Pharm II Block 1


  1. Chemotherapy Drugs
  2. Immunosuppressants and Immunomodulators
  3. Diuretics

Disclaimer: These notes do not cover diuretics, antianginal, antihypertensive, CHF, antiarrythmics, general anesthetics, NSAIDs, gout, rheumatoid arthritis, opioid drugs for block 1.



Q: Where on the DNA do alkylating agents alkylate DNA?
A: N7 of Guanine. KNOW THIS!!!!

Q: What are the adverse effects of alkylating agents?
A: Myelosuppression, secondary malignancies, anovulation (can be permanent if you’re over 30 yrs old)

Q: What secondary malignancies do chemotherapy agents cause?

Q: Why are alkylating agents called “radiomimetic”?
A: Because they are cell cycle non-specific, just like radiation therapy kills cells no matter what cell stage they are in.

Q: What are the three classes of Alkylating agents?
A: Nitrogen Mustard, Nitrosoureas, and “Others

Q: Chlorambucil, Melphalan, Cyclophosphamide, and Ifosfamide belong to what class of chemotherapy drugs?
A: Nitrogen mustards (“MCMCI”)

Q: Nitrogen Mustards is the M in MOPP. What is the MOPP regimen used to treat?
A: Hodgkin Lymphoma

Q: What’s the adverse effect of MOPP?
A: Sterility in males

Q: Which chemotherapy drug class have vesicant properties?
A: Nitrogen Mustard

Q: Nitrogen Mustards are bifunctional whereas Nitrosoureas are monofunctional. What does it mean to be bifunctional?
A: It means they are cross-linkers.

Q: Which Nitrogen Mustard drug is used to treat slow malignancies like low-grade lymphomas and CLL?
A: Chlorambucil

Q: Which Nitrogen Mustard drug is used to treat multiple myeloma?
A: Melphalan (“MMM”)

Q: What does Cyclophosphamide treat?
A: Breast Cancer (breast look like cycles)

Q: What does Ifosfamide treat?
A: Testicular Cancer (Ivan has testicles)

Q: Which chemotherapy drugs get metabolized into acrolein, which causes hemorrhagic cystitis?
A: Cyclophosphamide and Ifosfamide

Q: How do you block acrolein?
A: use MESNA, which has a free thiol that inactivates acrolein. KNOW THIS!!!

Q: What alkylating agent can be used to treat brain tumor and melanoma because it is fat soluble?
A: Nitrosoureas (i.e. Streptozocin)

Q: What drug can treat Islet Cell Tumors in pancreas?
A: Streptozocin. Benji thinks “streptozocin” sounds like “Zanzibar” (an island off of Tanzania), while Gundi thinks it sounds like “Stromboli” (an island off of Italy). It probably sounds like neither, but just try to find an island that you know of that sounds like “streptozocin” to remember that it is used for Islet Cell Tumors.)

Q: Which alkylating agent has antabuse effect (like disulfiram) so you need to be careful when taking it with alcohol?
A: Procarbazine

Q: What can Procarbazine treat?
A: Hodgkin Lymphoma. It’s one of the P’s in MOPP regimen for Hodgkin Lymphoma treatment.

Q: What alkylating agent can treat both Hodgkin Lymphoma and Melanoma?
A: Dacarbazine — which is the D in ABVD regimen treatment for Hodgkin Lymphoma. ABVD is now preferred over MOPP for the treatment for Hodgkin Lymphoma.

Q: What alkylating agent was used to treat CML before Gleevac was developed, but caused interstitial fibrosis and therefore not used anymore?
A: Busulfan

Q: Which drugs are used to treat melanoma?
A: Nitrosoureas and Dacarbazine.


Q: What are the four subtypes of antimetabolite chemotherapeutic drugs?
A: Anti-folates, Pyrimidine analogues, Purine analogues, and Hydroxyurea

Q: What phase of the cell cycle do Antimetabolite drugs work?
A: S-phase, when the cell is synthesizing DNA.

Q: If you are pregnant and have cancer, when should you NOT use antimetabolites?
A: Don’t use during 2nd and 3rd trimesters of pregnancy.

