Mechanism of Action (MOA); Types, Drugs Classificatons

Mechanism of action

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Mechanism of action (MOA) refers to the specific biochemical interaction through which a drug substance produces its pharmacological effect. A mechanism of action usually includes mention of the specific molecular targets to which the drug binds, such as an enzyme or receptor. Receptor sites have specific affinities for drugs based on the chemical structure of the drug, as well as the specific action that occurs there. Drugs that do not bind to receptors produce their corresponding therapeutic effect by simply interacting with chemical or physical properties in the body. Common examples of drugs that work in this way are antacids and laxatives. In comparison, a mode of action (MoA) describes functional or anatomical changes, at the cellular level, resulting from the exposure of a living organism to a substance.

Types of Mechanism of Action

a.  According to the overall interactions in the human body

1. Physical mechanisms

Transduction – The target molecules where the drugs act is linked with various biochemical reactions in the cells, resulting ultimately in response. These may be enzyme linked, Ca linked or g-protein linked.

Local Effect – When the drug effect occurs in the immediate vicinity of application, this is known as a local effect.

Systemic Effect – When the drug effect occurs away from the site of administration, this is known as the systemic effect.

Primary effect – the Primary effect is the effect for which the drug is administered or the treatment of the disease for which the drug is given.

Side effect – All other effects occurring, in addition, are known as secondary effects. When the secondary effects are undesirable by the patient, these are called adverse effects or side effects.

2.  Chemical mechanisms

Chemically acting antacids – Chemically acting antacids react chemically with HCl of the stomach, causing neutralization. Sodium bicarbonate chemically binds HCl forming NaCl and water.

Chelating agents – Chelating agents are the drugs used to treat poisoning with various metals. They incorporate or chelate metal ions into inner ring structure and in this way inactivate or neutralize the effects of metals.

Pralidoxime – Pralidoxime is a choline esterase reactivator. Poisoning of drugs like acetyl choline esterase inhibitors or organophosphate poisoning (insecticides, war gases) irreversible cause inactivation of acetyl choline esterase enzyme. This drug reacts chemically with phosphate of organophosphate compounds causing dephosphorylation. Thus acetyl choline esterase is released

3.  Drug- receptor interactions

Receptor

Macromolecules protein in nature which are target sites for drugs. Most drugs have to bind receptors to produce effects. Receptors are located mostly on the cell membrane but certain intracellular receptors are found as well.

There are three forms of binding to receptors

Ligands

Ligands are the endogenous substances, molecules or compounds which bind with receptors present in the body e.g. acetylcholine, adrenaline, noradrenaline, neurotransmitters like glutamate, aspartate, and GABA. They produce various effects and interfere with the flow of ions through channels called ligand gated channels. Their action may

  • Resemble with the natural ligand
  • Block the natural ligand

Agonists

Agonists are the drugs which when bind receptors, cause activation of receptors. They have the capacity to produce chain reactions in the receptors which ultimately bring about the effects. Agonists have two properties

  • Affinity for receptor
  • Capability to produce chain reactions in the cells having capability of intrinsic activity or efficacy

Coupling

Transduction process between occupancy of the receptor by agonist and response to occur is called coupling. Most agonists when bind to receptors cause activation. Most of them alter the second messenger systems in the cells.

There are three-second messenger systems

  • Cyclic AMP
  • Cyclic GMP
  • Calcium and phosphoinositol second messenger system

The levels of these second messenger systems may increase or decrease. This may occur in three steps

  • Drug binds receptor
  • Stimulation of g-regulatory protein occurs. G-regulatory protein exists in two forms; GS (stimulatory g-protein) and GI (inhibitory g-protein).
  • This causes the change in the effector element-enzyme or ionic channel depending on GS or GI.

Beta 1, beta 2, alpha 2, and dopamine 1 are the receptors associated with cAMP second messenger system.

Ligands include ACTH, catecholamines (beta adrenoreceptors), hCG, FSH, glucagon, histamine (H2 receptors), LH, MSH, PTH, serotonin, etc.

Calcium and Phospho-inositol system

Muscarinic and alpha 1 receptors are associated with calcium phospho-inositol system. Ligands include acetylcholine (muscaranic receptors), angiotensin, serotonin, vasopressin (V1 receptors), and catecholamines (alpha 1 adrenoreceptors).

