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EXAM 3 SMITH
| DRUG | CLASS | MOA/USE | ADRs | NOTES |
|---|---|---|---|---|
| Darbepoetin | Eythropoiesis stimulating agent (ESAs) | For anemia MOA: binds to erythropoeietin receptor on immature red blood cells, stimulates differentiation and proliferation | high RBCs, hyperviscosity, stroke, MI if given to pts without anemia HTN, no admin w/HTN reduce survival in H&N carcinomas development of antiboies against EPO (red cell aplasia) | lower binding affinity than epoetin alfa but longer half life Take about 10 days before erythrocyte progenitor cells are cont. released into circulation and longer for full effect, dont adjust dose too soon |
| Epoetin Alfa | Eythropoiesis stimulating agent (ESAs) | For anemia MOA: binds to erythropoeietin receptor on immature red blood cells, stimulates differentiation and proliferation | high RBCs, hyperviscosity, stroke, MI if given to pts without anemia HTN, no admin w/HTN reduce survival in H&N carcinomas development of antiboies against EPO (red cell aplasia) | higher binding affinity than darbepoetin but short half life Take about 10 days before erythrocyte progenitor cells are cont. released into circulation and longer for full effect, dont adjust dose too soon |
| Oral iron products | Ferrous sulfate, hydrated 325(65)mg Ferrous sulfate, desiccated 200(65)mg Ferrous gluconate 325(36)mg Ferrous fumarate 100(33)mg or 325(106)mg | used for heme - hemoglobin production to ensure efficacy of ESAs in anemia | Nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea | Constipation and diarrhea may be related to iron-induced changes in flora other GI effects lowering dose, making it a salt, or taking with food decrease ADRs |
| IV iron products | LMW iron dextran, iron sucrose, ferric glu/carb, deferasirox, deferiprone, ferric derisomaltose, polysaccharides iron complex | For pts unable to take oral iron, or severe anemia not maintained by oral therapy given as colloidal prep to prevent dose limiting toxicity | Iron overload needs to be monitored for anaphylaxis | LMW iron dextran has black box warning for significant ADRs especially with high miolecular weight preparations |
| Vitamin B12 (cyanocobalamin) | Vitamin | MOA: cofactor for many biochemical reactions, including prodcution of tetrahyrofolate | Deficiency from diet is not common, Vitn B12 deficiency can cause megaloblastic anemia or neurological symptoms | 1/6th absorbed from actual diet intake, stored in liver, absorbed by active transport across gut 3 |
| Folic acid | Deficiency is commonly caused by inadequate dietary intake, dihydrofolate reductase inhibitors can cause deficiency | Folic acid deficiency can cause megaloblastic anemia | no neurological symptoms unlike Vit B12 | |
| Sargramostim | GM-CSF (myeloid growth factor) | For Neutropenia MOA: Stimulates proliferation, differentiation and function of myeloid cells, used to recover from chemotherapy (neutropenia) stims CFU, GEMM, GM,M,E,Meg | Increase SCr, bilirubin, hepatic enzymes, dyspnea, transient supraventricular arrhythmia rxn to first dose | Can decrease leukocyte count synergistic effect with other hematopoietic growth factors |
| Filgrastim | G-CSF (myeloid growth factor) | For neutropenia MOA: Binds G-CSF on surface of immature neutrophils to enhance growth and production, reduced inflammation by inhibiting IL-2, TNF and interferon gamma, mobilizes hematopoietic stem cells | Prolonged high dose: bone pain, skin reactions, necrotizing vasculitis Prolonged use: marked granulocytosis (over 100,000/uL) and spleen enlargement (splenomegaly) | |
| Pegfilgrastim | G-CSF (myeloid growth factor) | For neutropenia MOA: Binds G-CSF on surface of immature neutrophils to enhance growth and production, reduced inflammation by inhibiting IL-2, TNF and interferon gamma, mobilizes hematopoietic stem cells | Prolonged high dose: bone pain, skin reactions, necrotizing vasculitis Prolonged use: marked granulocytosis (over 100,000/uL) and spleen enlargement (splenomegaly) | Longer half-life than filgrastim due to glomerular clearnace |
| Efbemalenograstim alfa-vuxw and Eflapegrastim-xnst | G-CSF (myeloid growth factor) | For neutropenia Decrease infection from febrile neutropenia in pts on myelosuppressive drugs | Efbemalenograstim alfa-vuxw: nausea, anemia, thrombocytopenia Eflapegrastim-xnst: same + back pain | Given once per chemo cycle, 24 horus after cytotoxic chemotherapy |
| Trilaciclib | Cyclin dependent kinase (CDK) 4/6 inhibitor | MOA: works on immune, hematopoietic and progenitors cells in cell cycle arrest, preventing them from being targeted by chemo therapy | 4/6 block S phase actions, keeps cells in G1, wears off after 32 hours and cells can grow | |
