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MedChem > Block 6 Putnam Stuff > Flashcards

Block 6 Putnam Stuff Flashcards

1
Q

Explain how regular insulin therapy works.

A

Exogenously delivers the insulin, replacing the insulin that’s missing.

  • it’s noted by an R on the label.
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2
Q

How is rapid acting insulin different than regular insulin therapy?

A

Rapid acting insulin has had its amino acid sequence modified, allowing for the rapid action.

When insulin is dimerized or hexamerized, it is not active. The monomeric formation is the active formation.

Rapid acting insulin works because it has been modified to decrease the formation of dimers and hexamers, allowing it to absorb more quickly.

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3
Q

Describe the MOA of long-acting insulin.

A

Changes in AA sequence:

  • changes isoelectric point
  • adds two ARG to the COOH terminal of the B chain
  • prevents deamination of acid-sensitive asparagine by replacing it with glycine (at the 21 position on the A chain)
  • aggregation in the cutaneous space
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4
Q

Tresiba and levemir both utilize changes to the amino acid in the 29th position on the B chain, but in different ways. What changes do they have?

A

Tresiba - hexadecanedioic acid conjugate to Lys on B29, allowing for the formation of multi-hexamers that causes slow release from tissues

Levemir - myristic acid conjugate to Lys on B29, allowing it to bind to albumin, from which it slowly dissociates

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5
Q

What is the MOA of metformin?

A

Decreases hepatic glucose production

Decreases intestinal absorption of glucose

Improves insulin sensitivity by increasing peripheral glucose uptake and utilization

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6
Q

What is the MOA of thiazolidinediones (glitazones)?

A

Binds to PPAR (peroxisome proliferator-activated receptor) gamma in adipocytes to promote adipogenesis and fatty acid uptake
- this decreases the amount of fatty acids present in circulation so that cells use more glucose

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7
Q

What is the MOA of sulfonylureas?

A

Bind to and close ATP sensitive K channels on the cell membrane of pancreatic beta cells
- this impacts the cell membrane structure and increases insulin secretion

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8
Q

What is the MOA of metaglinides?

A

Bind to ATP sensitive K channels on the cell membrane of pancreatic beta cells (like sulfonylureas)

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9
Q

How are metaglinides different from sulfonylureas?

A

Metaglinides have a weaker binding affinity and faster dissociation from the SUR1 binding site that results in a much shorter duration of action

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10
Q

What is the MOA of acarbose?

A

Acarbose is an alpha-glucosidase (glycoside hydrolase) and pancreatic alpha-amylase inhibitor
– thus, it blocks enzymes that digest carbohydrates in the small intestine, decreasing the rate at which carbohydrates are broken down into glucose

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11
Q

What is an incretin? Give an example of an endogenous incretin.

A

Incretins are molecules that stimulate insulin release and inhibit glucagon release.
– thus, they can directly and effectively lower blood glucose

Example: glucagon-like peptide 1 (GLP-1)

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12
Q

Define the function of DPP-4.

A

DPP-4 inhibits GLP-1 (and other incretins), thus inhibiting insulin release and allowing for glucagon release.

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13
Q

What is the MOA of DPP-4 inhibitors?

A

DPP-4 inhibitors block dipeptidyl peptidase 4 (DPP-4), thus blocking the inactivation of incretins.

  • the incretin is then able to stimulate the increase of insulin secretion and inhibit the release of glucagon
  • -> this lowers blood glucose
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14
Q

What suffix is associated with DPP-4 inhibitors?

Give at least 1 example of a DPP-4 inhibitor drug.

A

—Gliptin

Sitagliptin
Vildagliptin

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15
Q

What is the MOA of GLP-1 receptor agonists?

A

GLP-1 receptor agonists activate the incretin hormone receptor, leading to inhibition of glucagon release and stimulation of insulin release
— this lowers blood glucose levels

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16
Q

What suffix is associated with GLP-1 receptor agonists?

Give at least 1 example of a GLP-1 receptor agonist.

A

—tide

Exenatide (bydureon/byetta)
Liraglutide (victoza, saxenda)
Lixisenatide (lyxumia)
Albiglutide (tanzeum)
Dulaglutide (trulicity)
Semaglutide (ozempic)
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17
Q

What is the MOA of SGLT2 inhibitors?

