 
invasion, blocks viral replication
I. ANTIVIRAL AGENTS
KEY TERMS
Acquired immunodeficiency syndrome (AIDS)
 Collection of opportunistic infections and cancers that occurs
when the immune system is severely depressed by a decrease
in the number of functioning helper T cells
 Caused by infection with human immunodeficiency virus (HIV)
AIDS-related complex (ARC)
 Collection of less serious opportunistic infections with
HIV infection; the decrease in the number of helper T
cells is less severe than in fully developed AIDS
CCR5 coreceptor antagonist
 A drug that blocks the receptor site on the T cell
membrane that the HIV virus needs to interact with in
order to enter the cell
Cytomegalovirus (CMV)
 DNA virus that accounts for many respiratory ,
ophthalmic , and liver infections
Fusion inhibitor
 A drug that prevents the fusion of the HIV-1 virus with the
human cellular membrane, preventing it from entering
the cell
Helper T cell
 Human lymphocyte that helps to initiate immune
reactions in response to tissue invasion
Tissue hormone that is released in response to viral
Hepatitis B:
Nonnucleoside reverse transcriptase inhibitors
 A serious to potentially fatal viral infection of the liver ,
transmitted by body fluids  Drugs that bind to sites on the reverse transcriptase
within the cell cytoplasm, preventing RNA- and DNA-
Hepatitis C
dependent DNA polymerase activities needed to carry
out viral DNA synthesis; prevents the transfer of
 A usually mild viral infection of the liver that can progress
information that allows the virus to replicate and survive
to chronic inflammation, most often seen hepatitis after
blood transfusions
Nucleoside reverse transcriptase inhibitors
Herpes
 Drugs that prevent the growth of the viral DNA chain,
 DNA virus that accounts for many diseases, including preventing it from inserting into the host DNA, so viral
shingles, cold sores, genital herpes, and encephalitis replication cannot occur
Human immune deficiency virus (HIV) Protease inhibitors
 Retrovirus that attacks helper T cells, leading to a  Drugs that block the activity of the enzyme proteases in
decrease in immune function and AIDS or ARC HIV; protease is essential for the maturation of infectious
virus, and its absence leads to the formation of an
Influenza A immune and non infective HIV particle
 RNA virus that incaders tissues of the respiratory tract, Virus
causing the signs and symptoms of the common cold or
“flu”  Particle of DNA or RNA surrounded by a protein coat that
survives by invading a cell to alter its functioning
Integrase inhibitor
Agents for Influenza A Prototype
 A drug that inhibits the activity of the virus-specific and Respiratory
enzyme integrase (an encoded enzyme needed for viral viruses
replication, blocking this enzyme prevents the formation  Amantadine  Rimantadine (HF 25.4)
of the HIV-1 provirus)  Oseltamivir  Prophylaxis and
 Peramivir treatment of illness by
Interferon
 Ribavirin influenza A
 Rimantadine  Inhibits viral
  zenamivir replication, by AGENTS FOR HIV AND AIDS
uncoating the virus
Nucleoside Reverse Prototype
Route: oral Onset: Nonnucleoside

Prototype Transcriptase
Slow; Peak 6h Reverse
Inhibitors
 HF: 25.4 hrs; exreted
Transcriptase Zidovudine (HF 30-60 mins,)
unchanged in the  abacavir 
Inhibitors  Management of adults
urine  didanosine
 delavirdine  Nevirapine (HL 45 hrs; then 25- with symptomatic HIV
 Light-  emtricitabin
 efavirenz 30 hrs) infection in
headedness,dizzines e
 treatment of HIV-1 combination with other
s, insomnia,  etravirine
 lamivudine
infected patients who antiretrovirals;
depression  nevirapine
have experienced  stavudine
prevention of
 rilpivirine
clinical or  tenofovir maternal-fetal HIV
Agents for Herpes Virus immunological  zidovudine transmission
Prototype
and Cytomegalovirus deterioration in  AZT  A thymidine analogue
 acyclovir  acyclovir (HL 2.5-5) combination with other that is activated to a
 cidofovir  treatment of antiretrovirals triphosphate form,
 famciclovir herpes simplex  binds to HIV-1 reverse which inhibits
 foscarnet virus 1 and 2 transcriptase and replication of various
 ganiciclovir  inhibits viral DNA blocks replication of the retroviruses, including
 velacyclovir replication HIV by changing the HIV
 valganiciclovir  Route : Oral; structure of the HIV  Route: oral
Onset: Varies; enzyme Onset: varies
Peak: 1.5-2h  Route: Oral Peak: 30-90 mins
Duration :nk Onset: rapid  HF: 30 to 60 mins,
 HF: 2.5 to 5 hrs, Peak: 4h metabolized in the
excreted  HF: 45 hrs, then 25 to liver and excreted in
unchanged in 30 hrs; metabolized in the urine
urine the liver and excreted in  Headache, insomnia,
 Headache, the urine dizziness, nausea,
vertigo, tremors,  Headache, nausea, diarrhea, fever , rash,
nausea, vomiting vomiting, diarrhea, rash, bone marrow
, rash liver dysfunction, chills, suppression
fever
Protease Inhibitors Prototype Fusion Inhibitor Prototype CCR5 Prototype
 Atazanivir  Fosamprenavir (HF 7.7 hrs)  enfuvirtide  Enfuvirtide Coreceptor