| Eltrombopag | Trombopoietin receptor agonists | For thrombocytopenia MOA: thrombopoietin receptor agonist (TPO); induces proliferation and differentiation of megakaryocytes | Hemorrhage, thrombosis, ascites, disorder of liver, liver failure, portal vein thrombosis, cataracts pregnancy and breastfeeding risk | DDIs with calcium, antacids |
| Romiplostim | Trombopoietin receptor agonists | For thrombocytopenia MOA: thrombopoietin (TPO) receptor agonist; induces proliferation and differentiation of megakaryocytes | Acute myeloid leukemia, hemorrhage, increased reticulin in bone marrow, portal vein thrombosis Preg and feeding risk | SQ, other TPO agonists are oral Fc fragment |
| Avatrombopag | Trombopoietin receptor agonists | MOA: thrombopoietin receptor agonist (TPO); induces proliferation and differentiation of megakaryocytes has additive effect with TPO on platelet production | Portal vein thrombosis, thrombosis | Take with food |
| Rituximab | CD20 antibody | MOA in ITP: decrease in B cells from rituximab results in reduction of antibody producing cells that attach to platelets as well | Immunosuppressive because targets normal B cells, hypersensitivity | |
| Intravenous immune globin (IVIG) | MOA: prevent immune cells from attacking antibody coded platelets | rash, chills, headaches, shortness of breath, or hypotension; premedication used to prevent this | ||
| Rho(D) immune globin (anti-D immune globin) | Treat RhoD positive patients, RH-negative pregnancies MOA: destruction of anti-D red blood cells can save some platelets | possible severe vascular hemolysis | ||
| Goserelin, Leuprolide, Triptolerin | GnRH Agonists | For prostate cancer MOA: GnRH agonists suppress LH/FSH release by negative feedback, reducing testosterone production | Can cause disease flare from initial surge in LH/FSH, give androgen antagonists for 2-4 weeks to prevent surge | Can reduce testosterone to castration levels |
| Relugolix, Degarelix | GnRH Antagonists | Prostate cancer MOA: Do not let GnRH stimulate pituitary to reduce testosterone production | Teratogen, female partners must use birth control, do not use with preexisting QTc prolongation | No initial flare like agonist (otherwise no advantage over agonists) Relugolic is oral, degarelix is SQ |
| Finasteride | 5a-reductase inhibitors | For prosate cancer MOA: decrease DHT (highly active test) production | Teratogenic | Class of drugs can take 6 months to for max prostate shrinkage, reduces PSA by 50% Preferred over adrenergic antagonists for pts with arrhythmias, angina, on HTN meds, |
| Dutasteride | 5a-reductase inhibitors | For prostate cancer MOA: decrease DHT production decreases DHT more than finasteride | Teratogenic | Targets type 1/2 non selectively (finasteride is selective type 2), quicker and more effective than finasteride Finasteride 8hr half life dutasteride 5 weeks |
| Abiraterone acetate | CYP17 Inhibitors | MOA: Blocks 17a-hydroxylase (P450c17) and 17, 20-lyase, reduces synthesis of cortisol in the adrenal and gonadal testosterone precursors (DHEA) causes increase in ACTH and aldosterone synthesis, offset with dexamethasone (blocks ald activity) | Prodrug activated by CYP3A4, adrenocortical insufficiency, hepatotoxicity, HTN, hypokalemia, HF, inhibits Pgp and 2D6 | For metastatic prostate cancer that keeps growing at very low test levels docetaxel cuts off all androgen production so pair with prednisone BID |
| Anastrozole (non steroidal, potent and selective, effective in women who become resistant to tamoxifen), Letrozole (non steroidal) Exemestane (steroidal) | Aromatase inhibitors | Inhibit aromatase (test to est) to inhibit estrogen production in advanced breast cancer | Increased risk of osteoporotic fractures | Steroidal (Type 1): mimic androstenedione and bind irreversibly Non-steroidal (Type 2): reversible binding to heme group in aromatase |
| Tamoxifen (Nolvadex) | Selective estrogen receptor modulators (SERMs) | MOA: modifies estrogen receptors, beneficial in bone brain liver during post menopausal hormone therapy, agonist in bone and endometrium, antagonist in breast | increase incidence of endometrial cancer (because its a agonist in endometrium) by 4-6x, only used for up to 10 years | partial agonist in endometrium and bone, antagonist in breast |
| Raloxifene (Evista) | Selective estrogen receptor modulators (SERMs) | MOA: modifies estrogen receptors, beneficial in bone brain liver during post menopausal hormone therapy, ANTAGONIST activity in breast tissue and endometrium, agonsit in bone only used for treatment/prevention | Does not increase risk of endometrium cancer like tamoxifen Prevent osteoporosis in post menopausal women, breast cancer prophylaxis (PREVENTION ONLY), so safer but does work to treat only prevent | antagonist in breast and endometrium, agonist in bone |