Types of Receptors

There are four main types of receptors:

Type 1

Ligand gated ion channels

        Type 2

G-protein coupled receptors

Type 3

Kinase linked receptors

Type 4

Nuclear receptors

Location Membrane Membrane Membrane Intracellular
Effectors Ion channel Channel or enzyme Enzyme Gene transcription
Coupling Direct G-protein Direct Via DNA
Examples of Nicotinic acetylcholine receptor (nAchR), GABA type A Muscarinic acetylcholine receptor (mAchR), adrenoceptors Insulin, growth factor, cytokine receptors Steroid, thyroid hormone receptors
Structure Oligomeric assembly of subunits surrounding central pore Monomeric (occasionally dimeric) structure comprising seven transmembrane helices Single transmembrane helix linking extracellular receptor domain to the intracellular kinase domain Monomeric structure with separate receptor and DNA binding domains

An example includes suxamethonium (succinylcholine), which produces relaxation of skeletal muscles by

  • Activation of nicotinic receptors
  • Desensitization of receptors in the neuromuscular junction
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The reason for desensitization is not clear. In beta blockers (which act by cAMP), ultimately phosphorylation of proteins and accumulation of phosphosilines occurs, which increases the binding of beta receptors with proteins, known as beta arrestin. This beta arrestin interferes with the activity, ultimately leading to inhibition of adenyl cyclase enzyme.

The binding of the drug with the receptor may be of two types

  • Reversible binding
  • Irreversible binding

In reversible binding, the bond between the drug and receptor is very weak ionic, hydrogen or van der wall. This the effect is short lived. Prolong contact of tissues with the agonists results in decreased number of receptors in the tissues called down regulation of receptors. An example includes the patients suffering from bronchial asthma, in whom by prolonging usage of beta-agonists down regulation occurs. This the effect is reduced.

Spare Receptors

Sometimes it is seen, especially in isolated tissues, that when various amounts of drugs are added e.g. when in intestines of rabbits acetyl choline is added, this may lead to maximum effect. Only one percent of receptors might be occupied but the maximum response might be seen. This is due to the vast reserve. There are spare receptors, only very small amounts of drugs are required for maximum effect.

Antagonists

Binding of the drug with the receptor is the same. Most of the drugs binding receptors resemble the agonists but they cannot activate the receptors, and also prevent agonist binding. Thus opposite effect occurs in case of agonists and antagonists. They have two properties

  • Affinity
  • Do not have efficacy or intrinsic activity

Examples include atropine, which is the antagonist of acetylcholine. Propanolol is the antagonist of beta receptors. The binding of antagonist with the receptor is of two types

  • Reversible binding
  • Irreversible binding
  • Reversible binding is also known as competitive antagonism. E.g. atropine.

Non-competitive antagonism occurs when the binding effect of the antagonist is prolonged until the drug is excreted or new receptor is generated. An example includes phenoxybenzamine, which non-competitively blocks the action of catecholamines at beta receptors. Second generation H1 histamines are also non-competitive blockers.

Prolonged contact of tissues with the antagonists results in up-regulation of receptors or increase in the number of receptors in the tissues. The example includes patients suffering from arrhythmias or angina taking beta blockers, if we abruptly withdraw them, there will be reversing of the arrhythmia and angina. Up-regulation of catecholamines occurs which worsens the conditions.

Partial Antagonists

Partial antagonists have intermediate levels of efficacy. They bind with the receptors but have very small intrinsic activity and efficacy. It can be seen that even on 100 percent occupation of the receptors, the response is submaximal. Examples include beta blockers like pindolol and oxprenolol. They have ISA property (intrinsic sympathomimetic property) and are used in patients suffering from diabetes mellitus, peripheral vascular diseases, and bronchial asthma.

Inverse Agonists

When inverse agonists bind receptors, they cause activation of receptors but produce an effect opposite to the agonists. Examples include benzodiazepines used as sedative hypnotics. They produce sedation, relieve anxiety and relaxation of muscles. When beta-carbolines are administered, they bind benzodiazepines receptors causing the activation of receptors, producing stimulation, increase in tone, anxiety, and convulsions.

