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Pharmacodynamics for Medical Students Part 1/3 by Dr. WIlliam K Lim
- 2. Drug administered to patient arrives at site of action produces an effect Pharmacokinetics & Pharmacodynamics
- 3. Drug administered to patient arrives at site of action produces an effect pharmacokinetics pharmacodynamics Pharmacokinetics & Pharmacodynamics
- 4. Pharmacology Pharmacokinetics Pharmacodynamics Adsorption * How does the drug Distribution interact with the cell? Metabolism * How does the drug Excretion cause a therapeutic effect? What the body does What the drug does to the drug to the body
- 5. Pharmacology Pharmacokinetics Pharmacodynamics Adsorption * How does the drug Distribution interact with the cell? Metabolism * How does the drug Excretion cause a therapeutic effect? What the body does What the drug does to the drug to the body
- 11. Concept of Receptor Patient takes drug gets better
- 12. Concept of Receptor Patient takes drug gets better What did the drug do to the body? ?
- 13. Concept of Receptor Some drugs do not require a receptor for their effect: e.g. antacid: - changes pH of stomach aspirin: - forms covalent bond with enzyme kaolin: - adsorbs toxin in the gastrointestinal tract
- 14. Concept of Receptor Many drugs work by first binding to a receptorā¦.
- 15. Concept of Receptor cell Drug Molecules Langley 1878: āDrug binds to a receptive substance on the cellā (drugs must first bind to a receptor to produce their action)
- 16. Concept of Receptor cell surface receptor cell drug molecules
- 17. Concept of Receptor cell surface receptor cell drug molecules
- 18. Concept of Receptor cell surface receptor cell drug molecules
- 19. Main Families of Receptors
- 21. Main Families of ReceptorsIon Channels (open up for ions to pass) G protein Coupled Receptors (intracellular part of the receptor activate or inhibit cellular proteins)
- 22. Main Families of ReceptorsIon Channels (open up for ions to pass) G-protein Coupled Receptors (intracellular part of the receptor activate or inhibit cellular proteins) Receptor Tyrosine Kinase (phosphorylate intracellular proteins) Intracellular Receptors (enter nucleus, promote gene transcription)
- 23. Ion Channel Nicotinic cholinergic receptor on muscle membrane
- 24. Ion Channel
- 26. G-protein Coupled Receptor Receptor G proteins MODERN DRUG DISCOVERY NOVEMBER 2004 p24-28 Receptor G proteins Inside the cell Outside the cell Hormone
- 27. G-protein Coupled Receptor Receptor G proteins MODERN DRUG DISCOVERY NOVEMBER 2004 p24-28 Inside the cell Outside the cell Activate or inhibit other proteins, leading to final effect e.g. muscle contraction, enzyme secretion, etc.
- 29. Quantitation of Drug-Receptor Interactions ā¢ Drug acts on the cell by first binding to a receptor
- 30. Quantitation of Drug-Receptor Interactions ā¢ Drug has an affinity for its receptor e.g. drug A binds receptor A, not receptor B A B Drug A Receptor A Receptor B
- 31. Drug-Receptor Binding D = Drug R = Receptor D + R DR
- 32. Drug-Receptor Binding D = Drug R = Receptor D + R DR Effect
- 33. Drug-Receptor Binding D = Drug R = Receptor D + R DR Effect Principle: Drug-receptor binding follows the Law of Mass Action:
- 34. Drug-Receptor Binding D = Drug R = Receptor D + R DR Effect Principle: Drug-receptor binding follows the Law of Mass Action: ā¢ D and R bind after they collide randomly
- 35. Drug-Receptor Binding D = Drug R = Receptor D + R DR Effect Principle: Drug-receptor binding follows the Law of Mass Action: ā¢ D and R bind after they collide randomly D + R DR ā¢ After binding, D can dissociate from R D + R DR
