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PHAR 211 > Final > Flashcards

Final Flashcards

1
Q

What does metabolomics exclude?

A

enzymes, genetic material, structure molecules

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2
Q

What is the closest link to phenotype?

A

metabolomics

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3
Q

How does capiliary. electrophoresis work?

A

separate based on charge and partition coefficient

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4
Q

What can we do to speed up/ increase flow rate for Liquid chromatography?

A

sacrifice resolution

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5
Q

How do you calculate resolution?

A

R= (V2-V1)/(W1+W2/2)

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6
Q

What does it mean if R is >1.5?

A

good separation/resolution

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7
Q

What does particle size do to resolution?

A

smaller= better resolution

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8
Q

What can happen if high flow rate? Why?

A

loss of resolution due to back pressure

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9
Q

What is particle size for HPLC? WHat about flow rate?

A

5 microns
r8= 1ml/min

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10
Q

If column in LC is polar what happens?

A

polar things take longer to go through

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11
Q

What indicates the phase is non polar?

A

lots of carbons

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12
Q

What is difference between normal phase and reverse phase HPLC?

A

normal= stationary is polar
reverse= stationary is non polar

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13
Q

What is particle size for UPLC?

A

1.7-1.8 microns

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14
Q

For gas chromatography, what is the mobile phase?

A

gas- usually helium, H or N

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15
Q

For carrier gas what is pros and cons of each?

A

helium= best sensitivity, pricy
H= alright sense, flammable
N= bad sense but cheap

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16
Q

What is considered an abundant metabolite?

A

> 1 micro M

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17
Q

What is the database for metabolites?

A

HMDB

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18
Q

What is different between a targeted study vs a targeted?

A

target= know whats in sample

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19
Q

If someone is doing a metabolic fingerprint what can we assume?

A

dont know whats in it

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20
Q

What does metabolic profiling mean?

A

all involved in a disease state/ pathway

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21
Q

What is definition of pharmacometabolomics?

A

how metabolits change from a drug

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22
Q

WHat is path of biomarker discovery?

A

fingerprinting
then see if targets have
validation
clinical utility
approval

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23
Q

Why look at metabolomics?

A

fast, changes happen first before symptoms

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24
Q

What are the different matrixes for metabolomic study? pros and cons?

A

blood- easy but complex
Urine- not invasive, but different between age, gender
saliva= low amount
CSF- invasive
breathe- low concentration
tissue

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25
Q

Which matrixes are bad for proteomics?

A

urine and breathe

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26
Q

What makes antibodies?

A

B cells

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27
Q

Explain humoral immunity?

A

b cells bind to foreign and make antibodies
T cells bidn to antigen to kill
T helper bind to antigen and release cytokines to activate B and T cells

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28
Q

What is the structure of antibodies?

A

heterotetramer with 2 identical light and heavy chains

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29
Q

What portion of antibody binds to antigen and which binds to other cells?

A

Fab binds to antigen
Fc binds to cell

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30
Q

What do antibodies do?

A

neutralize, phagocytosis, lysis, NK

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31
Q

How are antibodies used in cancer?

A

stop angiogenesis= VEGFR and new interest in blocking checkpoints= nivolumab and iplimumab

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32
Q

Why can antibodies bind to many antigens?

A

diversity of CDR loops

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33
Q

How can we make a bunch of antibodies?

A

lots of immunoglobulin genes and recombination

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34
Q

What is the total diversity of antibodies in body?

A

> 1 billions

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35
Q

How can we produce (scientifically) antibodies?

A

humanized through hybridoma, through mice
bacteriophages
transgenic mice
human b cells

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36
Q

What has been a workhorse for protein engineering?

A

M13 bacteriophage

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37
Q

What is the success rate of MABs?

A

23% compared to 7% of small molecule drugs

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38
Q

How does bevacizumab work? How was it made?

A

stops VEGF= stop angiogenesis
made by humanized

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39
Q

How does mutations to Fc change function?

A

increase or decrease binding affinity

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40
Q

What are some bispecific antibodies mechanisms?

A

bridge two cells, double receptor inhibition/activation, piggybacck

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41
Q

What is a quadroma?

A

fuse two different hydroma to get bispecific
need advanced purification

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42
Q

What is knob-in holes tech?

A

mutate to get knob so that homodimerize doesnt happen so you get bispecific

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43
Q

What is cross mab tech?

A

knob to get proper bispecific but cross over happens on one of the heavy chain

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44
Q

What is the best success story of a bispecific antibody?

