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Medicinal Chemistry > Lectures 12, 13, 14, and 15 > Flashcards

Lectures 12, 13, 14, and 15 Flashcards

1
Q

What are the functions of beta 1 receptors?

A

Stimulate renin release in kidney and increase heart rate and contractile force of heart

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2
Q

What are the functions of beta 2 receptors?

A

Stimulate vasodilation of skeletal muscle and bronchodilation of lungs

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3
Q

What conformation do noradrenaline and adrenaline bind to an adrenergic receptor?

A

Trans conformation (w/ respect to nitrogen and beta OH)

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4
Q

Which absolute configuration is preferred in the adrenergic receptor?

A

R absolute configuration

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5
Q

What must be done to make a beta antagonist?

A
  • Retain high affinity for beta receptor
  • Eliminate intrinsic activity
  • Have higher affinity for beta vs. alpha receptors
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6
Q

What effect do isopropyl and t-butyl have on alpha and on beta receptors?

A
  • Alpha receptors – decrease potency

- Beta receptors – increase potency

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7
Q

What does an isopropyl N-substitution do?

A

Confers beta selectivity

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8
Q

What does addition of a sulfonamide to the meta position do?

A

Makes the molecule resistant to COMT, but still only a partial agonist

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9
Q

What does a para sulfonamide plus an isopropyl group do?

A

Makes the compound a weak antagonist

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10
Q

Is pronethalol or propranolol used more often and why?

A

Propranolol b/c pronethalol is toxic and possibly carcinogenic

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11
Q

What is the difference btwn arylethanolamine and aryloxypropanolamine?

A

Position of attachment of ethanolamine or oxypropanolamine w/ respect to ring substituents

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12
Q

Are arylethanolamines or aryloxypropanolamines more potent?

A

Aryloxypropanolamine

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13
Q

What are aryloxypropanolamines used for?

A

Binding to beta receptors

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14
Q

Does a t-butyl group produce beta 2 antagonist selectivity?

A

No, only beta 2 agonist selectivity

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15
Q

What effect do para substitutions of aryloxypropanolamines have?

A
  • Confer beta 1 vs beta 2 selectivity, so can produce cardioselective beta 1 antagonists
  • Must be single para substitutions
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16
Q

For arylethanolamine, the active isomer is ___

A

R and D

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17
Q

For aryloxypropanolamine, the active isomer is ___

A

S and D

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18
Q

How can effects of competitive antagonists of beta 1 (and sometimes beta 2) receptors be overcome?

A

Increased noradrenaline or adrenaline

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19
Q

What are some effects of beta antagonists?

A
  • Decrease heart rate, stroke volume, and force of contraction => decrease blood pressure
  • Decrease renin release in kidney (may be secondary mechanism to decrease BP)
  • Decrease intraocular pressure by decreased production of aqueous humor (used to treat glaucoma)
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20
Q

What effect do non-selective beta antagonists have on the lungs?

A

Can cause bronchoconstriction and precipitate an asthmatic attack in those w/ asthma

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21
Q

What makes the beta antagonists classified as class 2 antiarrythmic agents?

A

MSA (membrane stabilizing activity) or local anesthetic effect

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22
Q

In which beta antagonists is MSA higher?

A

Those w/ high LogP

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23
Q

When are MSA effects seen w/ beta antagonists?

A

At doses higher than what is needed for beta antagonist activity

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24
Q

What is the MSA of propranolol?

A

Potent MSA b/c can penetrate BBB and cause CNS effects

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25
Q

Nadolol is like the ___ version of propranolol

A

Hydrophilic

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26
Q

What is timolol mostly used for?

A

Glaucoma tx as eye drops

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27
Q

What is bunolol mostly used for and what is significant about it?

A
  • Glaucoma tx as eye drops

- One of the few beta antagonists that come as S isomer only

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28
Q

Which beta antagonists are arylethanolamines?

A

Sotalol and labetalol

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29
Q

What is pindolol used for? Does it have MSA?

A
  • Hypertension tx and as an adjuvant for depression tx

- Has MSA

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30
Q

What is a common characteristic of the structure of selective beta 1 antagonists?

A

Single para substituent that is typically an aliphatic straight chain and hydrophobic

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31
Q

Which beta 1 antagonists have MSA?

A
  • Metoprolol
  • Acebutolol (some MSA)
  • Betaxolol (some MSA)
  • Bisoprolol
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32
Q

What effect does an sp2 hybridized NH in the meta position have?