- 36. Drug-Receptor Binding D = Drug R = Receptor D + R DR Effect At equilibrium, ( or ) association rate = dissociation rate
- 37. Drug-Receptor Binding D + R DR ā¢ At equilibrium, some of the D is binding to R
- 38. Drug-Receptor Binding D + R DR ā¢ At equilibrium, some of the D is binding to R ā¢ If the number of R is constant, then if D increases, DR also increases D + R D R D+ R DR
- 39. Drug Dose/Concentration & Receptor Binding D + R DR Plot DR versus D: 100% 0 50% DR ( % of Receptor bound to Drug) D (Drug Concentration)
- 40. Drug ā Receptor binding experiment Receptor (in cell membranes) + drug Wait for equilibriumā¦ā¦
- 41. Drug ā Receptor binding experiment - - - - - - - - - - - - - - - - - - - - - drugBound ā R-- filter drugFree After equilibrium:
- 42. Drug ā Receptor binding experiment - - - - - - - - - - - - - - - - - - - - - drugBound ā R-- filter After equilibrium: measure radiation on filter paper
- 43. mg/mL drug 0.1 1 10 100 Wash over filter paper - - - - - - - - - - - - - - - - - - - - -
- 44. mg/mL drug 0.1 1 10 100 - - - - - - - - - - - - - - - - - - - - - measure radiation on filter paper
- 45. Drug Dose/Concentration & Receptor Binding D + R DR Plot DR versus D: 100% 0 50% DR ( % of Receptor bound to Drug) D (Drug Concentration)
- 46. Drug Concentration & Receptor Binding D + R DR Plot a graph of DR against D: D (Drug Concentration) [or amount] DR ( % of Receptor bound to Drug) 100% 0 50%
- 47. Drug Concentration & Receptor Binding D (conc) B (% Bound) 100 50 0 Rectangular Hyperbolic Curve
- 48. Drug Concentration & Receptor Binding D (conc) B (% Bound) ā¢ Equation: B (amt bound) Bmax . D D + Kd 100 50 0 Rectangular Hyperbolic Curve
- 49. Drug Concentration & Receptor Binding D (conc) B (% Bound) ā¢ Equation: B (amt bound) Bmax . D D + Kd ā¢ Kd = dissociation constant - concentration of drug when 50% of the receptors are bound. 100 50 0 Rectangular Hyperbolic Curve
- 50. Drug Concentration & Receptor Binding D (conc) B (% Bound) ā¢ Equation: B (amt bound) Bmax . D D + Kd ā¢ Kd = A measure of affinity of drug for receptor Every drug that can bind a receptor has a Kd value for that receptor. 100 50 0 Rectangular Hyperbolic Curve
- 51. Drug Concentration & Receptor Binding D (conc) B (% Bound) ā¢ Equation: B (amt bound) Bmax . D D + Kd ā¢ Kd = A measure of affinity of drug for receptor The higher the affinity, the smaller the Kd 100 50 0 Rectangular Hyperbolic Curve
- 52. Drug Concentration/Dose & Receptor Binding D (Drug conc) (or amount, mg) B (% receptor bound) 100 50 0 0 10 20 30 40 50 (mg/mL)
- 53. Drug Concentration/Dose & Receptor Binding B (% receptor bound) 100 50 0 0 10 20 30 40 D (Drug conc) (mg/mL)
- 54. Drug Concentration/Dose & Receptor Binding B (% receptor bound) 100 50 0 0 10 20 30 40 D (Drug conc) (mg/mL) Kd = 10 mg/mL
- 55. Drug Concentration/Dose & Receptor Binding B (% receptor bound) 100 50 0 0 5 10 20 30 40 D (Drug conc) (mg/mL) Drug A Drug B
- 56. Drug Concentration/Dose & Receptor Binding B (% receptor bound) 100 50 0 0 5 10 20 30 40 D (Drug conc) (mg/mL) Drug A Drug B Kd (Drug A) = 10 mg/mL Kd (Drug B) = 5 mg/mL
- 57. Drug Concentration/Dose & Receptor Binding B (% receptor bound) 100 50 0 0 5 10 20 30 40 D (Drug conc) (mg/mL) Drug A Drug B Kd (Drug A) = 10 mg/mL Kd (Drug B) = 5 mg/mL The higher the affinity, the smaller the Kd
- 58. Drug Concentration/Dose & Receptor Binding B (% receptor bound) 100 50 0 0 5 10 20 30 40 D (Drug conc) (mg/mL) Drug A Drug B Drug B has a higher affinity for the receptor than Drug A, so Kd for drug B is smaller. Kd (Drug A) = 10 mg/mL Kd (Drug B) = 5 mg/mL