A

SGLT2 (sodium glucose co-transporter 2) normally facilitates glucose reabsorption in the kidney
–so, SGLT2 inhibitors block the reabsorption of glucose in the kidney, thus increasing excretion and lowering blood glucose levels.

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18
Q

What suffix is associated with SGLT2 inhibitor drugs?

Give at least 1 example of an SGLT2 inhibitor.

A

—gliflozin

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)

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19
Q

What other disease state (besides hyperglycemia) can SGLT2 inhibitors be used to treat? Why?

A

SGLT2 inhibitors can efficiently pull volume off patients (increasing excretion of glucose can have a diuretic effect), so they can also be used to help with heart failure.

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20
Q

HGH is used to treat…

What is the MOA?

A

short stature of unknown cause

MOA - mimics natural growth hormone to stimulate growth and cellular reproduction

Examples: genotropin, norditropin, humatrope

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21
Q

What is chorex?

What is it used for?

A

human chorionic gonadotropin (hCG)

  • indicated to cause ovulation and treat infertility in women
  • can be used to increase sperm count in men
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22
Q

What is ovidrel and what is it used for?

A

recombinant hCG

induces ovulation by stimulating late phase follicular maturation and resumption of oocyte meiosis

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23
Q

Why are menotropins used to induce ovulation?

A

Menotropins are prepared from the urine of post-menopausal women. hCG is naturally occurring in post-menopausal women, and hCG induces ovulation.

24
Q

How does follistim work?

A

It stimulates ovarian follicular growth because it is made to resemble FSH

(FSH is the hormone produced in the anterior pituitary to normally stimulate follicular growth, maturation, and gonadal steroid production)

25
Q

What two drugs are based on the hormone vasopressin (ADH)?

A

Pitressin and Vasostrict

26
Q

What is pitocin used for?

A

It’s indicated for initiation or improvement of uterine contractions, as well in controlling postpartum bleeding

27
Q

What drug is used to treat hypothyroidism?

A

Levothyroxine - synthetic T4 (thyroxine)

28
Q

How do hyperthyroid treatment drugs work?

A

Methimazole, PTU, and Carbimazole (prodrug of methimazole) prevent iodine and peroxidase from interacting with thyroglobulin, thus preventing the production of T3 and T4.

M and C also interfere with the conversion of T4 to T3

29
Q

Describe the MOA of SERMs.

A

SERM stands for selective estrogen receptor modulator. They appear to act as estrogen agonists in the bone. They decrease bone resorption and turnover, along with increasing bone mineral density (BMD) and decreasing fracture incidence.

30
Q

Which natural molecule to bisphosphonates mimic? What is the difference between the two?

A

Bisphosphonates mimic pyrophosphate (a normal constituent of bone).
The oxygen in P-O-P (of pyrophosphate) is replaced with a carbon atom (in bisphosphonates) to create a non-hydrolyzable backbone.

31
Q

What are the effects of bisphosphonates?

How are they able to do this?

A

They inhibit osteoclast proliferation, decrease activity, reduce life span, and (as a result) decrease the number of sites along the bone surface where bone resorption occurs.

This is possible because they mimic pyrophosphate and can bind to the hydroxyapatite portion of the bone, aka they can bind to and stabilize calcium phosphate effectively

32
Q

Why is salmon the preferable source of calcitonin?

A

It has greater receptor affinity and a longer half-life than human calcitonin.

33
Q

How is Forteo able to work as a bone forming agent?

A

It increases the number of osteoblasts

34
Q

What is the MOA of prolia?

A

It is a RANKL receptor inhibitor
– binds to the receptor to inhibit osteoclast activation and formation

–> this is because when RANKL binds to its receptor on the surface of osteoclasts and osteoclast precursors, it stimulates formation and activation

35
Q

Can non-steroid based molecules be used to affect hormone levels?

A

Yes.

36
Q

What was the final force behind a meat inspection law and comprehensive food/drug law that eventually led to the passage of the 1906 “Federal Food and Drugs Act”?

A

Upton Sinclair’s “The Jungle”

37
Q

What was the Food, Drug, and Cosmetic Act (FD&C Act) of 1938 signed in response to? What did it mandate?

A

Death of over 100 people, many of whom were children, due to the addition of diethylene glycol (antifreeze) in a marketed form of sulfanilamide.

It established that manufacturers must prove the safety of their products prior to marketing.

