Capecitabine

PHARMACOKINETICS PHARMACODYNAMICS

Readily absorbed from GI tract. Protein Capecitabine is a fluoropyrimidine

binding: less than 60%. Metabolized in carbamate belonging to a group of
liver. Primarily excreted in urine. Halflife: 45 min. antineoplastic agents called
antimetabolites, which kill cancerous
cells by interfering with DNA synthesis.

INDICATIONS CONTRAINDICATIONS

Treatment of metastatic breast cancer as

monotherapy or in combination with : Severe renal impairment (CrCl less than 30 mL/min),
docetaxel after failure of prior dihydropyrimidine dehydrogenase (DPD)
anthracycline containing regimen. deficiency, hypersensitivity to capecitabine,
Treatment of metastatic colorectal cancer. 5-fluorouracil (5-FU). Cautions: Existing
Adjuvant (postsurgical) treatment of Dukes bone marrow depression, hepatic impairment, mild to
C colon cancer. OFFLABEL: Gastric cancer, moderate renal impairment,
pancreatic cancer, esophageal cancer, previous cytotoxic therapy/radiation therapy, elderly
ovarian cancer, neuroendocrine tumors, (60 yrs of age or older).
hepatobiliary cancer.

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Pemetrexed
PHARMACOKINETICS PHARMACODYNAMICS

Protein binding: 81%. Not metabolized. Inhibits biosynthesis of purine and

Excreted in urine. Half-life: 3.5 hrs. thymidine nucleotides. Inhibits protein
synthesis. Therapeutic Effect: Disrupts
folate-dependent enzymes essential for cell
replication.

INDICATIONS CONTRAINDICATIONS

Treatment of unresectable malignant pleural Severe hypersensitivity to PEMEtrexed.

mesothelioma in combination with CISplatin. Cautions: Hepatic/renal impairment,
Initial treatment of locally advanced or concurrent use of nephrotoxic medications,
metastatic non-squamous non– small-cell lung preexisting myelosuppression. Not indicated
cancer (NSCLC) (in combination with for squamous cell NSCLC.
cisplatin). Initial treatment of metastatic,
non-squamous NSCLC (in combination with
platinum chemotherapy and pembrolizumab) in
pts with no epidermal growth factor receptor
(EGFR) or anaplastic lymphoma kinase (ALK

tumor aberrations. Maintenance treatment

(single agent) of locally advanced or
metastatic non-squamous NSCLC if no
progression after 4 cycles of platinumbased
first-line therapy. Single-agent treatment
(after prior chemotherapy) of recurrent,
metastatic non-squamous NSCLC. OFF-LABEL:
Treatment of bladder, cervical, ovarian,
thymic malignancie
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Methotrexate
PHARMACOKINETICS PHARMACODYNAMICS

Widely distributed. Protein binding: 50%– Irreversibly binds to and inhibits

60%. Metabolized in liver. Primarily dihydrofolate reductase, inhibiting
excreted in urine. Removed by hemodialysis formation of reduced folates and
but not by peritoneal dialysis. Halflife: thymidylate synthetase, which inhibits
3–10 hrs (large doses, 8–15 hrs). purine/thymidylic acid synthesis.
Therapeutic Effect: Interferes with DNA
synthesis, repair, and cellular
replication.

INDICATIONS CONTRAINDICATIONS

Oncology-related: Treatment of breast, Hypersensitivity to methotrexate.

head/neck, non–small-cell lung, smallcell Breastfeeding. For pts with psoriasis,
lung carcinomas; trophoblastic tumors, juvenile idiopathic arthritis, or
acute lymphocytic, meningeal leukemias; rheumatoid arthritis: Pregnancy, hepatic
non-Hodgkin’s lymphomas (lymphosarcoma, disease, alcoholism, immunodeficiency
Burkitt’s lymphoma), carcinoma of syndrome, preexisting blood dyscrasias.
gastrointestinal tract, mycosis fungoides, Cautions: Peptic ulcer, ulcerative colitis,
osteosarcoma. Non-oncology uses: preexisting myelosuppression, history of
Psoriasis, rheumatoid arthritis (including chronic hepatic disease, alcohol
juvenile idiopathic arthritis). OFF-LABEL: consumption, obesity, diabetes,
Treatment of acute myelocytic leukemia, hyperlipidemia, use with other hepatotoxic
bladder carcinoma, ectopic pregnancy, medications, concomitant use of proton pump
management of abortion, systemic lupus inhibitors. Use of NSAIDs or aspirin with
erythematosus, treatment of and lower methotrexate doses for rheumatoid
maintenance of remission in Crohn’s arthritis.
disease.
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Alkylating agents- chlorambucil
PHARMACOKINETICS PHARMACODYNAMICS