- 59. Drug Concentration/Dose & Receptor Binding ā¢ Kd = dissociation constant : concentration of drug when 50% of the receptors are bound. = A measure of affinity of drug for receptor - The higher the affinity, the smaller the Kd
- 61. Drug Dose/Concentration & Response/Effect Free drug Drug binding to receptor Effect of receptor binding
- 62. Drug Dose ā Response experiment Add drug to cells Measure Ca2+ released
- 63. Drug Dose ā Response experiment Add drug to cells Measure Ca2+ released Measure Ca2+ released Measure Ca2+ released
- 64. Drug Dose/Concentration & Response/Effect D + R DR Response/Effect (Response Curve)(Binding Curve)
- 65. Drug Dose/Concentration & Response/Effect D + R DR Response/Effect Response (% max) Drug Dose or Conc 100 50 0 A ādose response curveā
- 66. Drug Dose & Response/Effect D + R DR Response (ED50) ED50 (effective dose 50%) = drug dose that give 50% of maximum response Response (% max) Drug Dose 100 50 0 A ādose response curveā
- 67. Drug Dose & Response/Effect D + R DR Response ED50 (effective dose 50%) or EC50 (effective conc 50%) =drug dose or conc giving 50% of max response Response (% max) Drug Dose or Concentration 100 50 0 A ādose response curveā
- 68. Drug Dose & Response/Effect D + R DR Response Every drug that can bind a receptor to produce a response has a EC50 or ED50 value for that response Response (% max) Drug Dose or Concentration 100 50 0 A ādose response curveā
- 69. Drug Dose & Response/Effect (ED50) Response (% max) Drug dose 100 50 0 A ādose response curveā Plotting response versus dose: a rectangular hyperbolic curve Drug concentration(EC50)or
- 70. Drug Dose & Response Plotting drug dose/concentration using log scale instead of arithmetic/linear scale
- 71. Drug Dose & Response 100 50 0 Log dose Response (% max) -9 -8 -7 -6 -5 -4 Plotting response versus log dose (or log conc):
- 72. Drug Dose & Response Plotting response versus log dose (or log conc): sigmoidal log-dose response curve 100 50 0 Log dose Response (% max) ā¢ Most important type of graph in pharmacology: ā¢ For comparing different drugs -9 -8 -7 -6 -5 -4
- 73. Drug Dose & Response 100 50 0 Response % Response % [Drug Dose] 100 50 0 (arithmetic scale) (log scale)
- 74. Drug Dose & Response 100 50 0 Response % Response % [Drug Conc] 100 50 0 (arithmetic scale) (log scale) Reasons to plot semi-log dose-response curves: ā¢ Easier to interpret: expands the scale at low concentrations
- 75. Drug Dose & Response 100 50 0 Response % Response % [Drug Conc] 100 50 0 (arithmetic scale) (log scale) Reasons to plot semi-log dose-response curves: ā¢ Easier to interpret: expands the scale at low concentrations
- 76. Drug Dose & Response 100 50 0 Response % Response % [Drug Conc] 100 50 0 (arithmetic scale) (log scale) Reasons to plot semi-log dose-response curves: ā¢ Easier to interpret: and compresses the scale at high concentrations.
- 77. Drug Dose & Response 100 50 0 Response % Response % [Drug Conc] 100 50 0 (arithmetic scale) (log scale) Reasons to plot semi-log dose-response curves: ā¢ Easier to interpret: ā¢Linear between 20 to 80% of maximal response - the dose range of drugs most commonly studied
- 78. Summary ā¢ Definition of pharmacodynamics ā¢ Concept of receptor ā¢ Concept of affinity of a drug for a receptor ā¢ Drug binding curve: definition of Kd ā¢ Dose response curve: definition of ED50(orEC50) ā¢ Plotting log dose-response curves
- 79. ā¢ What is potency? ā¢ What is efficacy? ā¢ What is an agonist? ā¢ What is an antagonist?