38
Q

The 1902 Biologics Control Act was enacted in response to…

A

13 children died from Jim the horse who had contracted tetanus (and whose tainted blood was used to treat patients)

39
Q

What are the current principal laws that govern biologics?

A

the FD&C act and the 1944 Public Health Service Act

40
Q

The Kefauver-Harris Amendments mandate…

A

efficacy as well as safety must be established before a drug can be marketed

and required the FDA to assess the efficacy of all drugs introduced since 1938.

41
Q

True or false: there were no generics allowed in the original 1938 FD&C Act, but the Kefauver-Harris Amendments allowed for all generic drugs to be approved.

A

FALSE
The Kefauver-Harris Amendments only allowed for generics for drugs approved before 1962 (the first ANDAs based on the literature)
The modern generic laws were passed in 1984 with the passage of the Drug Price Competition and Patent Term Restoration Act (aka the Hatch-Waxman Act)

42
Q

To make a biosimilar of a biologic, you must have:

A
  • proof of quality and similarity
  • PK bioequivalence
  • clinical safety and efficacy data
43
Q

When was an abbreviated approval pathway for biosimilars introduced?

A

The pathway is listed as part of the Biologics Price Competition and Innovation Act of 2009 (enacted as part of the ACA in 2010)

44
Q

Small molecule drugs are approved via _____ with a ____ for new drugs and a ____ for generics.

Biologics are approved via _____ with a ____ for new drugs and a _____ for biosimilars.

A

FDCA
NDA
ANDA

PHSA
Biologics License Application
Biosimilar Biologics License Application

45
Q

What does IRB stand for?

A

Institutional Review Board

46
Q

What are CDER and CBER?

A

The center for drug evaluation and research (for small molecule)

The center for biologics evaluation and research (for biologics)

47
Q

When can you submit an IND?

A

Once you have the basic chemistry and have completed animal trials (before human trials)

48
Q

What is the purpose of CMC (chemistry, manufacturing, and controls)?

A
  • assure that the drug sold will have quality attributes similar to those of the drug demonstrated to be safe and effective (meaning the ones being produced have the same quality attributes as the ones that were tested/approved)
  • assure the quality meets appropriate standards and is consistent
  • assure the drug you are using is the one described on the label
49
Q

What are the critical elements in CMC?

A
  • how and where is the drug made?
  • how are the raw materials tested and monitored?
  • what control procedures are in place to assure product consistency and quality?
  • are the quality attributes adequately identified and characterized for the product?
  • are the test methods used to monitor the product quality appropriate?
  • how long does the product maintain its quality after it is made (shelf-life/expiry)?
50
Q

Why is non-clinical research done?

A

to demonstrate that the drug is reasonably safe for use in initial small-scale clinical studies.

51
Q

what is evaluated in non-clinical drug development?

A

toxicity and efficacy through in vitro and in vivo lab animal testing

  • toxicology (acute, sub-chronic, chronic, genotoxicity (mutagenicity), and teratogenicity) - also dose escalation
  • pharmacology (ADME profile)
52
Q

When do GLP studies take place?

What takes place in them?

A

After the initial exploratory studies.

Further toxicology studies in at least two animal species (1 rodent and 1 non-rodent)

Further genotoxicity studies (including in vivo in addition to in vitro)

Safety pharmacology studies continue, including reproductive toxicity studies

Toxicokinetic studies

53
Q

What is the single most important factor in the approval or disapproval for a new drug?

A

Safety and effectiveness studies done in clinical trials - particularly the safety aspect

54
Q

Describe what takes place during phase 1 of clinical studies.

A

Takes place over the period of 1 year with 25-100 healthy subjects

Analyzes:

  • metabolic actions in humans
  • pharmacologic actions in humans
  • side effects with increasing doses
  • effectiveness of drug
55
Q

What is the primary goal of phase 2 clinical studies?

A
  • determine short-term side effects and risks associated with the drug in patients with the disease or condition

takes 1-2 years and studies effects in 150-300 PATIENTS

56
Q

when is the overall benefit-risk relationship of the drug evaluated during clinical studies?

A

Phase 3

57
Q

What provides the framework for how to conduct well-controlled studies?

A

Good Laboratory Practices

  • assures quality and integrity of data
  • provides overall accountability
  • facilitates study reconstruction

MedChem (4 decks)

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