  • Drugs having agonist effect at receptors have positive efficacy.
  • Drugs having inverse agonist effect at receptors have negative efficacy.
  • Drugs having an antagonist effect at receptors have zero efficacy.

4. Drug- enzyme interactions

ACE – inhibitors(angiotensin converting enzyme inhibitors)

ACE inhibitors convert angiotensin I into angiotensin II, which is a potent vasoconstrictor. ACE inhibitors are used in the treatment of hypertension.

Levo dopa – Levo dopa is metabolized by dopa decarboxylase in the periphery. Carbidopa competes with levo dopa for the dopa decarboxylase enzyme. Thus peripheral metabolism of levo dopa is decreased, more levo dopa enters brain producing more efficacy.

Ethanol – Ethanol (alcohol) undergoes metabolism in the body in two steps
  • Ethanol – is converted into acetaldehyde by alcohol dehydrogenase
  • Acetaldehyde – is converted into water and carbon dioxide by an aldehyde dehydrogenase.
  • Neostigmine – Neostigmine acts as a reversible acetylcholine esterase inhibitor. Thus in the treatment of myasthenia gravis, acetylcholine levels are reversibly increased in the NMJ.
  • Disulfiram – Disulfiram is used in alcohol aversion therapy. It inhibits aldehyde dehydrogenase enzyme. When a patient takes alcohol, an increase in plasma levels of acetaldehyde cause bad symptoms like nausea, vomiting, and flushing.
  • Allopurinol Allopurinol is used in the treatment of gout. Xanthine oxidase is inhibited which converts xanthine and hypoxanthine into uric acid.

5. Non Competitive Inhibition

The effects of noncompetitive inhibition are prolonged. These include

Irreversible anticholinestrases

These include the insecticides and the war gases. These are toxic compounds which can be absorbed through the skin.

Aspirin

Aspirin is an analgesic used in a headache, it inhibits cyclooxygenase enzyme in the platelets. It inhibits the synthesis of prostaglandins especially thromboxane A2. Life of platelets is only seven days. On maintenance therapy, aspirin is taken in low doses by cardiac patients.

Monoamine oxidase inhibitors

These are used to treat depression. They inhibit the monoamino oxidase enzyme which breaks down catecholamines. Thus decreased levels of noradrenalin and serotonin are coped by MAO inhibitors and increased levels are achieved.

Proton pump inhibitors

Proton pump inhibitors inhibit the hydrogen-potassium ATPase in parietal cells of the stomach, thus inhibit HCl secretion.

6.  Drug- channel interactions

Sodium Channels

Sodium channel drugs are used in cardiac arrhythmias and act by blocking the sodium channels. These include the local anesthetics which produce anesthesia in a localized area. Thus depolarization does not take place and there is no nerve conduction in that localized area.

Calcium channels

Calcium channel drugs are used in the treatment of hypertension and arrhythmias. They block the voltage gated calcium channels and release the vascular stiffness.

Potassium channels

Potassium channel drugs include amiodarone used in arrhythmias and block potassium channels. Thus there is a prolonged refractory period. Sulfonylureas are antidiabetic and block the ADP mediated potassium channels in the beta cells of the pancreas.

Chloride channels

Chloride channel drugs include benzodiazepines which produce sedation, used in epilepsy and are muscle relaxants. They increase the entry of chloride ions through the chloride channels causing hyper polarization.

7.  Miscellaneous mechanisms

Colchicines

Colchicines are used in the treatment of acute gout. The symptoms of gout are aggravated by the migration of leukocytes causing phagocytosis of uric acid crystals producing lactic acidosis leading to more inflammation and the cycle continues.  Colchicines binds tubulin of microtubules and prevents the migration of leukocytes.

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Vinca alkaloids

Vinca alkaloids are used in cancer chemotherapy. They too bind tubulin of microtubules of cancer cells, thus blocking mitosis.

Ionizing radiations

Ionizing radiations are used in cancer chemotherapy.

Levamisole

Levamisole is anthelmintic used to expel worms and parasites to treat worm infestation. They also cause stimulation of the immune system. When using immunosuppressive drugs, these are taken as immunostimulant drugs.

Immunosuppressive drugs

Immunnosuppressive drugs act by binding cytosolic protein aminophilin and are used in transplantation.