 Darunavir  Management of  Treatment of HIV-1 antagonist

adults with infected patients who  maravir  Maraviroc
 Fosamprenavi
symptomatic HIV have experienced oc  Combination antiretroviral
r
infection in clinical or treatment of adults infected
 Indinavir
combination with immunological with CCR5-tropic HIV-1
 Iopinavir
other antiretrovirals deterioration adter who have evidenced of
 Nelfinavir  Inhibits protease treatment with other viral replication and HIV-1
 Ritonavir activity, leading to agents, in combination strains resistant to multiple
 Saquinavir the formation of with other retrovirals antiretroviral agents
 tipranavir immature, non-  Prevents the entry of  Selectively binds to the
infectious virus the HIV-1 Virus into human chemokine receptor
particles cells by inhibiting the CCR5 on the cell
 Route: Oral fusion of the virus membrane preventing
Onset: varies membrane with the interaction of HIV-1 and
Peak: 1.5-4 min cellular membrane CCR5
 HF: 7.7 hrs;  Route: subcutan.  Route:oral
metabolized in the Onset: slow Onset: slow
liver and exreted Peak: 4-8 hr Peak: 0.5-4h
in the feces and  HF: 3.2 to 4.4 hrs;  HF: 14 to 28 hrs ; metabolized in the
urine metabolized in the liver, excreted in the feces and urine
 Headache, mood liver, tissues recycle  Dizziness, paresthesias, nausea,
changes, nausea, the amino acids, not vomiting, diarrhea, cough, upper
diarrhea, fatigue, excreted respiratory infection (URI) , fever,
rash, steven  Headache, nausea, musculoskeletal symptoms,
Johnson vomiting diarrhea, hepatotoxicity
syndrome, rash, anorexia,
redistribution of pneumonia, chills,
body fat (buffalo injection site
hump, thin arms reactions
and legs)
Integrase Inhibitor Prototype Anti- Hepa B Agents Prototype Anti- Hepa C Agents Prototype
 Dolutegravi  Raltegravir  adefovir  Adefovir  bococeprev  Simeprevir

r  In combination with  entecavir  Treatment of chronic ir  Treatment of chronic

other antiretroviral
 raltegravir
agents for the
treatment of HIV-1
infection in treatment
experienced adult
patients who have
evidence of viral
replication and HIV-1
strains resistant to
multiple antiretroviral
agents
 Inhibits the activity of
the virus-specific
enzyme integrase, an
encoded enzyme
needed for viral
replication. Blocking
this enzyme needed
for viral replication
 Route: oral
Onset: rapid
Peak: 3h
 HF: 9 hours,
metabolized in the
liver , excreted in the
feces and urine
 Headache, nausea,
dizziness, vomiting,
diarrhea, fever,
rhabdomyolysis
hepatitis B in adults
 telbivudine
with evidence of
active viral replication
and either evidence
of persistent
elevations in alanine
aminotransferase and
aspirate
aminotransferase or
histologically active
disease
 Inhibits hepatitis B
virus reverse
transcriptase, causes
DNA chain
termination, and
blocks viral
replication
 Route: Oral
Onset: rapid
Peak: .6-4h hr
Duration: unk
 HF: 7.5 hrs excreted
in the urine
 Headache, nausea,
asthenia, severe to
fatal hepatomegaly
with steatosis,
exacerbation of
hepatitis B when
discontinued
hepatitis C in adults
 simeprevir
with compensated
 sofosbuvir
liver dysfunction in
combination with
peginteferon and
ribavirin
 Inhibits hepatitis C
protease formation
preventing viral
replication
 Route : oral
Onset : Rapid
Peak 4-6 hr
Duration: unkn
 HF: 10-12 hrs;
excreted in the feces
 Fatigue, nausea,
diarrhea, rash
 II. ANTIFUNGAL AGENTS Azole Antifungals Prototype
 Fluconazole  Fluconazole
KEY TERMS Azole Topical Antifungals Prototype
 Itraconazole  Treatment of
 Butoconazole  Clotrimazole
oropharyngeal,
 Ketoconazole  Treatment of
azoles  Clotrimazole
esopharyngeal,
 Posaconazol oropharngeal
 A group of drugs used to treat fungal infections
and vaginal  Econazole
e candidiasis ;
candidiasis,  Ketoconazole
Candida prevention of
 Terbinafine
cryptococcal  Miconazole
oropharyngeal
 Fungus that is normally found on mucous membranes,  voriconazole meningitis,  Oxiconazole
candidiasis in
can cause yeast infections or thrush of the gas systemic fungal  Sertaconazole patients receiving
trointestinal (GI) tract and vagina in immunosupressed infections,
 Sulconazole radiation or
patients prophylaxis to
 Terbinafine chemotherapy
decrease the
 Terconazole  Binds to sterols in
Ergosterol incidence of
 tioconazole the fungal cell
candidiasis in bone
membrane,
 Steroid- type protein found in the cell membrane of fungi marrow transplants
changing
similar in configuration to adrenal hormones and  Binds to sterols in
membrane
testosterone the fungal cell
permeability and
membrane,
allowing leakage
Fungus changing
of intracellular
membrane
 A cellular organism with hard cell wall that contains chitin components,
permeability,
causing cell death
and many polysaccharides, as well as a cell membrane fungicidal or
 Not absorbed
that contains ergosterols fungistatic
systematically
 Route: Oral
 Troche, nausea,
Mycosis Onset: slow
vomiting,
Peak : 1-2 h
 Disease caused by a fungus abnormal liver
Duration: 2-4 D
function tests,
 HF: 30 hrs, metabolized in
Tinea topical: stinging,
the liver and excreted in the
redness, urticaria,
 Fungus called ringworm that causes such infections as urine
edema
athlete’s foot, jock itch, and others  Headache, nausea, vomiting,
diarrhea, abdominal pain,
rash
Echinocandin Antifungals Other antifungals  Protozoal intestinal infection that causes severe diarrhea Trypanosomiasis

and epigastric distress, may lead to serious malnutrition

 Anidulafungin  amphotericin B  African sleeping sickness inflames CNS, also chagas

 Caspofungin  flucystosine Leishmaniasis disease which causes serious cardiomyopathy

 micafungin  griseofulvin
 Skin, mucous membrane or visceral infection caused by ANTIMALARIALS Prototype
 nystatin
a protozoan passed to humans by the bites of sand flies  Chloroquine  Chloroquine
Other topical antifungals
 Mefloquine  Treatment and
Malaria prophylaxis of
 butenafine  naftifine  Primaquine
acute attacks of
 ciclopirox  tolnaftate  Protozoal infection with plasmodium, characterized by  Pyrimethamine
malaria caused by
 gentian violet  undecyclenic acid cyclic fever and chills as the parasite is released from  quinine
susceptible strains
ruptured red blood cells of Plasmodium;
treatment of
Plasmodium extraintestinal
III. ANTIPROTOZOAL AGENTS
amebiasis
 A protozoan that causes malaria in human, its life cycle
KEY TERMS  Inhibits protozoal
includes anopheles mosquito, which injects protozoa into
reproduction and
humans protein synthesis
amebiasis
 Route: oral
 Aamebic dysentery, which is caused by intestinal invasion of the
Pneumocystis jiroveci pneumonia
Onset: varies
trophozoite stage of the protozoan entameoba histolytica
Peak: 1-2 hr
 Opportunistic infection that occurs when the immune
Anopheles mosquito Duration 1wk
system is depressed ; frequent in AIDS patients
 HF: 70 to 120
 Type of mosquito that is essential to the life cycle of hrs, metabolized
Protozoa
plasmodium, injects the protozoa into humans for further in the liver and

maturation  Single0celled organism that pass through several stages excreted in the
urine
in their cycle
Cinchonism  Visual
Trichomoniasis disturbances,
 Syndrome of quinine toxicity characterized by nausea, retinal changes,
vomiting, tinnitus, and vertigo  Infestation with a protozoan that causes vaginitis in hypotension,
women but no signs or symptoms in men nausea, vomiting,
Giardiasis
 diarrhea
 Other Prototype IV. ANTIHELMINTIC AGENTS  Flatworms, including cestodes or tapeworms , worm that

ANTIPROTOZOALS can invade human intestine or other human tissues

KEY TERMS
 Atovaquone  Metronidazole (fluke)

 Metronidazole  Acute intestinal

Ascaris Schistosomiasis
amebiasis,
 Nitazoxanide
amebic liver
 Pentamidine  The most prevalent helminthic infection, fertilized round  Infection with a blood fluke that is carried by a snail
abscess,
 tinidazole worms are ingested
trichominasis,
Threadworms
acute infection
Cestode
caused by  Pervasive nematode that can send larvae into lungs,
susceptible  Tapeworm with a head ang segmented body parts liver, and cns
strains of
 Found in the soil
anaerobic Filariasis
bacteria Trichinosis
 Inhibits DNA  Infection of the blood and tissues of healthy individuals

synthesis of by worm embryos  Disease that result from ingestion of encysted

specific roundworm larvae in undercooked pork
Helminth
anaerobes,
 Trichinella spiralis
causing cell
 Worm that can cause disease by invading the human
death, Whipworm
body
mechanism of
action as an  Worm that attaches itself to intestinal mucosa and sucks
Nematode
antiprotozoal and blood
embicidal is not  Roundworms such as pinworm, whipworm, ascaris,
known ANTHELMINTICS Prototype
threadworms
 Route: oral Mebendazole
 Albendazole 
Onset: varies Pinworm  Treatment of
 Ivermectin
Peak 1-2 hr whipworm, pinworm,
 Mebendazoe
 Headache, dizziness,  Nematode that causes a common helminthic infection in
roundworm, and
 Praziquantel
ataxia, nausea, vomiting, humans; lives in the intestine and causes anal and hookworm infections
metallic taste, diarrhea  pyrantel
vaginal itching  Irreversibly blocks
glucose uptake by
Platyhelminth susceptible
 helminths, depleting  The generation of new blood vessels, cancer cells  Tumor that originates in the mesenchyme and is made
glycogen stores release an enzyme tgat will cause angiogenesis or the up of embryonic connective tissue cells
needed for survival growth of new blood vessels to feed the cancer cells
and reproduction, 2 types of cancer
causing death of Antineoplastic agent
1. Solid tumors
heminth
 Route: oral  Drug used to combat cancer or the growth of neoplasms 2. Haematological malignancies

Onset: slow
Autonomy ALKYLATING AGENTS Prototype
Peak 2-4 hr
 Altretamine  Chlorambucil
 HF: 2.5 to 9 hrs,
 Loss of the normal controls and reactions that ionhibit  Palliative
metabolized in the  Bendamustine
growth and spreading ; property of cancer cells treatment of
liver and excreted in  Busulfan
chronic
the urine  Carboplatin
Bone marrow suppression
lymphocytic
 Transcient  Carmustine
leukemia,
abdominal pain,  Inhibition of the blood forming components of the bone  Chlorambucil
malignant
diarrhea, fever
marrow  Cisplatin lymphomas, and
 Cyclophospha Hodgkin disease
Carcinoma
V. ANTINEOPLASTIC AGENTS mide  Alkylates cellular

 Tumor that originates in epithelial cells  Dacarbazine DNA interfering

KEY TERMS  Ifosfamide with the
Metastasis replication of
 Lomustine
Alopecia susceptible cells
 Mechlorethami
 Ability to enter the cicrculatory or lymphatic system and  Route Oral
ne
 Hair loss, a common adverse effects of antineoplastic travel to other areas of the body that are conducive for Onset: varies
 Melphalan
drugs growth and survival Peak: 1 h
 Oxaliplatin Duration: 15-20 h
Anaplasia Neoplasm  Procarbazine  HF: 60 to 90
 Streptozocin mins, metabolized
 Loss of organization and structure, property of cancer  New or cancerous growth ; occurs when abnormal cells
 temozolomide in the liver and
cells have the opportunity to multiply and grow excreted in the
urine
Angiogenesis Sarcoma
 Tremors, muscle
twitching,
 confusion, MITOTIC INHIBITORS Prototype
nausea,  Cabazitaxel  vincristine
hepatotoxicity, ANTINEOPLASTIC Prototype  acute leukemia,
 Docetaxel
bone marrox ANTIBIOTICS Hodgkin disease,
 Etoposide
suppression,  Bleomycin  Doxorubicin non Hodgkin
 Ixabepilone
sterility, cancer  Dactinomycin  To produce disease,
regression in  Paclitaxel
 Daunorubicin lymphoma
acute  Teniposide
 Doxorubicin  arrests mitotic
ANTIMETABOLITES Prototype lymphoblastic  Vinblastine division at the
 Epirubicin
 Capecitabine  Methotrexate lymphoma, acute  Vincristine stage of
 Idarubicin
 Cladribine  Treatment of myeoblastic  vinorelbine metaphase
gestational
 Mitomycin leukemia, wilms
 Clofarabine  Route: IV
choriocarcinoma;  Mitoxantrone tumor, Hodgkin
 Cytarabine Onset: varies
chorioadenoma,  Valrubicin and non Hodgkin Peak: 15-30 min
 Floxuridine
destruens, lymphomas  HF: 5 mins, 2.3
 Fludarabine Binds to DNA and
juvenile  hrs, 85 hrs,
 Fluorouracil rheumatoid inhibits DNA metabolized in
 Gemcitabine arthritis synthesis in a the liver
 Mercaptopurine  Inhibita folic acid susceptible cell,  Ataxia, cranial
 Methotrexate reductase, causing cell death nerve
 Pemetrexed leading to  Route: IV manifestations,
inhibition of DNA Onset rapid neuritic pain,
 Pentostatin
synthesis and Peak: 2 hr muscle wasting
 Pralatrexate
inhibition of Duration: 24-36hr
 thioguanine
cellular replication  HF: 12 mins, then
 Route: oral 3.3 hrs then 29.6 HORMONE AND Prototype
Onset: varies hrs, metabolized HORMONE
Peak: 1-4 hr in the liver MODULATORS
 HF: 2 to 4 hrs, excreted in urine  Abiraterone  Tamoxifen
excreted  Cardiac toxicity,  Treatment of
 Anasterazole
unchanged in complete but metastatic breast
 Bicalutamide
urine reversible alopeci cancer, reduction
 Degarelix
 Fatigue, malaise, of risk of invasive
 Enzalutamide
rashes, alopecia, breast cancer
 Estramustine  Competes with  Lapatinib the Bcr- Abl MISCELLANEOUS Prototype

 Exemestane estrogen for  Nilotinib tyrosine kinase ANTINEOPLASTICS

binding sites in  Palbociclib created by  Arsenic trioxide  Pegaspargase
 Flutamide
target tissues  Pazopanib Philadelphia  Asparaginase  Porfimer
 Fulvestrant
such as the  Regorafenib chromosome  Romidepsin
 Goserelin erwina
breast, a potent  Ruxolitinib abnormality in  Sipuleucel-T
 Histrelin chrysanthemi
antiestrogenic  Sorafenib CML and certain  Talc powder
 Letrozole  Belinostat
agent  Sunitinib tumor cells  Topotecan
 Leuprolide  Bexarotene
 Route: oral  Temsirolimus present in GIST  Tretinoin
 Megestrol Onset: varies  Trametinib  Route: oral  Decitabine  Vismodegib
 Mitotane Peak 4-7 hrs  Vemurafenib Onset: slow  Hydroxyurea  vorinostat

 Nilutamide  7 to 14 days,  Ziv-aflibercept Peak: 2-4 hr  Irinotecan

metabolized in the  HF: 18 to 40 hrs,  Naelarbine
 Tamoxifen
liver and excreted EPIDERMAL GROWTH metabolized in the
 Toremifene
in the feces FACTOR INHIBITOR liver excreted in
 triptorelin
 HF: 7 to 14 days  Erlotinib the urine
metabolized in the  Nausea, vomiting,
liver PROTEASE INHIBITOR bone marrow
 Hot flashes, rash,  bortezomib supression heart
nausea, vomiting, failure, headache,
gainal bleeding dizziness, edema,
rash,

CANCER CELL- Prototype

SPECIFIC AGENTS
 Afatinib  Methotrexate
 Axitinib  Treatment of
 Bosutinib adults with CML
 Ceretinib who are in blast
 Crizotinib crisis, chronic
 Dabrafenib phase
 Ibrutinib  Tyrosine kinase
 Idelalisib inhibitor that
 Imatinib selectively inhibits