A

emicizumab for hemophilia

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45
Q

What is the most common site for bispecific antibodies?

A

PD1 and HER 2

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46
Q

How many approved bispecific antibodies?

A

3

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47
Q

Cons of antibodies?

A

high cost, poor penetration

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48
Q

Pros and cons of scaffolds?

A

Pros- low cost, better penetrate
cons- immunogenicity and poor stability

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49
Q

What is RNA interference? WHat is a key requirment?

A

gene silencing
requires dsRNA

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50
Q

What enzyme is needed to make silencing RNA from long dsRNA?

A

dicer

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51
Q

How do siRNA work?

A

promote degrade of mRNA

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52
Q

Where can dsRNA come from?

A

hairpin, complementary RNA

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53
Q

What is structure of siRNA?

A

21-23 nucleotide what a 2 nucleotide overhang on each 3 prime end

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54
Q

Where does siRNA act?

A

on RISC which cleaves the passenger strand and the guide strand stays on AGO part of RISC to bind to complementary mRNA to cleave

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55
Q

Which is another name for passenger and guide strands?

A

passenger= sense
guide= antisense

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56
Q

What is miRNA

A

micro RNA= ds stem loop

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57
Q

WHat is process of miRNA

A

miRNA gene transcribed= ds
cleaved by Drosha to get pre-miRNA
exportin 5 sends it to cytoplasm
dicer cuts off loop then it binds to RISC and loses passenger strand and same process

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58
Q

What is a key difference between miRNA and siRNA?

A

miRNA is not fully complimentary so it can bind to more sites
and miRNA passenger strand is discarded not cleaved

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59
Q

WHat is a key pro of RNAi therapuetics?

A

act on gene target more of all classes of proteins
and can go into cells

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60
Q

Cons of RNAi?

A

vulnerable to nucleases
poor stability
poor delivery because they cant permeate

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61
Q

What are a delivery system form for RNAi

A

viral vectors - Lentiviruses or AAV

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62
Q

Cons of viral vectors?

A

immunogenicity
expensive
mutagenesis

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63
Q

What are non viral delivery mechanisms?

A

polymer or lipid based

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64
Q

Which is more efficient Viral or non viral delivery?

A

viral

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65
Q

Where si the site of target for RNAi?

A

anywhere

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66
Q

What is CRISPR-cas9

A

genome editing

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67
Q

How many FDA approved CRISPAR?

A

1

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68
Q

How does CRISPR work?

A

cas 9 chops virus DNA/RNA, uses some of the pieces and inserts it to remember the virus
when it cuts we can add or delete

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69
Q

What causes sickle cell?

A

mutation in hemoglobin-beta gene in chromosome 11

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70
Q

How can we use CRISPR in sickle cell?

A

edit gene that supresses fetal hemoglobin (gamma) which replaces beta unit

71
Q

What is innate vs adaptive immunity?

A

Innate= first line rapid
Acquired- second line, memory

72
Q

What are the cells of innate immunity and what they do?

A

NK
dendritic
mast- histmaine
neutrophils- most
basophil- parasites
macrophages

73
Q

How can innate recog pathogens?

A

PRR-recog toxins
DAMP-see molecules released by damaged cells
detecting missing self- recog healthy

74
Q

Which cells have MCH 1 and 2

A

1= all nucleated cells
2- macrophages, dendritic and B cells

75
Q

What are the two divisions of adaptive immuntiy?

A

cell mediated- cytotoxic t cells
humoral-b cells

76
Q

What is path of t cell maturation?

A

made in marrow
m,ature in thymus

77
Q

What is CD4+ and CD8+ t cells?

A

4= t helper
8= cytotoxic

78
Q

How do you activate cytotoxic t cells?

A

APC stims proliferation
activate by bond between cytotoxic t cell and MHC 1 and need secondary signal from CD28
CD80 and CD86 are co stim

79
Q

WHat are T regs?

A

suppress immune response

80
Q

How can B cells be activated?

A

binds to antigen, T cell, memory or dendritic

81
Q

What do each Ig do?

A

IgA= stop bacteria and viruses, in gi and resp
IgD= activate B cells and basophils in mucosa
IgE=hypersensitivity
IgG= viruses and bacetria
IgM= for humoral response

82
Q

Which Ig is most predominant?

A

IgG

83
Q

Which Ig is biggest?

A

IgM

84
Q

Which Ig gets released first for humoral immunity?

A

IgM

85
Q

What are the opioid receptors?

A

mu
kappa
delta
NOP

86
Q

What are our endogenous opioids?