| Fulvestrant (Faslodex) | Selective Estrogen Receptor Downregulators (SERDs) | MOA: antagonist in all tissue unlike SERMs, is steroidal, binds to ER with 100x affinity of tamoxifen, reducs number of ER in cells (downregulation) | Theorized to be safer longer and faster than SERMs, shows efficacy in tamoxifen resistant breast cancer, but trials cannot confirm it is more effective in anti-androgen actions compared to tamoxifen | |
| Bicalutamide | Anti-androgen (1st gen androgen receptor Antagonist) | MOA: inhibit androgens from binding to androgen receptors, do not decrease LH production, complete androgen blockage when given with GnRH agonists | Lower toxicity, better tolerability than others | Used to reduce tumor flares whenGnRH agonist are needed |
| Flutamide | Anti-androgen (1st gen androgen receptor Antagonist) | MOA: inhibit androgens from binding to androgen receptors, do not decrease LH production, complete androgen blockage when given with GnRH agonists | Rare fatal hepatotoxicity, tenderness, diarrhea | metabolized to active hydroxyflutamide |
| Nilutamide | Anti-androgen (1st gen androgen receptor Antagonist) | MOA: inhibit androgens from binding to androgen receptors, do not decrease LH production, complete androgen blockage when given with GnRH agonists | Risk of interstitial pneumonitis, nausea, alcohol intolerance, decreased vision at in dark | |
| Enzalutamide | Anti-androgen (2nd gen androgen receptor Antagonist) | MOA: inhibit androgens from binding to androgen receptors, do not decrease LH production, complete androgen blockage when given with GnRH agonists | Fractures, falls and cognitive impairment, back pain, fatigue | Greater affinity for AR compared to 1st gen, additional MOA of inducing apoptosis, metabolized to active N-desmethyl enzalutamide by CYP2C8 |
| Apalutamide | Anti-androgen (2nd gen androgen receptor Antagonist) | MOA: inhibit androgens from binding to androgen receptors, do not decrease LH production, complete androgen blockage when given with GnRH agonists | Increase QT interval and cause seizures, Fractures, falls and cognitive impairment, back pain, fatigue, inducer of 2C19, 3A4, 2C9 | 100% bioavailability |
| Darolutamide | Anti-androgen (2nd gen androgen receptor Antagonist) | MOA: inhibit androgens from binding to androgen receptors, do not decrease LH production, complete androgen blockage when given with GnRH agonists | NO CYP induction, ischemic heart disease, heart falure, urinary retention, pneumonia, hematuria | does not penetrate BBB, making seizures less common |
| Inavolisib | Phosphatidylinositol 3-kinase (PI3K) inhibitor | MOA: inhibit pi3k to prevent cell proliferation and induce apoptosis Used for breast cancer, PI3KCA mutation, HEr2 negative, HR positive | diarrhea, anemia, decreased white blood cells, UTIs | PI3Ka iso form is most associated with solid tumors because of PI3KCA |
| Zoledronic acid | Bisphosphonates | for bone metastasis MOA: binds to hydroxyapatite in bone to inhibit osteoclast mediated bone reabsorption | Atypical femur fracture, osteonecrosis of the jaw due to bone turnover supression | very long duration of action |
| Denosumab | RANK ligand inhibitor | for bone metastasis MOA: binds to RANKL and blocks it from binding to RANK on osteoclast precursor cells, inhibits osteoclastogenesis | peripheral edema, atypical femor fractures, osteonecrosis of the jaw, CI in pregnant women | |
| Radium 223 dichloride | for prostate cancer MOA: complexes with bone hydroxyapatite where bone is turning over. alpha particles break DNA in adjacent cells adn kill them | Range of alpha particles is less than 10 cell diameters | ||
| Sipuleucel-T | MOA: induces immune cell response against prostate acidic phosphate (PAP), expressed in most prostate cancers | for prostate cancer | ||
| Primary resistance | Inherent: no prior exposure but still resistant | |||
| Secondary resistance | Acquired: develops from exposure | |||
| Mechanisms of resistance | decreased activation of prodrugs, decreased uptake of drugs, alterations in drug transport systems, drug target, abilitu to repair damage, increased inactivation, decreased apoptosis abilities | |||
| Pleiotropic resistance | multi-drug resistance, even is structurally unrelated | |||
| Everolimus | Blocks mTOR of PI3K pathway in ER resistant pts | CYP3A4, edena, asthenia, HA, | for ER+/HER- advanced breast cancer previously treated with nonsterodial aromatase inhibitor (azole) | |
| Palbociclib | CDK 4/6 inhibitor | Blocks CDK 4/6 pathway in ER drug resistant pts | neutropenia, PE, embryo-lethal, CYP3A4 | goes in combination with letrazole as initial therapy with fulvestrant if pt has already undergone endocrine therapy |
| Ribociclb | CDK 4/6 inhibitor | used with aromatase inhibitor as inital therapy for postmenopausal women with HR positive, HER2 negative advanced or metastatic breast cancer |
Created by:
beezy41