Rapidly, completely absorbed from GI Inhibits DNA, RNA synthesis by crosslinking

tract. Protein binding: 99%. Metabolized with DNA strands. Therapeutic Effect:
in liver to active metabolite. Not removed Interferes with DNA replication and RNA
by hemodialysis. Half-life: 1.5 hrs; transcription.
metabolite, 2.5 hrs.

INDICATIONS CONTRAINDICATIONS

Treatment of chronic lymphocytic leukemia

(CLL), Hodgkin’s and non-Hodgkin’s : Hypersensitivity to chlorambucil.
lymphomas (NHL). OFF-LABEL: Nephrotic Previous allergic reaction to other
syndrome in children, Waldenström’s alkylating agents, prior resistance to
macroglobulinemia. chlorambucil, pregnancy. Extreme Cautions:
Treatment within 4 wks after full-course
radiation therapy or myelosuppressive drug
regimen. Cautions: History of bone marrow
suppression, head trauma, hepatic
impairment, nephrotic syndrome, seizure
disorder; administration of live vaccines
to immunocompromised pts.

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ifosfamide
PHARMACOKINETICS PHARMACODYNAMICS

Metabolized in liver. Protein binding: Inhibits DNA, protein synthesis by

negligible. Crosses blood-brain barrier crosslinking with DNA strands, preventing
(to a limited extent). Primarily excreted cell growth. Therapeutic Effect: Produces
in urine. Removed by hemodialysis. Half- cellular death (apoptosis).
life: 11–15 hrs (high dose); 4–7 hrs
(low dose).

INDICATIONS CONTRAINDICATIONS

Treatment of germ cell testicular

carcinoma (used in combination with other Hypersensitivity to ifosfamide. Urinary
chemotherapy agents and with concurrent outflow obstruction. Cautions:
mesna for prophylaxis of hemorrhagic Renal/hepatic impairment, compromised bone
cystitis). OFF-LABEL: Small-cell lung, marrow reserve, active urinary tract
non–small-cell lung, ovarian, cervical, infection, preexisting cardiac disease,
bladder cancer; soft tissue sarcomas, prior radiation therapy, conditions
Hodgkin’s, non-Hodgkin’s lymphomas; predisposing to infection (e.g., diabetes,
osteosarcom renal failure, immunocompromised pts, open
wounds). Avoid use in pts with WBC less
than 2,000 cells/ mm3 and platelets less
than 50,000 cells/ mm3.

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Bendamustine
PHARMACOKINETICS PHARMACODYNAMICS

Metabolized in liver and via hydrolysis to Alkylates and cross-links double-stranded

metabolites. Protein binding: 94%–96%. DNA. Therapeutic Effect: Inhibits tumor
Excreted in urine (50%), feces (25%). cell growth, causes cell death.
Halflife: 40 min.

INDICATIONS CONTRAINDICATIONS

Treatment of chronic lymphocytic leukemia

(CLL). Treatment of indolent B-cell non- Hypersensitivity to bendamustine. (Bendeka
Hodgkin’s lymphoma (NHL) that has only): polyethylene glycol 400, or
progressed during or within 6 mos of propylene glycol mono-thioglycerol.
treatment with riTUXimab or a riTUXimab- Cautions: Baseline cytopenias, hepatic/
containing regimen. OFF-LABEL: Treatment renal impairment, conditions predisposing
of mantle cell lymphoma, relapsed multiple to infection (e.g., diabetes, renal
myeloma. First-line treatment for failure, immunocompromised pts, open
follicular lymphoma. Treatment of wounds); dermatologic disease, HF,
Waldenström’s macroglobulinemia dehydration; pts at high risk for tumor
lysis syndrome (high tumor burden); history
of hepatitis B virus infection, herpes
zoster infection.

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Immunomodulators- lenalidomide
PHARMACOKINETICS PHARMACODYNAMICS

Widely distributed. Protein binding: 30%. Inhibits secretion of pro-inflammatory

Excreted in urine. Half-life: 3 hrs cytokines, increases secretion of anti-
(increased in renal impairment). inflammatory cytokines. Enhances cell-
mediated immunity by stimulation of T
cells. Therapeutic Effect: Inhibits myeloma
cell growth; induces cell cycle arrest and
cell death.

