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  • Pharmacology - Antidiabetic Agents: Block Degradation of GLP-1, Raise Circulating GLP-1 Levels

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    marie daitol
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    This document outlines various classes of antidiabetic agents, including their mechanisms of action and example drugs. It discusses sulfonylureas which increase insulin release from the pancreas, meglitinides which also regulate insulin release, DPP-4 inhibitors which block degradation of GLP-1, GLP-1 analogs which activate the GLP-1 receptor, thiazolidinediones which decrease insulin resistance, biguanides which reduce hepatic glucose production, alpha-glucosidase inhibitors which delay carbohydrate digestion, and islet amyloid polypeptide analogs which bind to amylin receptors. In total, 8 classes of antidiabetic drugs are described.

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    Antidiabetics

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    This document outlines various classes of antidiabetic agents, including their mechanisms of action and example drugs. It discusses sulfonylureas which increase insulin release from the pancreas, meglitinides which also regulate insulin release, DPP-4 inhibitors which block degradation of GLP-1, GLP-1 analogs which activate the GLP-1 receptor, thiazolidinediones which decrease insulin resistance, biguanides which reduce hepatic glucose production, alpha-glucosidase inhibitors which delay carbohydrate digestion, and islet amyloid polypeptide analogs which bind to amylin receptors. In total, 8 classes of antidiabetic drugs are described.

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    © All Rights Reserved
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    12 views2 pages

    Pharmacology - Antidiabetic Agents: Block Degradation of GLP-1, Raise Circulating GLP-1 Levels

    Uploaded by

    marie daitol
    This document outlines various classes of antidiabetic agents, including their mechanisms of action and example drugs. It discusses sulfonylureas which increase insulin release from the pancreas, meglitinides which also regulate insulin release, DPP-4 inhibitors which block degradation of GLP-1, GLP-1 analogs which activate the GLP-1 receptor, thiazolidinediones which decrease insulin resistance, biguanides which reduce hepatic glucose production, alpha-glucosidase inhibitors which delay carbohydrate digestion, and islet amyloid polypeptide analogs which bind to amylin receptors. In total, 8 classes of antidiabetic drugs are described.

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    of 2

    Pharmacology - Antidiabetic Agents

    A. Sulfonylureas
    i. MOA : ​Increase insulin release from the pancreas by binding to a 140-kDa high-
    affinity sulfonylurea receptor that is associated with a beta-cell inward rectifier
    ATP-sensitive potassium channel resulting in depolarization, opening a
    voltage-gated calcium channel and results in calcium influx and the release of
    preformed insulin.
    1. Member drugs
    a. 1st Generation ​Sulfonylureas
    i. Tolbutamide
    ii. Chlorpropamide
    iii. Tolazamide
    iv. Acetohexamide
    b. 2nd ​Generation ​Sulfonylureas
    i. Glyburide
    ii. Glipizide
    iii. Gliclazide
    iv. Glimepiride

    B. Meglitinides
    i. MOA: M​odulate beta-cell insulin release from the pancreas by regulating
    potassium efflux through the potassium channels similar to Sulfonylureas.
    1. Member drugs
    a. Repaglinide
    b. Mitiglinide
    c. Nateglinide (𝚫-Phenylalanine Derivative) - Stimulates rapid and
    transient release of insulin from beta cells through closure of the
    ATP-sensitive K​+ ​channel.

    C. Dipeptidyl Peptidase 4 (DPP-4) Inhibitors


    i. MOA: ​Block degradation of GLP-1, raise circulating GLP-1 levels
    1. Member drugs
    a. Sitagliptin
    b. Saxagliptin
    c. Linagliptin
    d. Alogliptin
    e. Vildagliptin

    D. Glucagon-Like Peptide-1 (GLP-1) Analogs


    i. MOA: Agonizes the Glucagon-Like Peptide-1 (GLP-1) Receptor
    1. Member drugs
    a. Exenatide
    b. Liraglutide
    c. Albiglutide
    d. Dulaglutide
    E. Thiazolidinediones
    i. MOA: Decrease insulin resistance by acting as ligands of ​peroxisome
    proliferator-activated receptor gamma (PPAR-​𝜸​).
    1. Member drugs
    a. Pioglitazone
    b. Rosiglitazone

    F. Biguanides
    i. MOA: Their primary effect is to activate the enzyme AMP-activated protein
    kinase (AMPK) and reduce hepatic glu- cose production.
    1. Member drug
    a. Metformin

    G. -Glucosidase Inhibitors
    i. MOA: Competitively inhibit the intestinal α-glucosidase enzymes and reduce
    post-meal glucose excursions by delaying the digestion and absorption of starch
    and disaccharides.
    1. Member drugs:
    a. Acarbose
    b. Miglitol
    c. Voglibose
    H. Islet Amyloid Polypeptide Analog
    i. MOA: ​Binds to amylin receptors
    1. Member drug
    a. Pramlintide

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