effectiveness
* combo: bactrim, septra
* tox:
+allergenic
+may precipitate in urine
+hematopoietic distrubances
74
trimethoprim
* MOA: inhibition of **folic acid synthesis**
+inhibits the enzyme **dihydrofolate reductase**
+blocks bacterial growth
* often combined with trimethoprim to enhance effectiveness
* combo: bactrim, septra
75
ketoconazole
antifungal
76
lamisil
antifungal
77
hydroxychloroquine
antiprotozoal agent
indication: malaria
78
metronidazole
antiprotozoal
adverse effect: black, hairy tongue
79
niclosamide
indication: parasitic worms
80
ivermectin
indication: parasitic worms
81
permethrin
indication: parasitic worms
82
acyclovir
* MOA:
* inhibits viral DNA synthesis
* converted into acyclovir triphosphate inside infected cells, then competes with **deoxyguanosine triphosphate** for incorporation into viral DNA
* once incorporated, acyclovir triphosphate acts as a **chain terminator** - it lacks a 3'-OH group, preventing further elongation of the DNA chain
* indications: HSV1, HSV2, VZV infections
* safe in pregnant women, can reduce shedding in c-section rate when given in last trimester of pregnancy
83
azidothymidine (AZT)
* drug class: antiretroviral nucleoside/nucleotide analog
* MOA:
+combined with other antivirals in HAART (highly active antiretroviral therapy)
+**inhibitor of reverse transcriptase**
84
lamivudine
* MOA: inhibits HBV DNA polymerase and HIV reverse transcriptase
85
cabotegrovir
| AKA PrEP
* Pre-exposure preventative
* blocks integration
86
interferon
* naturally occuring in human cells
* used with some success in preventing and treating viral infections
87
oseltamivir phosphate (tamiflu)
* influenza antiviral
* early treatment of flu (FDA approved)
88
zanamivir (relenza)
* must be taken BEFORE sx occur
* not rec for ppl with **asthma or COPD**
89
baloxivir marboxil (xofluza)
* polymerase inhibitor
* not rec for pregnant women, breastfeeding mothers, outpatients with progressive or complicated illness or hospitalized pts
* may reduce duration of flu by 1 day
* **one-time pill dose**
90
paxlovid
* COVID tx
* 2 antivirals, emergency use authorization (PO)
91
remdesivir
* FDA approved COVID tx
* chain terminator
* IV
92
COVID MABs
* COVID tx
* (3)
* block covid entry into cells
* IV
93
dexamethasone
* COVID tx
* cytokines
94
levodopa/carbidopa
* L-isomer of dopamine
* crosses the BBB (dopamine does not)
* improved uptake with carbidopa and COMT inhibitors (tolcapone)
* decreased toxicity (hallucinations) with pimavanserin (nuplazid)
* **MOA: restores dopa levels**
95
pimavanserin (nuplazid)
* drug class: a-typical antipsychotic
* inverse agonist ast 5-HT2A (visual cortex)
* interacts with the thalamus, which interacts with the substantia nigra
* combats hallucinations associated with parkinson's
96
pramipexole
* drug class: dopamine receptor agonist
* less effective than L-Dopa
* decreased SE
97
selegeline
* drug class: MAO-B antagonist
* minor effects alone
* increases dopamine levels
98
tolcapone
* drug class: COMT inhibitor
* catecholamines are inactivated by oral admin
* catecholamines are inactivated by catechol-O-methyltransferase (COMT)
* by inhibiting COMT, tolcapone **increases circulating dopamine**
99
apomorphine
* drug class: dopamine agonist
* useful to treat "off" periods of parkinson's
* decreases akinesia symptoms
100
baclofen
* drug class: muscle relaxant
* indication: cerebral palsy
* MOA: relaxes muscle movements associated with CP (hyper/hypotonia)
101
tetrabenazine
* drug class: VMAT2-inhibitor
* MOA: depletes dopamine (dopamine stimulates ACh receptors, leading to **Chorea associated with Huntington's Disease)**
102
haloperidol (haldol)
* drug class: antipsychotic
* MOA: dopamine receptor blocker
* treats Chorea symptoms associated with Huntington's Disease
103
riluzole
* drug class: sodium channel blocker
* MOA: blocks sodium channel binding
* extends quality of life in **ALS** patients
104
tacrine
* drug class: AChE-inhibitor
* MOA: inhibits the breakdown of AChE in the synapse to help with **Alzheimer's Disease** sx
105
ASA OD treatment
* activated charcoal
* IV fluids
* hemodialysis
106
memantine
* drug class: NMDA-R antagonist
* useful in the treatment of **Alzheimer's Disease**
107
echinacea
* sitmulation of immune system, anti-inflammatory
108
garlic
* HMG CoA reductase inhibitor
* "inhibits cholesterol synthesis"
109
ginko
* improved blood flow
* free radical scavenger
* "dementia: memory"
110
st. john's wort
* antidepressant
* **CYP450**
* not to be used with **MAO-i's and SSRI's**
111
ginseng
* memory
* immune system
* analgesia
112
milk thistle
* reduction in hepatotoxicity
113
saw palmetto
* BPH
114
kava kava
* anxiety, muscle relaxant, sedative
115
kombucha
* BP
* CA
* GI health
116
aloe
* laxative
* burn ointment
117
black cohosh
* menstrual discomfort
118
cyclophosphamide
drug class: alkylating agent - **nitrogen mustard**
* most common alkylating agent
* MOA:
1. forms highly reactive carbonium ion
2. transfers alkyl groups to nucleophilic sites on DNA bases
3. results in:
+cross linkage
+abnormal base pairing (cell cycle arrests)
+DNA strand breakage
**+decreased cell proliferation**
*also damages RNA and proteins*
119
chlorambucil
* least toxic nitrogen mustard alkylating agent
120
nitrosoureas
* alkylating agent that crosses BBB (useful in brain tumors)
121
cisplatin
* highly bound to plasma proteins
* concentrates in kidney, intestine, and testes
* poorly penetrates BBB
* slowly excreted in urine
* indications:
+testicular CA (85-95%)
+ovarian CA
+other solid tumors: lung, esophagus, gastric
* MOA:
1. cisplatin enters cell
2. Cl- ions released
3. forms highly reactive platinum (Pt) complexes
4. instra strand/interstrand x-linkage
5. DNA damage
6. inhibits cell proliferation
* adverse effects: emesis, nephrotox, peripheral neuropathy, ototox
122
methotrexate
* anti-metabolite drug
* inhibits dihydrofolate reductase (DHFR) and interferes with **DNA/RNA synthesis** by inhibiting **folate synthesis**
* cytotoxic actions:
+predominant on bone marrow
+ulceration of intestinal mucosa
+crosses placenta intereferes with embryogenesis (**fetal malformations and death**)
* immunosuppresive actions:
+prevents clonal expansion of B & T lymphocytes
* anti-inflammatory action
+interferes with release of inflammatory cytokines
123
antimetabolites
* 6-mercaptopurine (6-MP)
* 5-fluorouracil (5-FU)
124
vincristine, paclitaxel (taxol)
antineoplastic: **plant based**
125
dactinomycin, doxorubicin, bleomycin
antineoplastic: **anti-tumor abx**
126
corticosteroids, tamoxifen, fulvestrant
antineoplastics: **hormonal agents**
127
Imatinib, Trastuzuman, Rituximab
antineoplastics: **miscellanous -MABs & -ibs (growth factor inhibitors)**