A

Provides partial agonist activity but keeps competitive antagonist activity

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33
Q

What is labetalol used for?

A

Tx of high BP and heart rate

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34
Q

Is labetalol used often? Why or why not?

A

No b/c is a beta 1, beta 2, and alpha 1 antagonist

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35
Q

What is the main use of carvedilol?

A

Seen to decrease morbidity and mortality in heart failure and in post-acute MI patients

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36
Q

What are uses of beta blockers?

A
  • High blood pressure (not first line, and use is decreasing)
  • Arrhythmias (generally safe but not effective for prevention)
  • Heart failure
  • Angina*
  • MI/heart attack (life saving drug both during MI and for tx after)
  • Glaucoma*
  • Migraines (rare)
  • Tremors (rare b/c condition is rare)
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37
Q

What are some side effects of beta blockers?

A
  • Fatigue
  • Bronchospasm (only w/ asthmatics on non-selective beta blockers)
  • Cold extremities
  • Left ventricular insufficiency
  • GI (nausea, vomiting, diarrhea, abdominal pain)
  • CNS effects (hydrophobic beta blockers)
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38
Q

What are contraindications of beta blockers?

A
  • Asthma (beta 1 selective are fine)
  • Bradycardia
  • Diabetics (sometimes)
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39
Q

What effect does LogP have on a beta antagonist?

A

Increased LogP = increased hepatic metabolism, decreased t1/2, decreased urinary excretion of unchanged drug, and decreased bioavailability

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40
Q

What type of metabolism can aryloxypropanolamines undergo?

A
  • N-dealkylation (removal of isopropyl or t-butyl) => inactive metabolite, which can be oxidized by MAO
  • Aromatic hydroxylation => active metabolite
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41
Q

What is significant about esmolol?

A

Beta 1 antagonist that is metabolized by esterases, which decreases t 1/2 and allows HCP’s to have tight control over effect (rapid onset and quick elimination)

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42
Q

What is esmolol used for?

A

As continuous infusion for atrial fibrillation

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43
Q

Describe acebutolol metabolism?

A

Acebutolol (active) – amidase –> inactive – NAT –> diacetolol (active)

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44
Q

Acebutolol and diacetolol are ___ selective antagonists

A

Beta 1

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45
Q

What is different btwn diacetolol and acebutolol?

A

Diacetolol has longer t 1/2 and is found in higher concentration in plasma and has partial agonist activity

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46
Q

What should be given to a px that is having an MI or had an MI?

A

Beta blocker!!

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47
Q

Where and when is renin released?

A

Kidneys when BP sensing cells detect a decrease in BP

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48
Q

What is the function of angiotensin converting enzyme? How does it do this?

A
  • Converts angiotensin 1 into angiotensin 2 and makes bradykinin inactive
  • Cleaves histidine and leucine on C terminus to make angiotensin 2
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49
Q

What is the function of renin as an enzyme? How does it do this?

A
  • Converts angiotensinogen into angiotensin 1

- Cleaves valine and other aa’s on the C terminus to make angiotensin 1

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50
Q

What are the effects of angiotensin 2?

A
  • Vasoconstriction => increased BP
  • Increase ADH => vasoconstriction => increased BP
  • Increase ADH => increased H2O => increase blood volume, stroke volume, CO => increased BP
  • Increase aldosterone => increased Na+ and H2O and decreased K+ => increased BP
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51
Q

What are the effects of bradykinin?

A
  • Can increase prostaglandin synthesis => vasodilation

- Vasodilation => decreased SVR => decreased BP

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52
Q

What is another name for ACE and where is it primarily found?

A
  • Kininase 2

- Mostly found in lungs

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53
Q

What receptors does angiotensin 2 bind to and what does this cause?

A
  • Angiotensin 1 receptors (AT1)

- Causes vasoconstriction, increased release of aldosterone from adrenal cortex, and increased ADH

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54
Q

Angiotensin 1 receptors is G alpha __

A

q

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55
Q

What effects does the angiotensin 1 receptor have around the body?

A
  • Arterioles – vasoconstriction and increased BP
  • CNS – increase ADH
  • Adrenal cortex – increase aldosterone
  • Kidney - decrease renin through negative feedback
  • Cellular effects – increase phospholipase C, IP3, DAG, and intracellular calcium, and decrease K+ outflow
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56
Q

What are the ligands of angiotensin 1 receptor?

