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840 Exam #2 > Dr. Timmins > Flashcards

Dr. Timmins Flashcards

1
Q

Fuzeon

A
  • Long peptide
  • Blocks entry into CD4+ cell
  • Works on HIV 1 only
  • Not orally active
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2
Q

Why is Fuzeon not used?

A
  • Poor compliance

- Expensive

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3
Q

Maravioc (Selzentry)

A
  • Has oral bioavailability
  • Binds to host CCR5 coreceptor
  • Works on some strains of HIV 1
  • Need to test for virus tropism
  • Dose dependent on other CYP3A drugs
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4
Q

Maraviroc (Selzentry) Dosing for CYP3A inhibitors

A

-150mg BID

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5
Q

Maraviroc (Selzentry) Dosing for CYP3A inducers

A

-600mg BID

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6
Q

Maraviroc (Selzentry) Dosing for a patient with no other CYP3A drugs

A

-300mg BID

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7
Q

Purpose of Maraviroc (Selzentry) two ends (Med chem)

A

-Used for oxidation

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8
Q

What is the middle section of the Maraviroc (Selzentry) center of molecule used for?

A
  • N dealkylation

- This is major site of metabolism

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9
Q

Should you use Rifampin with Maraviroc (Selzentry)

A
  • Consider using rifabutin instead

- If you use Rifampin then you need to change the dose to 600mg BID

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10
Q

Which HIV drugs inhibit Reverse Transcriptase?

A

1) Nucleoside reverse transcriptase inhibitors
- modified at deoxyglucose function
- NOO 3’ hydroxyl group
2) Non-nucleoside reverse transcription inhibitors
- Uses a different mechanism of action

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11
Q

Viral Protease Inhibitors

A
  • Viral proteins are made as one long string
  • Needs to be cleaved by protease
  • If not cleaved the protein will not fold correctly
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12
Q

Protease Inhibitors medchem

A
  • All contain an amide or amide like group

- Are all big molecules

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13
Q

NRTIs and NNRTIs medchem

A
  • Lack 3’ OH

- Modified sugar

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14
Q

HIV integrase inhibitors MoA

A

-Integrase inhibitors prevent viral genome insertion into human CD4 cell genomes

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15
Q

HIV integrase inhibitor medchem

A

-Binds to viral integrase and inhibits its activity

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16
Q

How to remember NRTI and NNRTI drug names

A
  • Look like thymidINE so most end in “ine”
  • Except for Abaracadabara, and abacavir (magically a NRTI)
  • Ten middle fingers for TENofovir (awkward NRTI)
  • Efavirenz (NNRTI)
17
Q

How to remember Protease inhibitor drug names

A
  • ProteAse has an Amide or Amide like group

- So the end in “Avir”

18
Q

How to remember Integrase drug names

A
  • IntegRAse

- So they all end in “Ravir”

19
Q

Hep C treatment with old drugs

A
  • Major side effects

- New treatments = much less severe side effects

20
Q

NS5A medchem

A
  • Used to treat HepC
  • Dimeric protein
  • 2 zinc binding portions
  • Leading to symmetrical/near symmetrical drugs
21
Q

NS5B MoA

A
  • Used to treat HepC
  • RNA dependent RNA polymerase
  • Essential for viral replication
  • Can be non nucleoside or nucleoside
22
Q

What makes Sofosbuvir (Sovaldi) so special?

A
  • Pro drug of DFMU monophosphate
  • Cover up 2 negative charges
  • Then it gets 2 more phosphates in cell
  • Double prodrug
  • Orally absorbed
  • Gets into hepatocyte
23
Q

Why do we not just give DFMU triphosphate?

A

-Its log P is even worse than DFMU monophosphate

24
Q

How to remember HepC drugs

A
  • NS3/4A = previr
  • NS5A = asvir
  • NS5B = buvir
25
Q

What does NS3/4A target?

A
  • previr

- Targets a pair of proteases

26
Q

What does NS5A target?

A
  • asvir

- A pair of Zinc Ions

27
Q

What does NS5B target

A
  • buvir

- inhibits the build of new RNA genomes

28
Q

Are HIV/ Hep C drugs monotherapy or combination therapy

A
  • Combo therapy duhhh

- Monotherapy leads to an increased risk of resistance in HIV infections

29
Q

Why is resistance so much more likely to occur in viral infections over bacterial infections?

A

1) Time = you treat viral infections for much longer than bacterial
- Leading to an increased risk of mutation
2) Viral loads are many times higher than bacterial loads
3) Viral genome replication is more prone to error than bacterial replications
- Increased errors = increased mutations

840 Exam #2 (6 decks)

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