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Class: Immuno Block > Anti-Viral (NON-HIV) Drugs > Flashcards

Anti-Viral (NON-HIV) Drugs Flashcards

(55 cards)

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1
Q

DRUG CLASS 1: anti-DNA viruses

What is the mechanism of the drug treatments for HSV and CMV?

A

Nucleoside analogs that competitively bind VIRAL DNA POLYMERASE -> Most are chain terminators and inhibit viral DNA replication

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2
Q

Which two anti-HSV and anti-CMV drugs are so toxic that they can ONLY be used as TOPICAL agents?

A

Trifluridine

Vidarabine

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3
Q

How do the nucleoside analog drugs get converted to its active form?

A

Pro-drug form needs to be phosphorylated by HOST PT kinases -> Triphosphorylated form = active form

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4
Q

What is the one exception among the anti-HSV and anti-CMV drugs requiring host kinase for active phosphorylation?

A

ACYCLOVIR - Requires VIRAL thymidine kinase (TK) for the first phosphorylation event

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5
Q

Mutations of developing resistance to ACYCLOVIR

A

1) Mutations in the binding site of VIRAL DNA POLYMERASE

2) Mutations in VIRAL THYMIDINE KINASE - necessary for first phosphorylation

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6
Q

What are the drug treatments for Herpes Simplex Virus (HSV) and Cytomegalovirus (CMV) - DNA VIRUSES?

A 
"-clovirs"
Acyclovir
Ganciclovir
Cidofovir
Famciclovir

“-idines”
Trifluridine
Vidarabine

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7
Q

What is the chemical composition of ACYCLOVIR?

A 
Guanosine analog 
COMPETITIVE substrate (against dGTP) for VIRAL DNA Polymerase
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8
Q

How does ACYCLOVIR specifically get concentrated inside PARTICULARLY in viral-infected cells?

A

1st phosphorylation event is by VIRAL thymidine kinase (HSV-TK)
Then the 2nd and 3rd phosphorylation events by host kinases -> Gets trapped inside the virus

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9
Q

What is the chemical composition of CIDOFOVIR?

A 
CMP analog 
Competitive substrate (against dCTP) for VIRAL DNA Polymerase
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10
Q

How does CIDOFOVIR get activated within BOTH virus-infected and non-infected cells?

A

ONLY 2 PHOSPHORYLATION events by host kinases

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11
Q

Mechanism of CIDOFOVIR

A

CMP analog that competitively binds (against dCTP) for VIRAL DNA polymerase -> No 3’OH elongation -> Chain termination

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12
Q

Mechanism of resistance development for CIDOFOVIR

A

Mutations in the VIRAL DNA Polymerase

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13
Q

What does the CMP analog state of CIDOFOVIR imply in terms of pharmacoDYNAMICS?

A

Low oral bioavailability - because it is a charged molecule

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14
Q

Which agent is given commonly with CIDOFOVIR to increase its levels in pt? Name two reasons why.

A

PROBENECID

REASON 1: Blocks tubular transport of cidofovir -> Reduces renal clearance
REASON 2: Reduces associated nephrotoxicity

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15
Q

Which is the most broad-spectrum anti-viral drug in that it blocks all 3: HIV RT + VIRAL DNA polymerase + VIRAL RNA polymerase

A

FOSCAVIR

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16
Q

What is the chemical composition of FOSCAVIR?

A

Phosphate + Carboxylate moieties

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17
Q

Mechanism of resistance development against FOSCAVIR

A

Mutations in VIRAL DNA Polymerase

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18
Q

Why is FOSCAVIR also preferred with regards to resistance?

A

Retains its anti-DNA pol activity against GANCICLOVIR/CIDOFOVIR resistant strains

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19
Q

What are the three toxicities associated with FOSCAVIR administration?

A

1) NEPHROTOXICITY: Due to its negative charge (3-)
2) PENILE ULCERS: High levels of ionized urine
3) CNS TOXICITIES: Headache, hallucinations, seizures

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20
Q

DRUG CLASS 2: anti-Influenza (RNA - strand virus, orthomyxovirus)
What are the two subclasses?

A

SUBCLASS 1: Neuraminidase Inhibitors (Prevents viral escape)

SUBCLASS 2: Adamantanes - M2 protein Inhibitors (Prevents viral uncoating/unsheathing -> Prevents viral entry)

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21
Q

What are the 3 Neuraminidase inhibitors and routes of administration?

A

OSELTAMIVIR (Tamiflu) - Oral
ZANAMIVIR - Inhaled
PERAMIVIR - IV (single IV dose versus 5 days of oseltamivir)

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22
Q

What is the chemical composition of OSELTAMIVIR + ZANAMVIR + PERAMIVIR?

A

Sialic acid transition state analogs that INHIBIT viral neuraminidase activity

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23
Q

Mechanisms of resistance development in OSELTAMIVIR + ZANAMIVIR + PERAMIVIR

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A

Mutations in neuraminidase gene OR hemagglutinin (HA)

24
Q

Describe the prodrug -> activated drug conversion of OSELTAMIVIR

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A

Prodrug taken orally -> Activated by ESTERASES (GI/liver)