A

A2 and A3

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57
Q

What is the function of AT receptor blockers?

A

Prevent A2 from binding to AT 1 receptor

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58
Q

What are renin inhibitors used for?

A

Treating hypertension

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59
Q

What is the only approved renin inhibitor and what does it do?

A
  • Aliskiren
  • Mimics angiotensinogen, so blocks conversion of angiotensinogen into A1 => lower levels of A2 => decreased vasoconstriction, blood volume, and BP
  • Reversible competitive inhibitor
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60
Q

What is significant about teprotide?

A
  • First residue is a pyroglutamate (cyclic glutamate)
  • Has many proline residues that decreases proteolytic degradation
  • ACE inhibitor
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61
Q

What is a disadvantage to teprotide?

A

No oral bioavailability

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62
Q

What peptide can become the lead compound for developing a new drug from teprotide?

A

Ac-FAP (phenylalanine and proline)

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63
Q

What is an advantage and a disadvantage to Ac-FAP?

A

Binds to active site, but can be hydrolyzed by ACE

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64
Q

What effect does zinc have on Ac-FAP?

A

Polarizes the C=O bond, making it a better electrophile

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65
Q

What are S1, S1’, and S2’?

A

Binding pockets of ACE

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66
Q

What are disadvantages to captopril?

A
  • Causes taste disturbances and rashes
  • Can oxidize to form disulfide bonds
  • Very short t 1/2
  • Most problems attributed to high affinity zinc binding group SH (solution = dicarboxylate ACE inhibitors which replace SH w/ COOH)
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67
Q

What is significant about enalapril?

A

Pro-drug (catalyzed by esterases)

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68
Q

What is significant about lisinopril? (*common exam question)

A

Only ACE inhibitor that doesn’t need to be a pro-drug b/c di-zwitterion is electrically neutral

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69
Q

What are the dicarboxylate ACE inhibitors used for?

A
  • Heart failure
  • Hypertension
  • Acute and post-MI
70
Q

Which drugs are dicarboxylate ACE inhibitors?

A
  • Enalapril
  • Ramipril
  • Lisinopril
  • Quinapril
  • Perindopril
  • Trandolapril
71
Q

Phosphonate ACE inhibitors are metabolized by _____

72
Q

What are the uses of ACE inhibitors?

A
  • Hypertension (decrease SVR, dilate arteries, and BP decrease over long term)
  • Congestive heart failure (over time increase SV and CO, decrease remodeling of heart, and decrease sudden death and MI)
  • MI
  • Diabetes and renal failure
73
Q

What are some ACE inhibitor side effects?

A
  • Hypotension (esp. w/ first dose and captopril)
  • Cough
  • Hyperkalemia (not a problem w/ normal kidney function)
  • Acute renal failure
  • Fetopathic potential
  • Skin rash (more common w/ captopril)
74
Q

What usually causes the cough seen from ACE inhibitor use?

A

Increased bradykinin and/or prostaglandins in lungs

75
Q

How can the coughing side effect of ACE inhibitors be decreased?

A
  • Aspirin or iron supplementation

- Decrease dose or switch to ARB

76
Q

Can ACE inhibitors be taken during pregnancy?

77
Q

What do angiotensin 2 receptors blockers bind to?

A

AT1 receptors located at both vascular and adrenal sites

78
Q

When are angiotensin 2 receptors blockers used?

A

Px who need ACE inhibitor tx but can’t tolerate it

79
Q

____ was the first ARB

80
Q

What is important about losartan?

A

The carboxylate metabolite is 10-40x more potent than losartan itself

81
Q

What is losartan a competitive antagonist of and what does this cause?

A
  • Thromboxane A2 receptor

- Causes decreased platelet aggregation

82
Q

What is important about candesartan cilexetil?

A
  • More potent than losartan

- Pro-drug converted to candesartan by esterases

83
Q

What is important about telmisartan?

A

Only benzoic acid bi-phenyl ARB

84
Q

What is important about valsartan?

A

Only ARB w/ no imidazole or equivalent functionality

85
Q

Generally having more carboxylates will ____ oral absorption of a drug

A

Decrease (can get around this by adding an ester)

86
Q

What are some physicochemical properties of filtered components that should be considered?

A
  • MW below 50 kDa
  • Overall charge
  • Degree of plasma protein binding
87
Q

What are the 6 important regions of a nephron?