INDICATIONS CONTRAINDICATIONS

Treatment of low- to intermediate-risk Hypersensitivity to lenalidomide.

myelodysplastic syndrome (MDS) in pts with Pregnancy. Cautions: Renal/ hepatic
deletion 5q cytogenetic abnormality with impairment, conditions predisposing to
transfusion-dependent anemia. Treatment of infection (e.g., diabetes, renal failure,
multiple myeloma (in combination with immunocompromised pts, open wounds); pts at
dexamethasone). Treatment of pts with mantle risk for tumor lysis syndrome (high tumor
cell lymphoma that has relapsed or progressed burden); pts at risk for thrombosis
after 2 prior therapies (one of which included (immobility, indwelling venous
bortezomib). Maintenance treatment for multiple catheter/access device, morbid obesity,
myeloma (following autologous stem cell underlying atherosclerosis, genetic
transplant). Treatment of previously treated hypercoagulable conditions); history of
follicular lymphoma (in combination with venous or arterial thrombosis (e.g., CVA,
rITUXimab). Treatment of previously treated DVT, MI, pulmonary embolism). Avoid use in
marginal zone lymphoma (in combination with pts with glucose intolerance, lactase
riTUXimab). OFF-LABEL: Systemic amyloidosis, deficiency
lower-risk myelodysplastic syndrome, non-
Hodgkin’s lymphoma. Relapsed or refractory
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BEFORE DURING AFTER
Pomalidomide
PHARMACOKINETICS PHARMACODYNAMICS

Widely distributed. Metabolized in liver. Inhibits tumor cell proliferation and

Protein binding: 12%–44%. Peak plasma induces apoptosis (cell death) of
concentration: 2–3 hrs. Excreted in urine hematopoietic cells. Enhances T-cell– and
(73%), feces (15%). Half-life: 8–10 hrs. natural killer (NK) cell–mediated
immunity. Inhibits proinflammatory
cytokines. Therapeutic Effect: Inhibits
tumor cell growth and metastasis

INDICATIONS CONTRAINDICATIONS

Treatment of multiple myeloma in pts who

have received at least two prior therapies Hypersensitivity to pomalidomide.
including lenalidomide and a proteasome Pregnancy. Cautions: Anemia, HF,
inhibitor and who have demonstrated hepatic/renal impairment, smoking,
disease progression on or within 60 days breastfeeding, or prior history of CVA, MI,
of completion of the last therapy. DVT, PE.
Treatment of adults with AIDS-related
Kaposi sarcoma (KS) after failure of
highly active antiretroviral therapy
(HAART) or in pts with KS who are HIV
negative.

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BEFORE DURING AFTER
interferon alfa-2b
PHARMACOKINETICS PHARMACODYNAMICS

Well absorbed after IM, SQ administration. Binds to a specific receptor on cell

Undergoes proteolytic degradation during membrane to initiate intracellular
reabsorption in kidneys. Halflife: 2–3 activity, including suppression of cell
hrs. proliferation, augmenting specific
cytotoxicity of lymphocytes and increasing
phagocyte activity. Therapeutic Effect:
Prevents rapid growth of malignant cells;
inhibits hepatitis virus.

INDICATIONS CONTRAINDICATIONS

Treatment of hairy cell leukemia,

condylomata acuminata (genital, venereal Hypersensitivity to interferon alfa-2b.
warts), malignant melanoma, AIDS-related Decompensated hepatic disease, autoimmune
Kaposi’s sarcoma, chronic hepatitis C hepatitis. In combination with ribavirin:
virus infection (including children 3 yrs Women who are pregnant, men with pregnant
of age and older), chronic hepatitis B partners, pts with hemoglobinemias (e.g.,
virus infection (including children 1 yr sickle cell anemia), CrCl less than 50
and older), follicular non-Hodgkin’s mL/min).
lymphoma. OFFLABEL: Treatment of bladder,
cervical, renal carcinoma; chronic
myelocytic leukemia; laryngeal
papillomatosis; multiple myeloma;
cutaneous T-cell lymphoma; mycosis
fungoides; West Nile virus.

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PHARMACOKINETICS PHARMACODYNAMICS

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