A

enkephalin
dynorphin
Sub P
endorphin

87
Q

How does acetaminophen work? What enzyme for metabolism

A

COX inhibitor in CNS, boosts endocannabinoid levels
metabolized by CYP 2E1- can make toxic

88
Q

How is NSAIDs metabolized?

A

CYP 2C9 and 2D6

89
Q

How do cannabinoids work?

A

trick brain into thinking less pain
stops inflammation

90
Q

What distinguished enogenous opiods from exongenous?

A

endogenous are peptides

91
Q

What do opioids and cannabinoids both do the same thing to limit pain?

A

block neurotransmitter release from presynaptic

92
Q

What polymorphisms at each opioid receptors?

A

mu= 118 A to G= less analgesia
kappa= 36 Gto T= addiction
delta= none

93
Q

What polymoprhisms for NSAIDs?

A

GG= rofecoxib better than ibu
GC or CC= ibu better

94
Q

WHat polymoprhisms for cannabinoids?

A

none for effect
G1359A= T2DM
AAT= more abuse

95
Q

WHat are the three general; gene polymorphisms?

A

Poor= loss of at least 2 alleles
Normal
Ultra= at least 3 coppies of alleles

96
Q

What polymorphisms for tylenol?

A

more CYP 2E1= more hepatotoxicity through NAPQI

97
Q

What enzyme metabolizes codeine?

A

CYP 2D6

98
Q

WHat are the only actionable polymorphisms?

A

2D6- for codeine and tramadol
and OPRM1-morphine

99
Q

What can polymorphisms of opioids look like?

A

drug seeking behaviour

100
Q

What type of cancer is CAR-T for?

A

liquid tumours

101
Q

What do helper t cells do?

A

differentiation of b cells

102
Q

What is the TCR-CD3 complex?

A

TCR binds to CD3epsilon gama to alpha unit, epsilon delta to beta unti and CD3 theta

103
Q

How do cytotoxic T cells perform funtion?

A

perforin to make pores on target
granzyme for apop
granulysin for pores in microbes

104
Q

How can cancer evade cytotoxic t cells?

A

downreg of MCH 1
downreg CD80
over express CD47

105
Q

How do you do CAR T therapy?

A

collect T cells and add chimeric gene, grow t cells and infuse

106
Q

What is CAR core (first generation)?***

A

scFv binds cancer antigen and CD3 theta to bind ZAP70 and activate t cell
Hinge, transmembrane domain

107
Q

WHat is scFv?

A

like antibody but only the variable region to bind antigens

108
Q

What are added to future generations of CAR T?

A

co stimulators of CD28, 4-1BB, NFAT, JAK-STAT

109
Q

WHat is second gen CAR T?***

A

CD28 also

110
Q

What is 3rd gen CAR T?**

A

CD28 + 4-1BB

111
Q

What is 4th gen CAR T?

A

also NFAT

112
Q

What is 5th gen CAR T?

A

JAK-STAT

113
Q

What does addition of CD28 do for CAR T?

A

cytotox and proliferation

114
Q

What does core CAR T actually do?

A

cytotoxic

115
Q

WHat does 3rd gen actually do for CAR T?

A

cytotox, proliferation and survival

116
Q

WHat are cons of CAR T?

A

long time, pricey, t cell exhaustion

117
Q

Do we use core CAR T at all?

A

FUCK NO

118
Q

How many CAR T therapies are approved?

A

6

119
Q

EXplain B lymphocyte antigen CD19?

A

biomarker for lymphoma and leukemia

120
Q

What does BCMA tell us?

A

biomarker for myelomas

121
Q

WHat is Kymriah for/What costimulator?

A

targets CD19 for
has 4-1BB

122
Q

What is Yescarta for/What costimulator?

A

targets CD19 for diffuse B cell lymphoma and follicular lymphoma
co stim of CD28

123
Q

WHat is Tecartus for/What costimulator?

A

targets CD19 for mantle lymphoma
Co stim of CD28

124
Q

WHat is breyanzi for/What costimulator?

A

targets CD19 for diffuse B cell lymphoma
co stim of 4-1BB

125
Q

WHat is abecma for/What costimulator?

A

Targets BCMA for multiple myeloma
co stim of 4-1BB

126
Q

In what stage of B cell development does CD19 expressed?

A

early

127
Q

What is carvykti for/What costimulator?

A

targets BCMA for relapsed multiple myeloma
4-1BB

128
Q

What costimulator is better for lymphoblastic leukemia?

A

4-1BB

129
Q

Who made the first vaccine and what was it for?