A

1) Proximal convoluted tubule
2) Descending loop of Henle
3) Thick ascending limb of loop of Henle
4) Distal convoluted tubule
5) Late distal tubule and collecting duct
6) Distal collecting duct

88
Q

Where are the major sites of water reabsorption?

A
  • Proximal convoluted tubule

- Distal collecting duct

89
Q

Where do carbonic anhydrase inhibitors work and what do they do?

A
  • Proximal convoluted tubule

- Convert H2CO3 -> CO2 and H2O in luminal membrane; does the opposite inside the proximal tubule cell

90
Q

What occurs in the proximal convoluted tubule?

A
  • Antiport sends Na+ from luminal membrane into proximal tubule cell and H+ in the opposite direction
  • Symport sends Na+ and HCO3- from proximal tubule cell out to basolateral membrane
  • ATPase brings K+ into cell and Na+ out to basolateral membrane
91
Q

What occurs in the descending loop of Henle?

A
  • Surrounding medullary interstitium has high [Na+] compared to luminal fluid entering the loop of Henle
  • 15% of water from luminal fluid is drawn out by osmosis into interstitium and subsequently reabsorbed into bloodstream
92
Q

Luminal fluid is _____ as it flows through descending loop of Henle

A

Concentrated

93
Q

What occurs in the thick ascending limb of loop of Henle?

A
  • Na+/K+/2Cl- symporter
  • Passive channel transports K+ out to basolateral membrane and luminal membrane
  • ATPase pumps Na+ out to basolateral membrane and K+ inside loop of Henle
  • Passive transporter of Cl- to basolateral membrane
94
Q

What inhibits the Na+/K+/2Cl- symporter in the ascending limb of the loop of Henle?

A

Loop or high-ceiling diuretics

95
Q

What is the major site of Na+ reabsorption?

A

Ascending limb of loop of Henle

96
Q

Why are the ascending limb of the loop of Henle and the distal convoluted tubule thick?

A

To be a barrier to H2O

97
Q

What occurs in the distal convoluted tubule?

A
  • Na+/Cl- symporter
  • Passive transporters of Cl- and K+ to interstitium
  • ATPase
98
Q

What inhibits the Na+/Cl- symporter in the distal convoluted tubule?

A

Thiazide and thiazide-like diuretics

99
Q

What occurs in the late distal tubule and collecting duct?

A
  • Passive Na+ transporter into cell

- Passive K+ transporters into luminal fluid and interstitium

100
Q

Where does luminal fluid lead to?

101
Q

Where does interstitium lead to?

102
Q

What inhibits the passive Na+ transporter in the late distal tubule and collecting duct?

A

K+ sparing diuretics

103
Q

What does the late distal tubule and collecting duct dictate?

A

Final acidity and K+ content of urine

104
Q

What is the net water flow in the distal collecting duct?

A

From lumen -> interstitium

105
Q

What is aquaporin-2 and where is it found?

A
  • Found in distal collecting duct

- A water channel that passively reabsorbs water

106
Q

What occurs in the distal collecting duct?

A
  • Aquaporin-2
  • ADH binds to V2 (G alpha s), secreting adenylate cyclase, which releases cAMP to PKA and binding causes increased synthesis of aquaporin 2 channel
107
Q

What is the general function of diuretics?

A

Increase excretion of water from kidneys

108
Q

What are diuretics used for?

A
  • Edema (accumulation of fluid in interstitial spaces)

- Hypertension** (decrease blood volume, venous return, CO, and BP)

109
Q

What are present in almost all diuretics?

A

Sulfonamides, so px w/ sulfa allergies can’t take diuretics

110
Q

What is the most common thiazide diuretic?

A

Hydrochlorothiazide

111
Q

Are thiazide diuretics used as monotherapy?

112
Q

Describe the thiazide paradox

A
  • One acute effect of thiazides is decrease in blood volume
  • Blood volume returns to normal w/in 4-6 weeks of thiazide initiation, but lowered BP is still maintained
  • Mechanism unknown (thought to mediate blood vessel relaxation => decreased SVR)
113
Q

What is the difference btwn thiazide and thiazide-like drugs?

A

Thiazide-like drugs have an amide instead of a sulfonamide

114
Q

What are some thiazide-like drugs?

A
  • Metolazone
  • Indapamide
  • Chlorthalidone
115
Q

What extends the duration of metolazone?