Therapeutic antibodies

Therapeutic antibodies are used for isolation of cytokines which are responsible for inflammation. There are many medicines in the world and of them, drugs of modern medicine are widely used.

b.  Based on the mode of action, drugs can be categorized as following types

1.  Physically acting drugs

These are the drugs which do not react in the body with fluids or other biochemical substances. But they exert their effect just by being physically present at the location.

  • Bisacodyl – A drug of choic prescribed for peptic ulcer. This drug physically binds to the portion of the ulcer surface in the stomach. Thereby prevents the further attack of gastric acid on to it. Due to lack of further exposure to acid, the ulcer portion of stomach gets healed faster.
  • Charcoal – The activated charcoal is used as an antidote to poisons. Scientifically it is called activated as it in powered form and made to readily adsorb matter.

2.  Drugs acting by chemical reactions

Here drugs act to produce relief by reacting chemically with some or other body fluids.

  • When you have acidity in the stomach – you are advised to drink a solution of sodium bicarbonate. Acidity is caused due to the release of HCL in the stomach. HCl as we know is a strong acid. So when sodium bicarbonate a base (alkali) is consumed, it reacts with excess acid and neutralizes it to salt. Thus acidic pain is reduced. Other examples, in this case, are antacids tablets of aluminum hydroxide, magnesium hydroxide etc.
  • When there are kidney stones – physician advice consumption of a lot of citrus fruit juices like lemon, orange etc. These juices are acidic in nature. The kidney stones are mostly made of Calcium salts. Calcium is an alkaline substance. So when the acidic juice is taken in large quantities, it reacts with calcium (an alkali element) in the kidney stone and dissolves it. Also, any chances of further growth of the stone are inhibited by this citric juice.

3.  Drugs acting by physiological modifications

Here drugs produce some physiological effect and relief from symptoms of the disease.  This can be of three types.

  • Those producing opposite effect – In the case of severe diarrhea (loose motions without pain), the intestinal motility (movement) is very high. The movement is such that any food material in the intestine is pushed downwards i.e. towards the rectum for faster defecation. In this condition, doctors prescribe Morphine related drugs ( Ex; Loperamide).
  • Morphine has a special property in the gut. When taken orally, it reverses intestinal movement and instead of contents traveling downward, they travel up towards stomach and mouth. (Hence morphine consumption orally has symptoms like vomiting even undigested waste from mouth). For sever diarrhea, weaker derivatives of morphine are given to slow down the intestinal run downward and stop loose motion.
  • In patients with high blood pressure – diuretics are given. Blood pressure is one which exerts pressure on the blood vessels. When blood volume increases, the pressure also increases. So the drugs are given to enhance urine out put. Due to this blood volume decreases there by reducing the blood pressure.

5.  Those producing an unrelated effect

Here the symptoms are mitigated by producing unrelated changes in physiology.

  • Ex of such drugs is Zandu balm, index and other pain relieving balms. These gels show this unrelated mechanism of drug action. The volatile or essential oils present in these drugs produce irritation and redness in the region of application. Hence they are called as rubefacients. They are also called counter irritants.
  • When there is a pain, if the balm or gel is applied at the point of pain, they produce irritable and burning sensation at the place of application. This leads to high blood circulation at the point, causing redness and swelling of the region.  Hence the actual pain is nullified or forgot due to new irritating or burning feeling.

6.  Drugs acting through receptors 

This is a common method by which most drugs used in important disorders function. Receptors are situated at the cellular surface or rarely inside. When drugs bind to them, they bring changes at the cellular level and help relieve symptoms.

  • Most drugs used in depression, schizophrenia, anxiety, and drugs of abuse function through this mechanism.

7.  Drugs acting by replacement

Many vital drugs like anti-Parkinson’s,  anti-epileptics etc. act by this mechanism.

  • In Parkinson’s disorder, there is a low concentration ratio of Dopamine with that of acetylcholine in the brain. Hence the Parkinson symptoms are present. To minimize them, Levodopa is given. This is similar to dopamine in chemistry. In the brain, it breaks down into dopamine and enhances the concentration. Thus the imbalance in the ratio of dopamine and acetyl choline is minimized. Due to this, the Parkinson symptoms subside.