A

Ed Jenner for small pox

130
Q

What is a therapeutic vaccine?

A

stim immune response who is already infected

131
Q

What is a tolerogenic vaccine?

A

against self antigens so auto immune

132
Q

What are primary vs secondary lymph organs?

A

primary= marrow and thymus
secondary= nodes, spleen

133
Q

Explain the adaptive immune response?

A

dendritic present antigens to t helper, t helper mature and activate other t cells and b cells to make memory cells an d mount a better response

134
Q

Does a protein antigen ellicit a good immune response?

A

NO- need adjuvant

135
Q

How do Dendritic cells know self vs non self?

A

PAMPs on invaders and PRR on human cells

136
Q

Pros of using adjuvants in vaccine?

A

increase immunogenicity, reduce amount of antigen or frquency of shots, improve efficacy

137
Q

What delivery systems for vaccine?

A

MF59, PLG

138
Q

What vaccines prevent cancer?

A

HPV, Hep b

139
Q

WHat therapeutic vaccines do we have?

A

BCG and Sipuleucel T and stimuvax

140
Q

Explain stimuvax vaccine.

A

targets 25 AA sequence of MUC-1 in cancer cells

141
Q

Are we concerned about Covid vaccine changing our genome?

A

no stays in cytoplasm and RNA vaccine are very easily degraded

142
Q

What are inhibitory immune checkpoint molecules?

A

CTLA-4 (CD152) and PD-1

143
Q

What is CTLA-4?

A

binds CD80 and 86 or called B7, if blocked immune system will kill cancer cells

144
Q

WHat other site competes with CTLA-4?

A

CD28

145
Q

When is CTLA-4 highly present?

A

if cell exposed to antigen

146
Q

What happens if PD-1 and PD-L1 bind?

A

stops immune response

147
Q

How does iplimumab work?

A

CTLA-4

148
Q

How does Tremelimumab work?

A

CTLA-4

149
Q

WHat are the PD-1 drugs

A

Pembrolizumab
Nivolumab
Cemiplimab

150
Q

WHat are the PD-L1 drugs?

A

Atezolizumab
Avelumab
Durvalumab

151
Q

Most common ADRs of checkpoint inhibitors?

A

rash, diarrhea, fatigue
skin, chest, liver, renal disease
diabetes

152
Q

What is pseudo progression?

A

response after intitial increase in volume of cancer

153
Q

What is hyper progression?

A

acceleration of tumor growth during inhibition of checkpoints

154
Q

How does relatlimab work?

A

LAG-3 or CD223

155
Q

What is the most common form of cancer in women?

A

breast

156
Q

What is treatment of stage 1 Breast cancer?

A

Surgery
or radiation

157
Q

What is treatment of stage 2 breast cancer?

A

Surgery
radiation
chemo= AC-T, T AC, CAF

158
Q

WHat is treat of stage 3 breast cancer?

A

chemo, targeted, surgery

159
Q

What is treat of stage 4 breast cancer?

A

hormonal, chemo, targeted

160
Q

What causes the signalling of cancer from HER 2?

A

dimer with itself or EGFR

161
Q

What is MOA of trastuzumab?

A

subdoamin 4 of HER 2

162
Q

What is MOA of pertuzumab?

A

subdomain 2 blocks dimerization

163
Q

What does margetuximab do?

A

igG antibody that binds to HER2

164
Q

What is T-DM1?

A

trastuzumab with emastine

165
Q

What is fam-trastuzumab deruxtecan?

A

deruxtecan is topoisomerase inhibitor to get death

166
Q

What does lapatinib do?

A

TK inhibitor that REVERSIBLY binds to BOTH EGFR and HER2

167
Q

What does Neratinib do?

A

irreversibly bind tk inhibitor

168
Q

What does tucatinib do?

A

reversible inhibitor of HER2

169
Q

WHat are the CDK4 inhibitors?

A

palbociclib
ribociclib
abemaciclib
all stop cell going past R point

170
Q

How does everolimus work?

A

mTOR inhibitor

171
Q

How does Alpelisib work?

A

alpha specific PI3K inhibitor for patients with PIK3CA mutation

172
Q

How do olaparib / parib drugs work?

A

block DNA repair in cancer cells - DOESNT TARGET NORMAL CELLS

173
Q

Which is more efficient talazoparib or olaparib?

A

talazoparib

174
Q

What is therapy for triple negative cancer and what does it target?

A

sacituzumab govitecan
targets Trop-2

PHAR 211 (2 decks)

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