Pharm II (Chemo Id)

• 1. Anti estrogenic
• 2. Anti androgenic
• 3. Glucocorticoids

Blocks the Estrogen recepter (it is a weak estrogen)

• - thromboembolic disease
• - endometrial cancer
• - hot flushes
• - retinopathy

Faslodex (destroys the recepter)

Aminogluthemide

• Third Generations
• anastrozole
• letrozole
• exemestane

Tamoxifen--- used in both the pre and post menopausal settings.

Aromatase Inhibitors--- only be used in the post menopausal settings when the adrenal gland is the mojor source of the estrogen production.

• Flutamide
• Bicalutamide

• Toxicity:
• - hot flushes
• - impotence
• ** andropause (in men)

Leuprolide and Goserelin

Decreases the pituitary release of both LH and FSH--> decreased estrogen and testosterone

Prostate and breast cancers

Flare effect, Impotence

• - anti-nauseant
• - appetite stimulant
• - decreases cerebral edema
• - co-analgesic
• ___________________
• - fluid retention
• - glucose intolerance
• - proximal myopathy
• - insomnia
• - immunosuppression
• - increased appetite
• - skin changes
• - stress ulcers

• 1. EGFR (HER-2)
• -Lapetinib
• 2. EGFR (non HER-2)
• -Gefitinib
• -Eriotinib
• 3. VEGF
• -Sunitinib
• -Sorafanib
• 3. Product of mutated Oncogene
• -Imatinib

-Inhibits TK activity or the protein product or BCR:ALB oncogene seen in CML

• CML
• GI stromal Tumors (expression c-KIt)

Myalgia, Diarrhea, fluid retention

• 1. trastuzumab
• HER-2 expressing Breast cancers
• Cardiac toxicity
• 2. cetuximab
• k-ras wild-type colon cancer
• 3. panitunumab
• k-ras wild-type colon cancer

• bevacizumab
• - Colon cancer
• - Wound healing toxicity

• 1. CD 20 – rituxumab
• -B-cell lymphoma

• 2. CD 52 – alemtuzumab
• -B-cell lymphoma

M-TOR inhibitor

- Inhibited by bortezomib

• - activity:
• - multiple myeloma
• - mantle cell lymphoma

• •Interferons
• •Interleukins
• •Tumor necrosis factors

• - attempt to control human
• tumors by replicating this “interfering” property

Uses: Melanoma, RCC, Hairy cell leukemia, T-cell lymphoma, CML

Toxicity: Flu like symptoms, Myelosupression,

• 1. increased expression of target proteins
• 2. increased DNA repair
• 3. failure of drugs to enter a cell or
• increased efflux from cell regulated by multidrug resistance gene
• 4. inability of drug to penetrate tumor
• 5. target protein no longer available
• 6. target molecule altered
• 7. formation of trapping agent
• 8. decreased activation of prodrug

• 1. combination chemotherapy
• 2. dose intensity (1st does most important)
• 3. agents to reverse resistance

• •May be inherent
• eg. pancreatic cancer and gliomas

• •May be acquired
• eg. lymphoma and melanoma