Editor's Notes
- 2013 contd good feedback as lecturer, mention during lect which curve get which data, in revision class show all wrong interpretation cos cannot get Kd from response curve etc. Made EOB SEQ on which drug higher affinity from this curve (its response curve) and which more potent/effic- 121 students- max 15 marks, 7 got either 1 or 0 mark. Only 4 (3.3% of students) got 12 marks or more (able to say this curve cannot get affinity info: Yap Wen Nee, viviene jane, dylan harry, chai chang xian. Ave mark 5.4 (fail) 2013 45 min. no interaction, just give analogies- affinity for food, students bump into chairs, sit and stand. One asked is dose response related to michaelis menten enzyme kinetics- reaction rate v increases with substrate conc. Max is vmax, and substate conc for half Vmax is Km. http://medicaltextbooksrevealed.s3.amazonaws.com/files/11189-53.pdf āThe same mathematical relationships that define how a drug (ligand) interacts with a receptor to elicit or diminish a biological response also governs the ways in which substrates (ligands) interact with enzymes to generate metabolic end products. In fact, the terms KD and Emax (ceiling effect) can easily be redefined as Km and Vmax, which you recall from Michaelis-Menten enzyme kinetics.ā āDose ā response curves and enzyme kinetics. These are the same. The familiar dose-response curves are based on the Michaelis ā Menten model of enzyme substrate interactionā. http://www.frca.co.uk/article.aspx?articleid=101185. a dose response curve can obey first order Hill equation (Hill coefficient = 1) A first-order Hill function (means no cooperativity- binding of ligands are independent of each otherās binding) is sometimes called a Michaelis-Menten function). āThe fact that dose-response curves varied so much made pharmacology different from biochemistry. The concentration of a drug which produced a half-maximum response from a tissue, EC50, was not constant: with powerful agonists a maximum response was produced from the activation of only a small proportion of receptors.āhttp://www.pa2online.org/articles/?volume=1&issue=2. āSo the dissociation constant is a measure of the affinity of the drug for its receptor, just like the Michaelis-Menten constant (Km) is a measure of the affinity of a substrate for its enzyme. At equilibrium, the reaction can also be expressed by this equation which takes the same form as the Michaelis-Menten equation. āDrug concentration- effect relationship can be described by: 1) Michaelis-Menten equation for enzyme-substrate reactionā. So far can say if based on single site and no cooperative binding then dose response curve is similar to michelis menten where velocity become effect and EC50 is Km. End lect can use class name list to read out names of 4 students to ask them define at next class what is potency, efficacy, agonist and antag. A receptor can be any cellular macromolecule to which a drug binds to initiate its effect. Cellular proteins that are receptors for endogenous regulatory ligands (hormones, growth factors, neurotransmitters) are the most important drug receptors. Other receptors include enzymes (e.g., acetylcholinesterase), transport proteins (e.g., Na+,K+-ATPase), structural proteins (e.g., tubulin), and nucleic acids. When the relationship between receptor occupancy and response is linear, KD = EC50. If there is amplification between receptor occupancy and effect, such as if the receptor has catalytic activity when the receptor ligand is bound, then the EC50 lies to the left of the KD. 2012 50 min. student ask can binding curve also do semi log, and is binding curve same shape as response curve.- yes binding curve in log appear in lecture 2, will inform students there. In 3rd lect can give eg of real binding and response curve from journals, see same shape. 2011 had question why log scale is 1,10,100, 1000 ā does log make scale increase very fast (aside from initial one to 3 is sparser and 3 to 10 is compressed)? (yes it increase exponential not arithmetical) And we say is log scale but never need to get antilog, just read off, though axis is officially log? (yes cos never took log, just plot on a scale with different intervals) From the questions in āwhat else I want to knowā slips, some wonder how the binding/response expt is done so I put the binding expt pictorial in formative assessment 2010 45 min. supported by hard copy notes. if at end want to emphasise the impt of differentiate binding and effect curve then before show summary, show the diagram of drugs near the receptor with effect- put a dividing line and say again there are 2 different expt, 2 different part of the process, and first thing when see graph is ask what curve, then can know what info can get. Then I got 4 students to each read up on potency, effic, agonist and antag. Concept of receptor and how to analyse D-R binding How the drug at site of action produces an effect: receptor bind, quantitative analysis for comparing different drugs
- Concept of receptor and how to analyse D-R binding Note kinetic still occur after work at site, but it does mean dynamic cannot occur until drug arrive at site of action How the drug at site of action produces an effect: receptor bind, quantitative analysis for comparing different drugs
- Take a drug not just to metab and excrete it but cos you want it to act on body.
- Take a drug not just to metab and excrete it but cos you want it to act on body.
- Inhib cyclooxegenase which convert AA to PG, TX and Prostacyclin
- Before showing the main types of receptor, would be clearer to explain that in general drug bind receptor which then activate downstream signals to amplify and generate the effect.
- Before showing the main types of receptor, would be clearer to explain that in general drug bind receptor which then activate downstream signals to amplify and generate the effect. Not just stand at door, come in, start the action
- Receptors are types of doors, once activated, action starts receptor for the epidermal growth factor (EGF) ā receptor tyr kinase ifn= interferon receptor- class II cytokine receptor family. The Janus (JAK) family tyrosine kinases Tyk2 and Jak1 are constitutively associated with the IFNAR1 and IFNAR2c receptor subunits, respectively. Ligand binding results in the phosphorylation and activation of Tyk2 and Jak1 Tnf receptor- TNF is a cytokine which may induce either cell proliferation or apoptosis. TNF binds TNF Receptors (TNFRs), which are members of a superfamily of proteins known as Death Receptors, resulting in receptor aggregation and recruitment of adapters (i.e., TRAF [TNF Receptor-Associated Factor] proteins) TNFR complex formation activates Caspase 8, the SAP Kinase pathway (dependent on recruitment of Daxx), and the NFĪŗB pathway (which controls apoptosis versus proliferation).
