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med chem > exam 1 > Flashcards

exam 1 Flashcards

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1
Q
  1. What is the primary function of the Renin-Angiotensin-Aldosterone System (RAAS)?
A

Regulation of blood pressure

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2
Q
  1. Which are viable targets for antihypertensives acting on RAAS?
A

Renin
Angiotensin Converting Enzyme (ACE)
Angiotensin II Type I Receptor (Angiotensin II receptor type 1 or AT1)
Mineralocorticoid Receptor (aldosterone receptor)

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3
Q
  1. What is the purpose of renin and what is the general mechanism by which it works?
A

Rein is an aspartyl protease that cleaves angiotensinogen to convert to angiotensin I

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4
Q
  1. Why is renin a good target?
A

Renin catalyzes the rate-limiting step in the RAAS cascade

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5
Q
  1. How do sartans work as antihypertensives?
A

Angiotensin narrows your blood vessels which increases blood pressure and forces the heart to work harder.
Angiotensin II receptor blockers help relax your veins and arteries to lower your blood pressure and make it easier for your heart to pump blood.
Angiotensin II receptor blockers block the action of angiotensin II.

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6
Q
  1. How do phosphodiesterase 5 (PDE5) inhibitors act as antihypertensives?
A

Vasodilators:
allow cGMP (secondary messenger) to stay active and thus relax smooth muscle

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7
Q
  1. What is the rationale behind designing antagonists from agonists and what strategies are used?
A

Since agonists are known to already interact with the target, they are a good starting point for design of antagonists.
By adding more functional groups, additional interactions can be utilized to alter the induced fit to inhibit the target.

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8
Q
  1. Why did the chain extension of histamine along with guanidine result in antagonist activity?
A

The guanidine group interacts with both the agonist and antagonist area of the H2 receptor, however the chain extension allowed the guanidine to specifically interact with the antagonist region.

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9
Q
  1. How do dipoles play a role in drug activity?
A

Proper alignment of dipoles in substrate and target will allow for stronger intermolecular interactions.

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10
Q
  1. Why are proton pump inhibitors superior over H2 antagonists?
A

They are downstream of the receptors that initiate the release of gastric acid (Release of gastric acid is promoted by acetylcholine, gastrin and histamine)

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11
Q
  1. What are the drug targets within the molecular pathway for adrenergic receptors?
A

AEEMPTV

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12
Q
  1. What is the major difference between beta-1 and beta-2 adrenergic receptors?
A

2-Adrenoceptors predominate in the airways
1- Adrenoceptors predominate in the heart

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13
Q
  1. How does insulin work?
A

Insulin binds to its receptor (receptor tyrosine kinase) which is activated to autophosphorylate then further phosphorylate other proteins to activate the signaling cascade which ultimately causes translocation of glucose transport proteins to the cell surface.

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14
Q
  1. Explain the difference between type 1 and type 2 diabetes.
A

Type 1 is caused by the immune system attacking beta-islet cells in the pancreas, thus insulin is not produced. Type 2 is caused by a decreased sensitivy of insulin, or less insulin produced.

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15
Q
  1. Why is Teplizumab useful against type 1 diabetes but not type 2?
A

CD3-directed monoclonal antibody that is suspected to target the T-cells responsible for the attack on β-islet cells. Since T cells are not involved in type 2 diabetes, immunosuppressive therapy would not be useful for type 2 diabetes.

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16
Q
  1. Briefly explain biguanides and incretin mimetics as diabetes therapeutics.
A

incretin mimetics Induce the pancreas to make more insulin
biguanides limit the liver’s ability to make and release sugar

17
Q
  1. What role does the FcRn (neonatal Fc receptor) have for mAb therapeutics?
A

This receptor interacts with the Fc portion of mAbs, and allows for recycling back into circulation as opposed to catabolism.

18
Q
  1. How can engineering the Fc region enhance mAb therapies?
A

It can be utilized to alter pharmokinectic properties through the FcRn and also induce stronger interactions with immune effector cells.

19
Q
  1. How can mAbs be utilized as effective anti-cancer agents?
A

a.Direct tumour cell killing can be elicited by receptor agonist activity, such as an antibody binding to a tumour cell surface receptor and activating it, leading to apoptosis (represented by the mitochondrion).
It can also be mediated by receptor antagonist activity, such as an antibody binding to a cell surface receptor and blocking dimerization, kinase activation and downstream signalling, leading to reduced proliferation and apoptosis.
An antibody binding to an enzyme can lead to neutralization, signalling abrogation (preventing a biological function) and cell death, and conjugated antibodies can be used to deliver a payload (such as a drug, toxin, small interfering RNA or radioisotope) to a tumour cell.
b | Immune-mediated tumour cell killing can be carried out by the induction of phagocytosis; complement activation; antibody-dependent cellular cytotoxicity (ADCC); genetically modified T cells being targeted to the tumour by single-chain variable fragment (scFv); T cells being activated by antibody-mediated cross-presentation of antigen to dendritic cells; and inhibition of T cell inhibitory receptors, such as cytotoxic T lymphocyte-associated antigen 4 (CTLA4).
c | Vascular and stromal cell ablation(removal) can be induced by vasculature receptor antagonism or ligand trapping (not shown); stromal cell inhibition; delivery of a toxin to stromal cells; and delivery of a toxin to the vasculature. MAC, membrane attack complex; MHC, major histocompatibility complex; NK, natural killer.

20
Q
  1. What are typically considered antigens for mAbs?
A

Overexpressed receptors on cancerous cells, in tumor microenvironment, receptors with known oncogenic mutations

21
Q
  1. What is the theory behind ADCs?
A

The antibody can specifically target tumor antigens to allow for specific release of highly potent drugs

22
Q
  1. Concerning ADCs, what are some of the design principles that are most important?
A

Linker should be stable enough to withstand circulation but still enable release of active drug, drug should have proper physicochemical properties which enable uptake into neighboring tumor cells,

23
Q
  1. Why is it necessary to have extremely potent drugs for ADCs?
A

ADCs typically have a DAR (drug to antibody ratio) that is very low therefore the drugs must induce an effect at very low concentrations

24
Q
  1. How can heterogeneity be improved for DAR?
A

Incorporate unnatural amino acids to have specific conjugation, utilize enzyme-directed conjugation, utilize new chemistry to make use of disulfide bridges at hinge region without disrupting antibody structure

25
Q
  1. Explain why 3rd generation ADCs have a greater therapeutic window than the previous generations.
A

Improved chemistry has allowed for more homogeneous DAR, stable linkers, enhanced PK profiles, dual targeting, dual drug loading, more potent drugs

med chem (3 decks)

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