A

It binds to carbonic anhydrase in erythrocytes, which acts as a reservoir of drug, extending duration

116
Q

What are some side effects of thiazide and thiazide-like drugs?

A
  • Loss of Na+, Cl-, K+, and water
  • Hypokalemia (dose dependent)
  • Hyperuricemia could precipitate gout
  • Hyperglycemia (dose dependent)
117
Q

What is the function of loop or high-ceiling diuretics?

A

Inhibit Na+/K+/2 Cl- symporter in thick ascending limg of loop of Henle => massive loss of Na+, K+, Cl-, and water

118
Q

What are loop or high-ceiling diuretics mostly used to treat?

A

Edema (especially w/ heart failure)

119
Q

What are 2 loop or high ceiling drugs?

A
  • Furosemide

- Bumetanide

120
Q

Are loop or high ceiling drugs used for hypertension?

121
Q

What are some side effects of loop or high ceiling drugs?

A
  • Hypokalemia
  • Hyponaturemia
  • Hypochloremia
  • Dehydration
  • Hyperuricemia could precipitate gout
  • Ototoxicity (rare and usually reversible)
122
Q

What is the function of potassium sparing diuretics?

A

Inhibit passive Na+ transporter in late distal tubule and collecting duct => modest diuresis

123
Q

What are 2 examples of potassium sparing diuretics?

A

Amiloride and triamterene

124
Q

What are potassiums sparing diuretics mostly used for?

A

To counteract hypokalemia from thiazide and loop diuretics (triamterene supplied in combination products w/ HCTZ)

125
Q

What is the function of aldosterone in the late distal tubule?

A

Increases expression of passive Na+ transporter and Na/K ATPase => increased Na+ and decreased K+ reabsorption

126
Q

What is used for aldosterone insufficiency?

A

Fludrocortisone

127
Q

What is spironolactone?

A

Mineralocorticoid receptor antagonist (K+ sparing diuretic)

128
Q

When is spironolactone given?

A

W/ thiazide or loop diuretics to decrease risk of hypokalemia

129
Q

What is hemostasis?

A

Natural process to prevent blood loss from a damaged blood vessel

130
Q

What is an embolism?

A

Thrombus migration (in brain = stroke; in heart = MI)

131
Q

What is the general process of hemostasis?

A

Tissue injury -> vasoconstriction -> primary hemostasis, platelet aggregation -> secondary hemostasis, coagulation

132
Q

What occurs in primary hemostasis?

A
  • Platelets adhere to injured blood vessel
  • Platelets aggregate primary hemostatic plug
  • Platelets stimulate coagulation factors
133
Q

What occurs in secondary hemostasis?

A
  • Coagulation cascade starts
  • Fibrin clot forms
  • Reinforces primary hemostatic platelet plug
134
Q

What causes platelet adhesion?

A

GP1a/2a and GP1b are receptors that bind to collagen and von Willebrand factor (respectively), causing platelets to adhere to sub-endothelium of a damaged blood vessel and become activated

135
Q

What do adherent platelets release?

A

Substances that activate nearby platelets and recruit them to the site of injury

136
Q

What forms the primary hemostatic plug?

A

Activated platelets

137
Q

What initiates the coagulation system?

A

Tissue factor, which is in the subendothelium, via the extrinsic coagulation pathway

138
Q

What is the coagulation cascade?

A
  • Series of steps that ultimately lead to fibrous reinforcement of the primary hemostatic plug
  • Series of clotting factors in a cascading activation
139
Q

What are clotting factors?

A

Serine proteases that recognize a very specific sequence, often 4-5 aa’s long

140
Q

What do clotting factors begin as?

A

Inactive form cleaved by another clotting factor to become active (this is indicated w/ an “a” after the factor)

141
Q

Does one protease activate only one clotting factor?

A

No, can activate many

142
Q

____ augment the activation of clotting factos

A

Phospholipids and Ca2+

143
Q

What does thrombin do?

A

Stimulates platelet activation and aggregation

144
Q

What are differences btwn the intrinsic and extrinsic pathways?

A
  • Intrinsic is slow (takes seconds to produce fibrin) and stays active longer
  • Extrinsic is rapid (takes milliseconds to produce fibrin) and stays active for less time
145
Q

How is the coagulation process stopped?

A

Endogenous inhibitors of coagulation factors

146
Q

What is the function of antithrombin?