8. Drugs acting by substitution

This is the mechanism of action of anticancer, antiviral,  antibiotic drugs. They substitute a vital metabolite of cell physiology with a function-less molecule and lead to the death of cancer cells, bacteria, and virus

  • This is a list of all the possible mode of drug actions. Most of the drugs fall into one or other category of the mechanism of action as mentioned above.

 Importance of mechanism of action

Elucidating the mechanism of action of novel drugs and medications is important for several reasons:

  • In the case of anti-infective drug development, the information permits anticipation of problems relating to clinical safety. Drugs disrupting the cytoplasmic membrane or electron transport chain, for example, are more likely to cause toxicity problems than those targeting components of the cell wall (peptidoglycan or β-glucans) or 70S ribosome, structures which are absent in human cells.
  • By knowing the interaction between a certain site of a drug and a receptor, other drugs can be formulated in a way that replicates this interaction, thus producing the same therapeutic effects. Indeed, this method is used to create new drugs.
  • It can help identify which patients are most likely to respond to treatment. Because the breast cancer medication trastuzumab is known to target protein HER2, for example, tumors can be screened for the presence of this molecule to determine whether or not the patient will benefit from trastuzumab therapy.
  • It can enable better dosing because the drug’s effects on the target pathway can be monitored in the patient. Statin dosage, for example, is usually determined by measuring the patient’s blood cholesterol levels.
  • It allows drugs to be combined in such a way that the likelihood of drug resistance emerging is reduced. By knowing what cellular structure an anti-infective or anticancer drug acts upon, it is possible to administer a cocktail that inhibits multiple targets simultaneously, thereby reducing the risk that a single mutation in microbial or tumor DNA will lead to drug resistance and treatment failure.
  • It may allow other indications for the drug to be identified. Discovery that sildenafil inhibits phosphodiesterase-5 (PDE-5) proteins, for example, enabled this drug to be repurposed for pulmonary arterial hypertension treatment, since PDE-
  • 5 is expressed in pulmonary hypertensive lungs.
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Drugs Classification according to the mechanism of action

PENICILLINS
CEPHALOSPORINS
FLUOROQUINOLONES
AMINOGLYCOSIDES
MONOBACTAMS
CARBAPENEMS
MACROLIDES
OTHER
Natrual
First generation
Ciprofloxacin (Cipro)
Levofloxacin (Levaguin)
Moxifloxacin (Avelox)
Norfloxacin
 Amikacin
Gentamicin
Kanamycin
Neomycin
Tobramycin
 Aztreonam Ertapenem
Imienem
Meropenem
Azithromycin
Clarithromycin
Dirithromycin
Erythromycin
Clindamycin
Vancomycin
Rifampin
Doxycycline
Linezolid
Tetracycline
Trimethoprim/ sulfamethoxacole
Penicillin G
Penicillin-VK
Cephalothin
Cefazolin (Ancef, Kefzol)
Cephapririn
Cephalexin (Keflex)
other
Penicillinase Resistant
Second Generation
Methicillin
Nafcillin
Oxacillin
other
Cefacor
Cefotetan (Cefotan)
other
Aminopenicillins
Third Generation
Ampicillin Ceftriaxone (Rocephin)
other
Fourth Generation
Cefpirome
Cefepim

 

Antibiotic Grouping By Mechanism
Cell Wall Synthesis Penicillins
Cephalosporins
Vancomycin
Beta-lactamase Inhibitors
Carbapenems
Aztreonam
Polymycin
Bacitracin
Protein Synthesis Inhibitors Inhibit 30s Subunit
Aminoglycosides (gentamicin)
Tetracyclines
Inhibit 50s Subunit
Macrolides
Chloramphenicol
Clindamycin
Linezolid
Streptogramins
DNA Synthesis Inhibitors Fluoroquinolones
Metronidazole
RNA synthesis Inhibitors Rifampin
Mycolic Acid synthesis inhibitors Isoniazid
Folic Acid synthesis inhibitors Sulfonamides
Trimethoprim

 

