NUSCTX 110 Midterm 1 2025 Newest Complete Exam/ Actual Questions
with 100% Correct Verified Answers/ Graded A+
1. On-Target Toxici- Toxic effect due to the drug interacting with the intended
ty therapeutic target
2. Off-Target Toxici- Toxic effect due to the drug interacting with an unintended
ty biological target or unintended tissue
3. Idiosyncratic drug reactions that occur rarely and unpredictably
drug reactions
4. Idiopathic drug when the cause of toxicity in a drug is unknown
reactions
5. Rosiglitazone •It was prescribed as an insulin sensitizer for diabetics
by binding to PPAR-gamma receptors in adipocytes•First
released in 1999, annual sales peaked at 2.5 billion in
2006 and use has declined dramatically after drug was
found to increase risk of heart attacks.•Adverse effects
subject to over 13,000 lawsuits and has been estimated
to have caused 83,000 heart attacks in the US•Rosigli-
tazone causes on-target edema which can put people at
risk for congestive heart failure—occurs through reduced
renal excretion of sodium and increase in sodium and
water retention
6. Non-Steroidal Non-Steroidal Anti-Inflammatory Drugs—Aspirin, Ibupro-
Anti-Inflammato- fen, Diclofenac, Naproxen, acetaminophen•Used for pain
ry Drugs relief, inflammation, fever reduction and swelling, arthritis,
headache•Acetylsalicilic acid (active ingredient of aspirin)
is produced by plants including willow bark and spiraea
7. Rofecoxib •COX2-selective inhibitor with very little gastrointestinal
(Vioxx) side-effects•Prescribed to over 20 million people as a pain
reliever for arthritis•was found to be responsible for in-
creased risk of heart attack and stroke•Recalled in 2004;
Financial damage: nearly $6 billion in litigation•Largest
drug recall in history•Merck and FDA criticized for ignor-
ing evidence of dangers of Vioxx before its eventual re-
call•140,000 people could have suffered serious coronary
heart disease from taking the drug in just the U.S.•Studies
, NUSCTX 110 Midterm 1
have shown that COX2 is responsible for synthesis of
prostacyclins in the vasculature which are cardioprotec-
tive•COX2-selective inhibition reduces the cardioprotec-
tive prostacyclin and causes cardiac events
8. Diphenhy- •Diphenhydramine also crosses the blood brain barrier
dramine where H1 histamine receptor antagonism causes sleepi-
ness.•Modern antihistamines, such as claritin, do not
cross the blood brain barrier
9. Toxicology Toxicology is the study of adverse effects of chemicals
on living systems, including:•Mechanisms of action and
exposure to chemicals as a cause of acute and chronic
illness.•Recognition, identification, quantification of haz-
ards from occupational exposure to chemicals. •Discov-
ery of new drugs and pesticides and characterizing their
safety, ADME, toxicology.•Development of standards and
regulations to protect humans and the environment from
adverse effects of chemicals.
10. Terfenadine a non-sedating antihistamineformerly used for treatment
of allergic conditions by Sanofi Aventis•Was used by over
100 million patients by 1990 and made over $440 mil-
lion•Replaced by fexofenadine in the 1990s due to risk of
cardiac arrhythmia
11. Thalidomide •Thalidomide was an anti-nausea and sedative drug that
was introduced in the late 1950s to be used to help
with morning sickness•1950s to 1960s: more than 10,000
children in 46 countries were born with deformities such
as phocomelia involving shortened limbs R-thalidomide
stimulates the GABA receptor to cause sedative effects.
•S-thalidomide binds to a protein and inactivates a protein
called cereblon (CRBN), an E3 ubiquitin ligase that, when
bound to thalidomide, recruits neo-substrates to ubiq-
uitinate and proteasomally degrade them—including a
recently identified transcription factor called SALL4 which
is involved in limb outgrowth and development
12.