- Nicotinic cholinergic receptor - Composed of 5 peptide subunits: 2Ī±, 1Ī², 1Ī³, 1Ī“ Receptor on muscle fibre eg respiratory muscles- how does it contract. Nerve release NT bind to receptor.
- The two binding sites for AcCho are nonidentical and can be distinguished by differential binding of some competitive antagonists. In particular, d-tubocurarine (TC) binds with dissociation constants that differ by -100-fold
- May need show more cascade and recoupling, else some wonder what is G doing
- May need show more cascade and recoupling, else some wonder what is G doing
- May need show more cascade and recoupling, else some wonder what is G doing
- Affinity is bind with tenacity
- Like all stand and move, but eyes close, move quietly so have random collisions.
- randomly meet at party but after talk, can dissociate and meet others
- there are some binding and others unbinding- so arrow in 2 direction, at equib, rate is equal. at any moment, some (not all) are bound At first more DR formed. Later, more DR dissociate. At equib, rate is same. Rate of nos sitting down is same as nos standing up from sitting. Illus; 10am shopping centre open and number of people inside increases. Till 11am there is 100 inside though 30 enter from 11-12 yet only 100 total inside- cos 30 also leave- equib. But no matter how many inside (30, 50 then 100, majority are at one shop, the most popular one (MPH book, Guess jeans, CD,DVD, Nike shoes) then customer has highest affinity for that store. Lower affinity for other store and no affinity for certain store. Collide = all move blindfold and no noise Case of where nos of people of shopping centre the same though new one go in, cos some go out, and more will be at fav store- higher affinity
- Till all receptors bound
- Till all receptors bound
- Can be dose or conc. Dose is what you give, conc is level in blood. More dose, more conc. Plot whichever
- Can be dose or conc. Dose is what you give, conc is level in blood. More dose, more conc. Plot whichever
- For ease just say receptor binding If you bring in more student (eg 1000 student in this room of 100 chairs) eventually every chair will be occupied- 100% receptor bound.
- Draw higher affinity plot to compare
- Draw higher affinity plot to compare
- Draw higher affinity plot to compare
- Draw higher affinity plot to compare
- Draw higher affinity plot to compare
- Can you do this
- Can you do this What is kd?
- Can you do this Now draw a 2nd drug of higher affinity
- Can you do this
- Can you do this
- Can you do this
- Can you do this
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
- In clinical use of drug we donāt give patient one range, only one dose. We give range in pharmacol expt to see the property of the drug. If give more drug will not increase response cos every system has a max, like you cannot increase HR to 1 million beat per min, and cannot make car go faster when at max speed by putting more petrol (need to change engine). Does not mean higher affinity drug give more response- affinity is binding, response is how you change shape of receptor after bind. Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!! or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc Now effect- not binding (lab science)- in ward interested in effect, so from here canāt tell Kd or affinity.
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!! or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc Now effect- not binding (lab science)- in ward interested in effect, so from here canāt tell Kd or affinity.
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!! or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc Now effect- not binding (lab science)- in ward interested in effect, so from here canāt tell Kd or affinity.
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!! or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc Now effect- not binding (lab science)- in ward interested in effect, so from here canāt tell Kd or affinity. I like to call dose
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. Dose is on log scale. Just plot on this scale give you log value, no need take log and antilog. Scale is log: see the exponential increase. Name of shape: sigmoidal not rect hyperbola
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. Dose is on log scale. Just plot on this scale give you log value, no need take log and antilog. Scale is log: see the exponential increase. Name of shape: sigmoidal not rect hyperbola The units of EC50 and [D] are concentration, but log[D] is unitless.Ā
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. Dose is on log scale. Just plot on this scale give you log value, no need take log and antilog. Scale is log: see the exponential increase. Name of shape: sigmoidal not rect hyperbola
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT. Small dose not compressed together, large dose not flat plateau Linear middle segment
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT. Small dose not compressed together, large dose not flat plateau Linear middle segment
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT. Small dose not compressed together, large dose not flat plateau Linear middle segment
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT. Small dose not compressed together, large dose not flat plateau Linear middle segment
- Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT. Small dose not compressed together, large dose not flat plateau Linear middle segment
- Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. or ED50 Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc