PRINCIPLES
TARGEIS
FOR
DRUG
ACTION
phavmacoiogy
body And
drugs their
interautions
with of
Stndy
majordivisions
of pharmaulogy
pharmokinetits f
to drug
does
drng +ne
whatbody
andmovementofthe
alferation bythe
drng of
body
abSorption
From
thesiteof administration
Intotheblood
distribution
bloodstream
from
metabolism.
reversibly tothe
distribute interstitial
fluids
dvnqis detoxified orinautivated climination
excvetion
pharmacodynamics y
whatdvug doesto body
beneficialandharmtui
etfect @ppropnate determine
the
mechanismof action range0oSlfoy patients
targetsfor drngaction
receptors
chemicai
endogenous andrespondtD
signalsrecognise
agonists
toachieve
veceptor activation
altivate
receptoY
1001ligand
(endogenous)
> binds a
no
antagcnists
toayeleptor
prodncesbinds
(exogenons)
when
effect it ligandth0t a
block+eactionof agonists
Salbutamol
( bvonchodilator) (anaigesic) codeine
n gonists
receptoy
adregenic ßz receptoropiod
channels
10n2,
Itdocaine(localanaesthetic) ( Sedative)diazepam
blocks
(90 promotes
Antagonist
opening
Natchannel modmatoys
channelCI*
cavviers 3.
omedrazole
(Anti-nicer) fluoxetine
(antidepressant)
Ihibits inhibits
protonpumpthatpvodnces seydtonivi
q0stvicacid
vempt fvd ake of
cleft
Synaptic
m
©olivia_liying
, 4. enzumes
(anaigesic) aspirin 5-finoronraul
lanti-Cancer)
Inhibits
inhibits
that prodnce
cyuiodxygenase (repiaces urauilin puxine b;
intlammatovy mediators thymidyiate
Synthase
*t
pentcillin ( antibiotics)
interautions
Withtayget
inhibrts dyn?
sh ape
transpeptidase that form lock- and-key
bacteviau cemwall inducedHit
charge distribntion
tupe of bonds
false snostrate
(weakest) VAn
waals dev
v
Co abnormalmetabolite
prodnced covavent
bonds
lstnngest)
-
prodvng
nutivedrug AN.medication
thatis inactivenntil metabolized
into
reduce side effeit
vesistant
dissolvrnq and
Cynshing to
impvove phaymacokinetits
Bo nttive dvug
receptors
ligand aated
Ton
channels
ionotropic receptor
whenopen andaltow iondiffusion
divect action milliseconds
todvnalmgonist),
bind wim
channel
AcH nicotine
canses
skeietal muscletocontralt) CACH
nicotinic receptor huperpolavisation ordepolarisation
Signaitransdnition
G veceptor coupledpvdtein
metabotropic reueptor
subi
polypeptide &BA
nitstransmembrane
bindwithGDP
Subunit) (d
helites Y a
-
protein G
Gs
Stimmiatov AC>cAmpactivates
channels Calt
activates
Gitt
adenylyicyciase
inhibitovy
inhibltsadenylyicyciase
Ac--
aitivates
Ktchanneis
Gl
'activates C
phospholipase hydyolyzed
GDP GTP
©olivia_liying ond subnnit
restingstate
when drngIongerpresent, reverts
thereveptor nDiSTD
dealtivatedACiS
,••.
fast in aution( seconds)
AcH muscavine
-
mnstarinic
veceptor smooth
mnscie
contraltion
adyenoreceptor
a1 adrenaline agonistlvasoconstriution)
(blodd vesser) musuie brazosin
Smooth antagonist
ola
CNSmenvons
BI bisoprotol antagonists
(heart muscie)
myocardium (+reat hypertension)
B: salbntamolagonist
smoothmnscie Chiood vessel,bronchus
llungs))
selective MOreto B2
enzyme
Ckinase)-linkedreceptors A
large extracelularligand-bindingdomain than BI
to intraceuuiqr domain
connetted
insmin
growth ( cancex
imatinib
fautors blocker,
growth inhibitor)
tyrosinekinase
l.ligandbindina
seif dimerization2. receptor serine, threonine
kinase
Cytokine receptor
gnanylyluyciase-linked
receptor
tyro Sine tyvosine minutes SI D in aition-
P ®
3. antophosphovyiation
enbughVlaY
4.phosphormiation
0ther ofvoteins
(signalcascade)
-
Nnclearorintraceiniarreueptor
CIASS vecepto Y sterdid
Ibcateoin cytoplasm
form homodimers
destro@en veceptor
lígands aveendocrine:
steroid
noymone
class II
located in nnclens hoymone
thyvoid
form heterddimers receptor
ligandsmetabolite lrgandlipids Ayelfatty auids)
8IoWin aution( hours)
gene Proteinsynthesistranscription
©olivia_liying
, ACTION
OF
DRUG
QUANTIFICATION 11
agonist And
doseresponse curve
curve
response gradeddose
or
.
patientresponse
collected
fromisorated animals 130SYONGN.
tissmes,
mensnredrespons e
ugainstdosingthemagnitnde
of
Emax
maximalresponse th e
indicates
theefticacy of agonist
of maximal
response Emax
k.
100 ED50
dose
effective 0+50°/-
poteny a
of gonistindicates
th e
50 -ED 50
=
half of Emax
EmAx 801.ED50basedon401.
=
•
kd(y- aris ). reteptorsKd
ocuupied)
equilibriumdissociation
Constant
which
concentyation 0tof
ngonist
I0 (D0 1000
agonist Concentration
10000
dose
avaiabie
decnpied
are
releptors 50:lofthe
ELD01 indruates
theaftinity of agonist
10-foldincrease unittoanother
fromone
affinitn
describes
thestrength
with aligandbinds
whith toreleptoy a
gveateraffinity lower
Kd
efficacy
ability ofAn
ALtiON
inducesconformational
oreleptoxtoevoke
agonisttoautivate
change
an
occupation nctivatio n
R AR AR->aLtiON
affimity efticacY
Mnactivated activated ngonist fMM
fun agonist paytial agonst
(AR+)nighefficaly higherEmax,
higherefticnly
partial agonist
lowefficacy(AR)
cannot
evoke
maximum
response,even
when theavailable
occupying all
veceptors
, ofadrngproduceaeffelt
potency
giventoamount
needed
lower
EC5o greater the
potency ofDlesser amonnt
maximaieffelt
toachieve
is needed haif
conc.
=
ED50
3 Dedose) ( C=
affinity tendto have
high
©olivia_liying
TARGEIS
FOR
DRUG
ACTION
phavmacoiogy
body And
drugs their
interautions
with of
Stndy
majordivisions
of pharmaulogy
pharmokinetits f
to drug
does
drng +ne
whatbody
andmovementofthe
alferation bythe
drng of
body
abSorption
From
thesiteof administration
Intotheblood
distribution
bloodstream
from
metabolism.
reversibly tothe
distribute interstitial
fluids
dvnqis detoxified orinautivated climination
excvetion
pharmacodynamics y
whatdvug doesto body
beneficialandharmtui
etfect @ppropnate determine
the
mechanismof action range0oSlfoy patients
targetsfor drngaction
receptors
chemicai
endogenous andrespondtD
signalsrecognise
agonists
toachieve
veceptor activation
altivate
receptoY
1001ligand
(endogenous)
> binds a
no
antagcnists
toayeleptor
prodncesbinds
(exogenons)
when
effect it ligandth0t a
block+eactionof agonists
Salbutamol
( bvonchodilator) (anaigesic) codeine
n gonists
receptoy
adregenic ßz receptoropiod
channels
10n2,
Itdocaine(localanaesthetic) ( Sedative)diazepam
blocks
(90 promotes
Antagonist
opening
Natchannel modmatoys
channelCI*
cavviers 3.
omedrazole
(Anti-nicer) fluoxetine
(antidepressant)
Ihibits inhibits
protonpumpthatpvodnces seydtonivi
q0stvicacid
vempt fvd ake of
cleft
Synaptic
m
©olivia_liying
, 4. enzumes
(anaigesic) aspirin 5-finoronraul
lanti-Cancer)
Inhibits
inhibits
that prodnce
cyuiodxygenase (repiaces urauilin puxine b;
intlammatovy mediators thymidyiate
Synthase
*t
pentcillin ( antibiotics)
interautions
Withtayget
inhibrts dyn?