25
Name the 2 Adamantane drugs that prevent M2 protein and thus Influenza viral entry
Amantadine | Rimantadine
26
What is the specific mechanism of action of AMANTADINE + RIMANTADINE?
Binds and inhibits by clogging the M2 protein (H+/ion pore) -> Inhibits viral uncoating/unsheathing for its entry into host cell
27
What is the mechanism of developing resistance against AMANTADINE + RIMANTADINE?
Mutation in viral M2 protein * Currently most circulating strains are all resistant to this and currently waiting for a strain to emerge for which we can use the adamantanes *
28
DRUG CLASS 3: anti-Hepatitis C (RNA virus, + sense) | What is the overall goal/benchmark for anti-hepatitis therapy?
SUSTAINED virologic response (SVR) * Often times, the virologic response may be suppressed only temporarily due to a small pool of infected cells that emerges thereafter *
29
Does a vaccine exist for Hepatitis C? How about Hepatitis B?
Hep B- YES | Hep C - NO
30
HBV is responsible for the majority of which cases of cancer?
Hepatocellular carcinoma (one of the most common cancers)
31
What was the first ALL ORAL TREATMENT for Hepatitis C virus (HCV)?
SOFOSBUVIR/ RIBAVARIN
32
What is the chemical composition of SOFOSBUVIR and its mechanism of action?
UMP analog - NUCLEOTIDE pro-drug bec it carries one phosphate Terminates chain elongation of HCV RNA-dependent RNA polymerase
33
What drugs do you have to be careful administering together with SOFOSBUVIR? Hint: Think [drug]
Drugs that induce the p-glycoprotein drug efflux pump SOFOSBUVIR is a substrate for this pump SOFOSBUVIR + pump-inducing drugs -> Increases drug efflux -> Lowers [SOFOSBUVIR]
34
What is the chemical composition of RIBAVARIN
``` Guanosine analog (similar to acyclovir in this sense) DIFFERENCE from Acyclovir: Acyclovir requires VIRAL thymidine kinase for first phosphorylation event followed by host kinases for the other phosphorylations. Ribavarin is phosphorylated 3x all by host kinases ```
35
What are the targets of RIBAVARIN? (3)
1. GTP-synthesis enzymes: LOWERS cellular GTP 2. Inhibits mRNA capping 3. Inhibits VIRAL RNA-dependent RNA polymerase -> Inhibits RNA virus replication
36
What is the main difference between the 2 nucleoside analogs: SOFOBUVIR + RIBAVARIN
Sofobuvir - UMP analog that TERMINATES chain elongation of HCV RNA-dependent RNA polymerase Ribavarin - Guanosine analog that does NOT terminate chain elongation. Rather targets the 3 specific enzymes
37
What drug is the latest HCV NS3 protease inhibitor?
SIMEPREVIR | * Note photosensitivity w/ drug use *
38
Name the 2 HCV protease inhibitor drugs.
SIMEPREVIR + PARITAPREVIR
39
Name the two anti-HCV NS5A protein inhibitors.
LEDIPASAVIR + OMBITSAVIR
40
What do LEDIPASAVIR + OMBITSAVIR target?
Block NS5A protein (DIMER) that is conserved among HCV genotypes - HCV structural protein with NO inherent enzymatic activity BUT this inhibition blocks viral RNA replication + packaging
41
What is the importance of LEDIPISAVIR binding and inhibiting the DIMER form of NS5A protein?
Ledipisavir binds the dimer form VERY tightly that it leads to inactivation within picomolar ranges
42
What confers specificity of LEDIPASAVIR to HCV?
Viral NS5A has no human homolog
43
ALL/ORAL Combo Pill: LEDIPISAVIR + SOFOSBUVIR
HARVONI - 96% success rate
44
Most important precaution with taking SOFOSBUVIR or other SOFOSBUVIR-based drugs (e.g. HARVONI) with regards to drug/drug interaction
Should not take AMIODARONE (heart drug) + SOFOSBUVIR-base -> Results in slower heartbeat Worry about CV issues
45
What is the name of the non-nucleoside inhibitor of HCV RNA-dependent RNA polymerase?
DASABUVIR
46
ALL ORAL HCV treatment: DASABUVIR + OMBITSAVIR + PARITAPREVIR + RITONAVIR (paritaprevir booster)
VIEKIRA PAK
47
VIEKIRA PAK contains which drugs?
DASABUVIR (Non-nucleoside inhibitor of RNA pol) OMBITSAVIR (NS5A inhibitor) PARITAPREVIR (NS3 protease inhibitor) RITONAVIR (NS3 booster)
48
Precaution with drug-drug interactions with VIEKIRA PAK
DASABUVIR - metabolized by CYP2C8 PARITAPREVIR - metabolized by CYP3A4 RITONAVIR - CYP3A4 INHIBITOR
49
Why is pegylated-Interferon NOT a first-line drug of treatment for HCV?
1) Long course of treatment that only works for 50% of HCV patients 2) SO SO MANY ADVERSE EFFECTS
50
DRUG CLASS 4: anti-Hepatitis B (DNA virus that replicates via RNA intermediate) Name the two drugs used for anti-HBV treatment.
ENTECAVIR | TENOFOVIR
51
What are the first line-treatments of HBV?
1) INTERFERONS (really unfortunate bec there's so many side effects such as reduced P450 metabolism, neurotoxicity, autoimmunity, hepatotoxicity) 2) NUCLEOSIDE ANALOG RNA pol Inhibitors: TENOFOVIR + ENTECAVIR
52
How does ENTECAVIR get activated?
ENTECAVIR (guanosine analog) gets phosphorylated 3x by HOST kinases
53
Mechanism of action of ENTECAVIR
Entecavir gets incorporated into first or second strand DNA synthesis -> Has 3'OH for elongation -> Additional bases are added BUT DNA is DISTORTED -> Blocks further synthesis * Chain terminator by causing DNA distortion *
54
How long does a pt have to be on ENTECAVIR? Why?
For their LIFETIME | ENTECAVIR only SUPPRESSES HBV. If off treatment, REBOUNDING can occur
55
Resistance properties of ENTECAVIR
1. Emerged slowly - BEC resistance requires 2 mutations 2. Cross-resistance to Lamivudine (anti-HIV) - If pt is taking lamivudine and develops resistance against this as well, ENTECAVIR resistance accelerates

Class: Immuno Block (13 decks)

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