A
  • Inhibits thrombin (2a), Xa, IXa

- Acts like a substrate for clotting factor, trapping it in an acyl-intermediate

147
Q

What does antithrombin require for activity?

A

Naturally produced heparins

148
Q

What is needed on heparin to bind to antithrombin?

A

In the A domain, a penta-saccharide minimum sequence

149
Q

What is the pharmacological use of heparin?

A

Stop blood coagulation

150
Q

What differentiates one heparin from another?

A

Number of monosaccharides, types of monosaccharides, and presence of charges on them

151
Q

What is the significance of the neutral region of heparin?

A
  • Not critical to interaction w/ antithrombin or thrombin
  • Suppressing charges in this region don’t affect anticoagulant activity, but can decrease undesired interactions (esp. w/ platelet proteins)
  • 2-3 disaccharide units
152
Q

What is the minimum chain length of heparin that is required for substantial thrombin inhibition?

A

16 saccharide units

153
Q

What is the function of the T-domain of heparin?

A
  • Binds to exosite 2 of thrombin, but only if total length of molecule is 16 saccharide units or more
  • Must be charged for binding to thrombin
154
Q

What are the various types of heparin?

A
  • Unfractionated heparin
  • Low molecular weight heparin
  • Synthetic heparin
  • Differ in mechanism of action, MW, pharmacokinetics, and side effects
155
Q

What is the size of unfractionated heparin?

A

18 or more mono-saccharides

156
Q

What is the function of unfractionated heparin on thrombin (IIa)?

A
  • Inhibits thrombin (IIa) by binding to antithrombin and an exosite 2 on IIa via negative charges at the end of the extended heparin chain
  • Called the bridging mechanism and increases the rate of reaction btwn IIa and antithrombin
  • Also induces a conformational change in RCL of antithrombin that increases rate of reaction btwn antithrombin and thrombin (conformational change mechanism)
157
Q

What is the function of unfractionated heparin on Xa?

A

Inhibits Xa by inducing conformational change in RCL of antithrombin that increases rate of reaction btwn antithrombin and Xa; requires binding by penta-saccharide to antithrombin

158
Q

What is the size of low molecular weight heparin?

A

Less than 18 mono-saccharides

159
Q

What is the function of low molecular weight heparin and synthetic heparin?

A

Inhibits Xa by inducing conformational change in RCL of antithrombin that increases rate of reaction btwn antithrombin and Xa (same as unfractionated heparin); requires binding by penta-saccharide to antithrombin

160
Q

What is the size of synthetic heparin?

A
  • 5 mono-saccharides (fondaparinux)

- Almost exactly the same as the Heparain penta-saccharide, except fondaparinux has an additional methy-group

161
Q

What is the ratio of anti-Xa:IIa for the various types of heparin?

A
  • Unfractionated – 1:1
  • Low molecular weight – 2-4:1 (inhibits Xa more)
  • Fondaparinux – >100:1
162
Q

What are the mechanisms of the various types of heparin?

A
  • Unfractionated= bridging and conformation

- Low molecular weight and fondaparinux = antithrombin conformation

163
Q

How is unfractionated heparin administered?

A

Continuous IV administration

164
Q

How is low molecular weight heparin administered?

A

Subcutaneous injection

165
Q

Can heparin be used in pregnancy?

166
Q

What drugs does heparin interact w/?

A
  • ASA, NSAIDs, dextran, dipyridamole, ticlopidine

- IV nitroglycerin decreases heparins anti-coagulation effect, so may need to use higher doses

167
Q

What are some side effects of heparin?

A
  • Bleeding
  • Heparin induced thrombocytopenia (more common in unfractionated)
  • Osteoporosis (very very rare)
  • Allergy
168
Q

What are the uses of heparin?

A
  • Prevent venous thromboembolism
  • Treat deep vein thrombosis
  • Prevent thrombosis during surgery, dialysis
  • LMWH SC injection where oral anticoagulants are contraindicated
  • MI (typically unfractionated via continuous IV)
  • May be used in pregnant px prone to miscarriages to prevent miscarriages (only LMWH or UFH w/o benzyl alcohol as a preservative)
169
Q

Which heparin has dose-dependent kinetics?

A

Unfractionated

170
Q

What is unique about the structure of carvedilol?

A
  • Has meta sp2 hybridized NH, but doesn’t produce partial agonist activity
  • No isopropyl or t-butyl substitution on N

Medicinal Chemistry (14 decks)

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