, NUSCTX 110 Midterm 1
1.How do a.Most small-molecule drugs bind to a pocket in a protein
most small-mol- and inhibits or activates that protein, but that protein is not
ecule drugs that degraded
are in the clin- b.Most small-molecule drugs bind to a gene and turn on
ic work to exert or turn off that gene
their therapeutic c.Most small-molecule drugs edit your genome to repair
action? inborn errors
d.Most small-molecule drugs bind to a pocket in a protein
and gets degraded
13. 2.What is in- a.Target selection, screening small-molecule libraries to
volved in a typi- discover hits, take the hit compound and file an IND to
cal drug discov- the FDA and enter Phase I clinical trials
ery campaign to b.Target selection, screening small-molecule libraries to
get to clinical tri- discover hits, hit to lead medicinal chemistry optimiza-
als? tion to improve potency, selectivity, and pharmacokinet-
ic/pharmacodynamic parameters to get to a developmen-
tal candidate (DC), testing safety, metabolism, efficacy,
optimizing process chemistry and formulation, filing an
Investigational New Drug Application (IND) to Food and
Drug Administration (FDA), and entering Phase I clinical
trials
c.Formulating a nutrient supplement cocktail, announce
its efficacy on social media and news outlets, sell to
patients online
d.Hearing rumors about the efficacy of a drug, touting
to the media and press that it cures a potentially lethal
disease, and strong-arming the FDA to cross-indicate
the drug for the lethal disease by passing emergency
approval of the drug before clinical trials are finished
14. 3.What is the
therapeutic
mechanism of
action of the
non-steroidal
anti-inflammato-
ry drug
ibuprofen? What
with 100% Correct Verified Answers/ Graded A+
1. On-Target Toxici- Toxic effect due to the drug interacting with the intended
ty therapeutic target
2. Off-Target Toxici- Toxic effect due to the drug interacting with an unintended
ty biological target or unintended tissue
3. Idiosyncratic drug reactions that occur rarely and unpredictably
drug reactions
4. Idiopathic drug when the cause of toxicity in a drug is unknown
reactions
5. Rosiglitazone •It was prescribed as an insulin sensitizer for diabetics
by binding to PPAR-gamma receptors in adipocytes•First
released in 1999, annual sales peaked at 2.5 billion in
2006 and use has declined dramatically after drug was
found to increase risk of heart attacks.•Adverse effects
subject to over 13,000 lawsuits and has been estimated
to have caused 83,000 heart attacks in the US•Rosigli-
tazone causes on-target edema which can put people at
risk for congestive heart failure—occurs through reduced
renal excretion of sodium and increase in sodium and
water retention
6. Non-Steroidal Non-Steroidal Anti-Inflammatory Drugs—Aspirin, Ibupro-
Anti-Inflammato- fen, Diclofenac, Naproxen, acetaminophen•Used for pain
ry Drugs relief, inflammation, fever reduction and swelling, arthritis,
headache•Acetylsalicilic acid (active ingredient of aspirin)
is produced by plants including willow bark and spiraea
7. Rofecoxib •COX2-selective inhibitor with very little gastrointestinal
(Vioxx) side-effects•Prescribed to over 20 million people as a pain
reliever for arthritis•was found to be responsible for in-
creased risk of heart attack and stroke•Recalled in 2004;
Financial damage: nearly $6 billion in litigation•Largest
drug recall in history•Merck and FDA criticized for ignor-
ing evidence of dangers of Vioxx before its eventual re-
call•140,000 people could have suffered serious coronary
heart disease from taking the drug in just the U.S.•Studies
, NUSCTX 110 Midterm 1
have shown that COX2 is responsible for synthesis of
prostacyclins in the vasculature which are cardioprotec-
tive•COX2-selective inhibition reduces the cardioprotec-
tive prostacyclin and causes cardiac events
8. Diphenhy- •Diphenhydramine also crosses the blood brain barrier
dramine where H1 histamine receptor antagonism causes sleepi-
ness.•Modern antihistamines, such as claritin, do not
cross the blood brain barrier
9. Toxicology Toxicology is the study of adverse effects of chemicals
on living systems, including:•Mechanisms of action and
exposure to chemicals as a cause of acute and chronic
illness.•Recognition, identification, quantification of haz-
ards from occupational exposure to chemicals. •Discov-
ery of new drugs and pesticides and characterizing their
safety, ADME, toxicology.•Development of standards and
regulations to protect humans and the environment from
adverse effects of chemicals.
10. Terfenadine a non-sedating antihistamineformerly used for treatment
of allergic conditions by Sanofi Aventis•Was used by over
100 million patients by 1990 and made over $440 mil-
lion•Replaced by fexofenadine in the 1990s due to risk of
cardiac arrhythmia
11. Thalidomide •Thalidomide was an anti-nausea and sedative drug that
was introduced in the late 1950s to be used to help
with morning sickness•1950s to 1960s: more than 10,000
children in 46 countries were born with deformities such
as phocomelia involving shortened limbs R-thalidomide
stimulates the GABA receptor to cause sedative effects.
•S-thalidomide binds to a protein and inactivates a protein
called cereblon (CRBN), an E3 ubiquitin ligase that, when
bound to thalidomide, recruits neo-substrates to ubiq-
uitinate and proteasomally degrade them—including a
recently identified transcription factor called SALL4 which
is involved in limb outgrowth and development
12.
, NUSCTX 110 Midterm 1
1.How do a.Most small-molecule drugs bind to a pocket in a protein
most small-mol- and inhibits or activates that protein, but that protein is not
ecule drugs that degraded
are in the clin- b.Most small-molecule drugs bind to a gene and turn on
ic work to exert or turn off that gene
their therapeutic c.Most small-molecule drugs edit your genome to repair
action? inborn errors
d.Most small-molecule drugs bind to a pocket in a protein
and gets degraded
13. 2.What is in- a.Target selection, screening small-molecule libraries to
volved in a typi- discover hits, take the hit compound and file an IND to
cal drug discov- the FDA and enter Phase I clinical trials
ery campaign to b.Target selection, screening small-molecule libraries to
get to clinical tri- discover hits, hit to lead medicinal chemistry optimiza-
als? tion to improve potency, selectivity, and pharmacokinet-
ic/pharmacodynamic parameters to get to a developmen-
tal candidate (DC), testing safety, metabolism, efficacy,
optimizing process chemistry and formulation, filing an
Investigational New Drug Application (IND) to Food and
Drug Administration (FDA), and entering Phase I clinical
trials
c.Formulating a nutrient supplement cocktail, announce
its efficacy on social media and news outlets, sell to
patients online
d.Hearing rumors about the efficacy of a drug, touting
to the media and press that it cures a potentially lethal
disease, and strong-arming the FDA to cross-indicate
the drug for the lethal disease by passing emergency
approval of the drug before clinical trials are finished
14. 3.What is the
therapeutic
mechanism of
action of the
non-steroidal
anti-inflammato-
ry drug
ibuprofen? What