Q: Which class of chemo drugs can cause mucositis?
A: Antimetabolites

Q: Which Anti-folate chemotherapy drug treats Choriocarcinoma?
A: Methotrexate. In fact, it was the first treatment ever for a solid tumor!

Q: Which chemo drug does not cross BBB and therefore must be injected intrathecally if you want to use it in the brain?
A: Methotrexate

Q: Which chemo drug collects in the “third spacing” like pleural effusions and ascitic fluid, and causing a slow release of the drug into the body?
A: Methotrexate

Q: Which anti-folate chemotherapy drug is used to treat mesothelioma?
A: Pemetrexed (peMEtrexed for MEsothelioma)

Q: Which anti-folate chemotherapy drug is used to treat colorectal and breast cancer?
A: Raltitrexed (R for “rectal and bReast”)

Q: What chemotherapy drug competitively inhibits Dihydrofolate reductase (DHFR) from converting inactive oxidized folate (dihydrofolate) into active reduced folate (tetrahydrofolate)?
A: Methotrexate

Q: Normally what is tetrahydrofolate used for?
A: It’s needed for thymidylate synthetase.

Q: What is thymidylate synthetase normally used for?
A: Converting dUMP –> dTMP, or UMP –> TMP, which can then be incorporated into the newly synthesized DNA

Q: If you have methotrexate overdose, what do you do?
A: Treat with Leucovorin (folinic acid), which is basically reduced folate that can go ahead and stimulate thymidylate synthetase to continue to function normally. Remember the DHFR that normally makes reduced folate is not available because it is inhibited by the methotrexate. It “rescues” normal cells with normal growth fractions that require less folate than cancer cells.

Q: Which pyrimidine analog is basically a “fake uracil,” replacing normal uracil from making normal thymine during DNA synthesis?
A: 5-FU

Q: What scaffold is needed for 5-FU to convert to 5FdUMP or 5FUMP?

Q: What inhibits PRPP, adn therefore inhibits 5-FU conversion to 5-FdUMP/5FUMP and therefore decreases the effect of 5-FU during chemotherapy?
A: Allopurinol… so gout patients watch out!

Q: What does allopurinol do to 6-Mercaptopurine (a purine analogue chemo drug) levels?
A: Allopurinol blocks XO, which blocks 6-MP. Therefore Allopurinol increases 6-MP.

Q: So in conclusion, what does allopurinol do to 5-FU and 6-MP levels?
A: Allopurinol decreases 5-FU activity but increases 6-MP activity

Q: Flucytocine is normally used as an antifungal but why can it be used in chemotherapy?
A: Because it is converted to 5-FdUMP

Q: What is 5-FU mainly used to treat?
A: Colorectal cancer

Q: What chemo agent is a 5-FU prodrug?
A: Capecitabine

Q: What is the adverse effect of capecitabine?
A: Hand-Foot Syndrome

Q: What chemo drug is a cytidine analogue that treats AML but causes cerebellar dysfunction?
A: ARA-C, aka Cytosine Arabinoside, Cytarabine

Q: What is the mechanism of resistance for ARA-C?
A: cells increase cytidine deaminase or decrease deoxycytidine kinase.

Q: What chemo drug is a cytosine analogue used as a key drug in the treatment of pancreatic cancer?
A: Gemcitabine

Q: What are the three mechanisms of action of purine analogue chemo drugs?
A: 1. incorporated wrongly into DNA
2. decrease HGPRT, which normally recycles purines
3. blocks the first committed step in DNA synthesis (Glutamine + PRPP –> R5P)

Q: Which chemo drugs are guanine analogues?
A: 6-Mercaptopurine, 6-Thioguanine

Q: What are the guanine analogues used to treat?
A: mainly leukemia.

Q: Which chemo drug is an adenosine analogue?
A: Fludarabine

Q: What is Fludarabine used to treat?
A: Low Grade Lymphoma (“F is a Low Grade”)

Q: What chemo drug inhibits ribonucleotide reductase (RNR), which converts RNA to DNA?
A: Hydroxyurea, a urea analogue.

Q: What three chemo drugs treat (either now or in the past) CML?
A: Imatinib mainly, but also Hydroxyurea, and Busulfan, which is not used anymore because it caused interstitial fibrosis.


Q: What type of fungus are the fungal antiobiotic-derived chemo drugs from?
A: Streptomyces

Q: Naturally occurring chemo drugs can come from either plant or fungal antibiotics. The often get multidrug resistance (MDR). What is MDR mediated by?
A: P-Glycoprotein (efflux pump). KNOW THIS!!!

Q: What are the five fungal antibiotic chemo drugs we covered?
A: Anthracyclines, Anthracenediones, Dactinomycin, Mitomycin, Bleomycin

Q: Which fungal antibiotic chemo drug intercalates DNA and inhibits topoisomerase-2?
A: Anthracyclines

Q: What fungal antibiotic chemo drug generates oxygen free radicals, which causes heart toxicity (because heart has no SOD)?
A: Anthracyclines

Q: What are the adverse effects of anthracyclines?
A: Heart Toxicity (most distinctive), Alopecia after 3 weeks, Myelosuppression, secondary malignancy

Q: What do you use in conjunction with anthracyclines to prevent heart toxicity?
A: Dexrazoxane, which is an iron chelating agent that helps prevent formation of free radicals.

Q: What other drug causes heart toxicity and should not be given together with anthracyclines?
A: Trastuzumab

Q: What suffix do all the anthracyclines end with?
A: -rubicin — like Doxorubicin, Daunorubicin, Idarubicin, and Epirubicin.

Q: What is Doxorubicin used to treat?
A: Non-Hodgkin Lymphoma. Doxorubicin is the H in CHOP regimen, used for Non-Hodgkin Lymphoma. Yes, I know — the H in chop is Hydroxydoxorubicin.

Q: What is Daunorubicin used to treat?
A: AML, like ARA-C! (“Dawn is during AM”)

Q: What is Idarubicin used to treat?
A: Hematologic Malignancies

Q: What color are anthracyclines?
A: Red. Hence “rubicin” in its name. This isn’t that important, but it’s fun fact.

Q: What drug is an anthracenedione?
A: Mitoxantrone

Q: Who do you use anthracenedione/mitoxantrone with?
A: Frail patients, because it is just like anthracyclines except it is less active and less toxic… and it’s blue instead of red 🙂

Q: What is Dactinomycin (or Actinomycin D) used to treat?
A: Pediatric tumors, like Wilms Tumor. It’s gold color.

Q: What drug prefers hypoxic conditions and therefore used to treat big tumors with low growth fractions like bladder and anal cancers?
A: Mitomycin.

Q: What is the adverse effects of mitomycin?
A: TTP (thrombotic thrombocytopenic purpura), which causes CNS disturbance, kidney dysfunction, and small vessel angiopathy. (Mitomycin is purple and causes purpura, and treats big tumors — “my big toe is purple”)

Q: What is the only chemo drug that is cell cycle specific to the G2 phase?
A: Bleomycin. (“Lance Armstrong drinks Gatorade G2”)

Q: What is the MOA for bleomycin?
A: intercalates DNA, like most of the other fungal antibiotics (except mitomycin, which is an alkylator)

Q: Why didn’t Lance Armstrong want to take bleomycin for his testicular cancer?
A: Because it causes lung toxicity (because it produces free radicals), which would be detrimental to his career.

Q: Besides testicular cancer what else does bleomycin treat?
A: Hodgkin Lymphoma. Bleomycin is the B in the ABVD regimen

Q: What plant-derived chemo drug prevents spindle formation by causing depolymerization of the microtubules?
A: Vinca alkaloids (Vincristine, Vinblastine, Vindesine, Vinorelbine)

Q: What plant-derived chemo drug prevents spindle dissociation by causing tubulin polymerization?
A: Taxanes (Paclitaxel, Docetaxel)

Q: What phase of the cell cycle do vinca alkaloids and taxanes work?
A: M-phase, because it involves microtubules needed for mitosis.

Q: What are Vinca Alkaloids used for?
A: Hodgkin Lymphoma (V in ABVD, and O in MOPP) AND Non-Hodgkin Lymphoma (O in CHOP). V obviously stands for vincristine. O stands for oncovorin, the trade name of vincristine.

Q: What is the most important adverse effect of most vinca alkaloids?
A: peripheral neuropathy, because it effects your microtubules in neurons. sensory neuropathy is usually reversible whereas motor neuropathy is not. You see this less in vinblastine.

Q: What does Paclitaxel treat?
A: Ovarian cancer

Q: What is the unique adverse effects of taxanes?
A: Skin and nail toxicity. Obviously you also get neural problems because your microtubules are effected.

Q: What plant-derived chemo drug inhibits topoisomerase-2?
A: Podophyllotoxins (i.e. Etoposide), like anthracyclines (fungal antibiotic chemo drug)

Q: What is podophyllotoxins used to treat?
A: Testicular cancer (like ifosphamide, bleomycin), small cell lung carcinoma, and Non-Hodgkin Lymphoma (the P in CHOP regimen). Think about a pea pod for podophyllotoxin, and inside the pod there are two peas, like testicles.

Q: What three drugs we covered treat testicular cancer?
A: PIB — Podophyllotoxin, Ifosfamide, Bleomycin. “Mr. PIB”

Q: What plant-derived chemo drug inhibits topoisomerase I?
A: Camptothecins (Irinotecan, Topotecan)

Q: What is Irinotecan used to treat?
A: Colon Cancer

Q: What is the adverse effect of irinotecan?
A: excessive diarrhea (and therefore treat with antimotility agent), acute cholinergic effects (and therefore treat with atropine). “I ran to the can” to release my excessive diarrhea.

Q: What does Topotecan treat?
A: Small Cell Lung Carcinoma and Ovarian cancer.

Q: What all treats small cell lung carcinoma?
A: Topotecan and Podophyllotoxins (“Topo & Podo”)


Q: What is the MOA for platinum-derived chemo drugs (cisplatinum, carboplatinum, oxaliplatinum)?
A: They alkylate DNA

Q: What are the adverse effects of platinum-derived chemo drugs?
A: NEUROTOXICITY (leading to hearing loss), since heavy metals are hard for the body to get rid of.

Q: How do you prevent neurotoxicity in platinum-derived chemo drugs?
A: Infuse patient with Calcium and Magnesium

Q: Besides Neurotoxicity, what other adverse effect does cisplatinum have?
A: Nephrotoxicity

Q: What do you use to treat nephrotoxicity in cisplatinum?
A: Amifostine, which scavenges reactive cisplatin metabolites in the tissue.

Q: Besides Neurotoxicity, what other adverse effect does carboplatinum have?
A: myelosuppression. It has less nephrotoxicity than cisplatinum.

Q: Besides Neurotoxicity, what other adverse effect does oxaliplatinum have?
A: Cold intolerance

Q: What is cisplatinum used for?
A: Germ Cell Tumor

Q: What is Carboplatinum used for?
A: Breast, Ovarian, Lung.

Q: What is Oxaliplatinum used for?
A: Colon Cancer!!!! unique among platinum-derived chemo drugs.

Q: What chemo drug destroys asparagine available for tumor protein synthesis (especially since tumors already have low asparagine synthetase)?
A: L-Asparaginase.

Q: What does L-Asparaginase treat?
A: Pediatric ALL.

Q: What are all the drugs that treat colon cancer?
A: Raltitrexed, Oxaliplatinum, Bevacizumab, Panitunumab, Irinotecan, Cetuximab, 5-FU. “ROB PIC 5”


Q: What is the adverse effect of Tamoxifen?
A: Thrombus, endometrial cancer

Q: What is the adverse effect androgen receptor blockers (flutamide, bicalutamide)?
A: andropause, impotence

Q: Where is the primary and secondary (like during post-menopause) estrogen source?
A: Primary — Ovary, Placenta, Corpus Luteum
Secondary — Adrenal, Liver, Breast

Q: What cancers are prednisone used to treat?
A: both Hodgkin Lymphoma (P in MOPP) and Non-Hodgkin Lymphoma (P in CHOP)

Q: What is the adverse effect of prednisone?
A: Fluid retention, glucose intolerance, PROXIMAL MYOPATHY (because break down muscle to increase glucose in blood), increased appetite.

Q: What stage in cell cycle do anti-hormonal drugs work?
A: G1


Q: What chemo drugs inhibit the tyrosine kinase on her2/neu EGFR?
A: Lapatinib

Q: What chemo drugs inhibit the tyrosine kinase on non-her2/neu EGFR?
A: Gefitinib, Erlotinib

Q: What are the adverse effects of the EGFR Antagonists?
A: Acneiform Rash

Q: What is Lapatinib used to treat?
A: Breast Cancer

Q: What is Gefitinib and Erlotinib used to treat?
A: Non small cell lung carcinoma. Erlotinib also treats pancreatic cancer.

Q: What two drugs inhibit the tyrosine kinase receptors on VEGF?
A: Sunitinib and Sorafanib

Q: What do the VEGF inhibitors treat?
A: Sunitinib treats GI Stromal Tumors (GIST) and kidneys. Sorafanib treats kidney, liver.

Q: Which drugs inhibit the tyrosine kinase receptors of bcr-able proteins in CML and GIST?
A: Imatinib and Nilotinib

Q: What are the adverse effects of imatinib and nilotinib?
A: diarrhea, MYALGIA, fluid retention

Q: So in summary, what drugs act during these cell cycle stages?
A: M: Vinca, Taxanes
G1: Steroids
S: Antimetabolites
G2: Bleomycin
G0: none


Q: What monoclonal antibodies target EGFR?
A: Trastuzumab, Cetuximab, Panitunumab

Q: What are the adverse effects of EGFR-targetting monoclonal antibodies?
A: Cardiotoxicity, ACNEIFORM RASH

Q: What does trastuzumab treat?
A: her2/neu-overexpressed breast cancer. Trastuzumab is commonly known as herceptin

Q: What does cetuximab treat?
A: squamous cell HEAD AND NECK cancers and k-ras colon cancers

Q: What does Panitunumab treat?
A: k-ras colon cancer

Q: What monoclonal antibodies target VEGF?
A: Bevacizumab

Q: What does Bevacizumab treat?
A: Colon Cancer

Q: What is the adverse effect of bevacizumab?
A: decreased wound healing

Q: What monoclonal antibody target CD20 B lymphocyte receptors and therefore good at treating B Cell Lymphomas?
A: Rituxumab

Q: What monoclonal antibody target CD52 B lymphocyte receptors and therefore good at treating B Cell Lymphomas?
A: Alemtuzumab


Q: What chemo drugs are M-TOR Inhibitors and what do they treat?
A: Temsirolimus and Everolimus. They treat Renal Cell Cancer!!!

Q: How do M-TOR Inhibitors work?
A: They bind to MTOR and prevent IL-2 signal translocation. T-lymphocytes do not proliferate.

Q: What chemo drug is a proteosome inhibitor and treats multiple myeloma and mantle cell lymphoma?
A: Bortezomib

Q: What is it called when you resect as much of the cancer as you can first, then blast the rest with chemotherapy?
A: Adjuvant Chemotherapy (i.e. Breast cancer)

Q: What is it called when you give a high dose of chemo to quickly and forcefully attack the cancer?
A: Induction Chemotherapy (i.e. ALL)

Q: What is it called when you just inducted chemo and need to maintain the response?
A: Consolidation Chemotherapy if at high dose. Maintenance Chemotherapy if at low dose. (i.e. Acute Leukemia)

Q: What is it called when you shrink the tumor with enough (like with radiotherapy) so that you can resect it?
A: Neoadjuvant Therapy (i.e. Breast, Rectal cancer)

Q: What is it called when the primary goal of the chemo is not to extend life but to simply improve life?
A: Palliative Chemotherapy

Q: What 3 things do you need to put in CSF Support?
A: Granulocyte Colony Stimulation Factor to decrease infection (but adverse effect is bone pain), Erythropoietin (to increase RBC to decrease need for transfusion), Megakaryocyte Growth Factor

Q: What cancers are resistant to chemo?
A: Pancreatic cancer, Gliomas

Q: What cancers have acquired resistance?
A: Lymphomas, Melanomas

Q: When is the nadir blood count?
A: 7-14 days post-chemotherapy


Q: What two general conditions do immunosuppressants treat?
A: Transplant rejection and Autoimmune Disease. For transplant rejections, it can be used as prophylactic, maintenance, and chronic therapy.

Q: What are the general adverse effects of immunosuppressants?
A: Infections, secondary cancer

Q: What are 5 classes of immusuppressants?
A: Calcineurin inhibitors, mTOR inhibitors, Antimetabolites, Antibodies, and Glucocorticoids.


Q: Which calcineurin inhibitor acts by binding cyclophilin, which blocks calcineurin, which prevents it from phosphorylating NF-AT, which then blocks IL-2 transcription, leading to suppression of immunity?
A: Cyclosporine

Q: What is the difference between the mechanism of action of Cyclosporine and Tacrolimus?
A: Although they are both calcineurin inhibitors, Cyclosporine binds cyclophilin, which blocks calcineurin, whereas Tacrolimus binds FKBP-12, which then blocks calcineurin.

Q: Why shouldn’t you take cyclosporine and tacrolimus together?
A: Because it can lead to nephrotoxicity!

Q: What is Cyclosporine used to treat?
A: Rheumatoid arthritis, psoriasis, dry eye syndrome, rejection of kidney/liver/heart.

Q: What happens when you use cyclosporine and drink grapefruit juice?
A: grapefruit juice prevent the metabolism of cyclosporine by P450. Therefore it will cause your cyclosporine concentration to increase, causing you to have more infections.

Q: Besides nephrotoxicity, what is another high-yield adverse effect of cyclosporine?
A: Gum hyperplasia! (see in cyclosporine, phenytoin, and nifedipine).

Q: Why is tacrolimus often more preferred over cyclosporine?
A: Because it is less toxic. It is also 10-100x more potent than cyclosporine, so you don’t need as much.

Q: What is tacrolimus used to treat?
A: Graft vs Host disease (along with methotrexate, mycophenolate). Remember GVHD is when donor attacks host (rather than host attacking donor like in regular rejection). You can also use it to treat atopic dermatitis and psoriasis.


Q: What does the “mTOR” stand for in “mTOR inhibitor”?
A: Mammalian Target of Rapamycin. Sirolimus (aka Rapamycin) inhibits mTOR.

Q: What is the MOA of Sirolimus?
A: Binds FKBP-12 –> blocks mTOR –> blocks IL-2 signal needed for T cells to proceed from G1 stage to S (synthesis) stage to proliferate. In contrast, the calcineurin inhibitors prevent T cells from being transcribed in the first place. Sirolimus also prevents B cells from maturing into plasma cells.

Q: What is Sirolimus mainly used for?
A: To coat stents. SRL-coated stents prevent the re-stenosis of blood vessels by decreasing the proliferation of endothelial cells (prevent G1 –> S phase of cell cycle).

Q: Sirolimus is also nephrotoxic, like calcineurins, but how does it compare?
A: It is less nephrotoxic than calcineurins.


Q: What is the MOA of Methotrexate?
A: It competes with dihydrofolate (oxidized folate) to inhibits dihydrofolate reductase (DHFR), which normally converts the inactive dihydrofolate to active tetrahydrofolate, needed to make purine and pyrimidines of DNA. Since you can’t make DNA anymore, your cells stop proliferating (cytotoxic).

Q: Besides autoimmune diseases, transplant rejections, and cancer, what else is methotrexate used to treat?
A: It is the first choice DMARD used to treat Rheumatoid Arthritis, but with completely different reasons than that for cancer. While inhibition of DHFR does happen, the main MOA for the treatment of RA is the inhibition of purine metabolism, leading to accumulation of adenosine, which is anti-inflammatory.

Q: What is the MOA of Azathioprine?
A: It is the prodrug of 6-Mercaptopurine (6-MP, a guanine analogue, “fake guanine”).

Q: Why should you not take allopurinol with azathioprine?
A: Because Azathioprine is a prodrug version of a purine, it is metabolized by XO. Rememebr Allopurinol inhibits XO, and therefore would increase the concentration of azathioprine in your body, leading to too much suppression.

Q: What is considered the newest, safest, and best antimetabolite immunosuppressant?
A: Mycophenolate Mofetil — there is less myelosuppression and less opportunistic infections.