sh ape
transpeptidase that form lock- and-key
bacteviau cemwall inducedHit
charge distribntion
tupe of bonds
false snostrate
(weakest) VAn
waals dev
v
Co abnormalmetabolite
prodnced covavent
bonds
lstnngest)
-
prodvng
nutivedrug AN.medication
thatis inactivenntil metabolized
into
reduce side effeit
vesistant
dissolvrnq and
Cynshing to
impvove phaymacokinetits
Bo nttive dvug
receptors
ligand aated
Ton
channels
ionotropic receptor
whenopen andaltow iondiffusion
divect action milliseconds
todvnalmgonist),
bind wim
channel
AcH nicotine
canses
skeietal muscletocontralt) CACH
nicotinic receptor huperpolavisation ordepolarisation
Signaitransdnition
G veceptor coupledpvdtein
metabotropic reueptor
subi
polypeptide &BA
nitstransmembrane
bindwithGDP
Subunit) (d
helites Y a
-
protein G
Gs
Stimmiatov AC>cAmpactivates
channels Calt
activates
Gitt
adenylyicyciase
inhibitovy
inhibltsadenylyicyciase
Ac--
aitivates
Ktchanneis
Gl
'activates C
phospholipase hydyolyzed
GDP GTP
©olivia_liying ond subnnit
restingstate
when drngIongerpresent, reverts
thereveptor nDiSTD
dealtivatedACiS
,••.
fast in aution( seconds)
AcH muscavine
-
mnstarinic
veceptor smooth
mnscie
contraltion
adyenoreceptor
a1 adrenaline agonistlvasoconstriution)
(blodd vesser) musuie brazosin
Smooth antagonist
ola
CNSmenvons
BI bisoprotol antagonists
(heart muscie)
myocardium (+reat hypertension)
B: salbntamolagonist
smoothmnscie Chiood vessel,bronchus
llungs))
selective MOreto B2
enzyme
Ckinase)-linkedreceptors A
large extracelularligand-bindingdomain than BI
to intraceuuiqr domain
connetted
insmin
growth ( cancex
imatinib
fautors blocker,
growth inhibitor)
tyrosinekinase
l.ligandbindina
seif dimerization2. receptor serine, threonine
kinase
Cytokine receptor
gnanylyluyciase-linked
receptor
tyro Sine tyvosine minutes SI D in aition-
P ®
3. antophosphovyiation
enbughVlaY
4.phosphormiation
0ther ofvoteins
(signalcascade)
-
Nnclearorintraceiniarreueptor
CIASS vecepto Y sterdid
Ibcateoin cytoplasm
form homodimers
destro@en veceptor
lígands aveendocrine:
steroid
noymone
class II
located in nnclens hoymone
thyvoid
form heterddimers receptor
ligandsmetabolite lrgandlipids Ayelfatty auids)
8IoWin aution( hours)
gene Proteinsynthesistranscription
©olivia_liying
, ACTION
OF
DRUG
QUANTIFICATION 11
agonist And
doseresponse curve
curve
response gradeddose
or
.
patientresponse
collected
fromisorated animals 130SYONGN.
tissmes,
mensnredrespons e
ugainstdosingthemagnitnde
of
Emax
maximalresponse th e
indicates
theefticacy of agonist
of maximal
response Emax
k.
100 ED50
dose
effective 0+50°/-
poteny a
of gonistindicates
th e
50 -ED 50
=
half of Emax
EmAx 801.ED50basedon401.
=
•
kd(y- aris ). reteptorsKd
ocuupied)
equilibriumdissociation
Constant
which
concentyation 0tof
ngonist
I0 (D0 1000
agonist Concentration
10000
dose
avaiabie
decnpied
are
releptors 50:lofthe
ELD01 indruates
theaftinity of agonist
10-foldincrease unittoanother
fromone
affinitn
describes
thestrength
with aligandbinds
whith toreleptoy a
gveateraffinity lower
Kd
efficacy
ability ofAn
ALtiON
inducesconformational
oreleptoxtoevoke
agonisttoautivate
change
an
occupation nctivatio n
R AR AR->aLtiON
affimity efticacY
Mnactivated activated ngonist fMM
fun agonist paytial agonst
(AR+)nighefficaly higherEmax,
higherefticnly
partial agonist
lowefficacy(AR)
cannot
evoke
maximum
response,even
when theavailable
occupying all
veceptors
, ofadrngproduceaeffelt
potency
giventoamount
needed
lower
EC5o greater the
potency ofDlesser amonnt
maximaieffelt
toachieve
is needed haif
conc.
=
ED50
3 Dedose) ( C=
affinity tendto have
high
©olivia_liying