Q: What is Mycophenolate mofetil used to treat?
A: Lupus nephritis, psoriasis, kidney/liver transplants.

Q: What is the MOA of Mycophenolate mofetil?
A: It inhibits inosine monophosphate dehydrogenase (IMPDH), which is used to synthesize guanosine in B and T cells.

Q: Which antimetabolite immunosuppressant inhibits Dihydroorotate Dehydrogenase, leading to the inhibition of pyrimidine synthesis?
A: Leflunomide

Q: What is Leflunomide used to treat?
A: Rheumatoid Arthritis

Q: What is cyclophosphamide used to treat when used in small dose? large dose?
A: Small dose used to treat SLE. Large dose used to treat transplant rejection.

Q: Remember what is the AE of cyclophosphamide?
A: It has acrolein, which causes hemorrhagic cystitis (bloody pee). Therefore use MESNA in conjunction when using cyclophosphamide and iphosphamide to reduce this adverse effect.


Q: Which polyclonal antibody immunosuppressant is used to treat aplastic anemia if patient can’t get a bone marrow transplant?
A: Antithymocyte Globulin (ATG)

Q: What is the adverse effect of ATG?
A: Cytokine Release Syndrome, leading to fever. Because ATG is made from animal serum, your body reacts to it by releasing a whole bunch of IL-2 and TNFa. If this happens, use Basilixumab and Daclizumab (both monoclonal antibody immunosuppressants) instead.

Q: How does Rh(D) Immunoglobin help prevent hemolytic disease of the newborn?
A: You give the Rh IgG to an Rh(-) mother within 72 hours of exposure to her first Rh(+) baby. The Rh IgG binds the Rh antigen from the baby’s blood, prevening the mother from developing anti-Rh-antigen antibodies against her future Rh(+) children.

Q: What is the MOA of Muromonab-CD3 (OKT3)?
A: It binds CD3 receptors on human T cells.

Q: How does Daclizumab and Basiliximab work?
A: They both inhibit CD25 on regulatory T cells (specifically the IL-2 receptor alpha chain).

Q: How does Daclizumab and Basiliximab differ?
A: DacliZUmab is humanized. BasiliXImab is chimeric.

Q: How does the naming system of monoclonal antibodies reflect the intensity of immune reaction?
A: omab = murine (except muromonab) which means it’s from a mouse, most immune reaction AE.
ximab = chimeric
zumab = humanized
umab = human (least immune reaction AE)

Q: Which monoclonal antibody is an anti-VEGF antibody used to treat colon cancer?
A: Bevacizumab. High yield!!

Q: Which monoclonal antibody is an anti-TNFa receptor antibody and is used to treat RA, Crohn’s Disease?
A: Infliximab. High yield!!

Q: Which monoclonal antibody is an anti-IgE antibody and is a last resort for severe asthma?
A: Omalizumab

Q: Which monoclonal antibody is an anti-Her-2-receptor antibody and is used to treat Her-2 breast cancer?
A: Trastuzumab aka Herceptin. High yield!!!

Q: Which monoclonal antibody is an anti-RSV fusion protein antibody used to prevent RSV infection?
A: Palivizumab

Q: Which monoclonal antibody is an anti-CD20 (on B cell) antibody used to treat Non-Hodgkin Lymphoma (B cell lymphoma)?
A: Rituximab. High yield!!!


Q: What are immunomodulating agents?
A: They are the opposite of immunosuppressants. They amplify your immune system so it can fight certain cancers and diseases.

Q: Which immunomodulating agent is a recombinant IL-2, and therefore increases cytotoxic T lymphocytes and NK cells to treat renal cell carcinoma and malignant melanoma?
A: Aldesleukin. It’s great at treating renal cell carcinoma because it is excreted in the kidneys.

Q: Besides being used as a vaccine against TB, what else can you use Bacille Calmette-Guerin (BCG) for?
A: It is an immunomodulator. You can inject it into bladder, stimulating the immune system there, preventing bladder cancer.

Q: Which interferon is used to treat MS?
A: INF-beta

Q: Which interferon is used to treat CML, malignant melanoma, and hepatitis B and C?
A: INF-alpha



Leave a Reply

Your email address will not be published. Required fields are marked *