Aztreonam

Inhibits Cell Wall Synthesis
Penicillins
(bactericidal: blocks cross linking via competitive inhibition of the transpeptidase enzyme)
Class/Mechanism Drugs Indications (**Drug of Choice) Toxicity
Penicillin Penicillin G
Aqueous penicillin G
Procaine penicillin G
Benzathine penicillin G
Penicillin V
Strep. pyogenes (Grp.A)**
Step. agalactiae (Grp.B)**
C. perfringens(Bacilli)**
Hypersensitivity reaction
Hemolytic anemia
Aminopenicillins Ampicillin
Amoxicillin
Above +
↑ Gram-negative:
E. faecalis**
E. Coli**
 Above
Penicillinase-resistant-penicillins Methicillin
Nafcillin
Oxacillin
Cloxacillin
Dicloxacillin
Above +
PCNase-producingStaph. aureus
Above +
Interstitial nephritis
Antipseudomonal penicillins Carbenicillin
Ticarcillin
Piperacillin
Above +
Pseudomonas aeruginosa**
 Above
Cephalosporins
(bactericidal: inhibits bacterial cell wall synthesis via competitive inhibition of the transpeptidase enzyme)
1st generation  Cefazolin
Cephalexin
Staph. aureus**
Staph. epidermidis**
Some Gram-negatives:
E. Coli
Klebsiella
Allergic reaction
Coombs-positive anemia (3%)
2nd generation Cefoxitin
Cefaclor
Cefuroxime
Above +
↑ Gram-negative
Allergic Reaction
ETOH Disulfiram reaction
3rd generation Ceftriaxone
Cefotaxime
Ceftazidime
Cefepime (4th generation)
Above +
↑ Gram-negative
Pseudomonas
Allergic Reaction
ETOH Disulfiram reaction
Other Cell Wall Inhibitors
Vancomycin 
(bactericidal: disrupts peptioglycan cross-linkage)
 Vancomycin MRSA**
PCN/Ceph allegies**
S. aureus
S. epidermidis
Red man syndrome
Nephrotoxicity
Ototoxicity
Beta-lactamase Inhibitors 
(bactericidal: blocking cross linking)
Clavulanic Acid
Sulbactam
Tazobactam
S aureus**
S epidermis**
E.Coli**
Klebsiella**
Hypersensitivity Reaction
Hemolytic anemia
Carbapenems Imipenem (+ cilastatin)
Meropenem
Doripenem
Ertapenem
Broadest activity of any antibiotic
(except MRSA, Mycoplasma)
Aztreonam ive rods
Aerobes
Hospital-acquired infections
Polymyxins Polymyxin B
Polymyxin E
Topical Gram-negative infections
Bacitracin Bacitracin Topical Gram-positive infections
Protein Synthesis Inhibition
Anti-30S ribosomal subunit
Aminoglycosides
(bactericidal: irreversible binding to 30S)
Gentamicin
Neomycin
Amikacin
Tobramycin
Streptomycin
Aerobic Gram-negatives
Enterobacteriaceae
Pseudomonas
Nephrotoxicity
Ototoxicity
Tetracyclines
(bacteriostatic: blocks tRNA)
Tetracycline
Doxycycline
Minocycline
Demeclocycline
Rickettsia
Mycoplasma
Spirochetes (Lyme’s disease)
Hepatotoxicity
Tooth discoloration Impaired growth
Avoid in children < 12 years of age
Anti-50S ribosomal subunit
Macrolides
(bacteriostatic: reversibly binds the 50S)
Erythromycin
Azithromycin
Clarithromycin
Streptococcus
H. influenzae
Mycoplamsa pneumonia
Coumadin Interaction (cytochrome P450)
Chloramphenicol
(bacteriostatic)
Chloramphenicol H influenzae
Bacterial Meningitis
Brain absces
Aplastic Anemia
Gray Baby Syndrome
Lincosamide
(bacteriostatic: inhibits peptidyl transferase by interfering with amino acyl-tRNA complex)
Clindamycin Bacteroides fragilis
S aureus
Coagulase-negative Staph & Strep
Excellent Bone Penetration
Pseudomembranous colitis
Hypersensitivity Reaction
Linezolid
(variable)
Linezolid Resistant Gram-positives
Streptogramins Quinupristin
Dalfopristin
VRE
GAS and S. aureus skin infections
DNA Synthesis Inhibitors
Fluoroquinolones
(bactericidal: inhibit DNA gyrase enzyme, inhibiting DNA synthesis)
1st generation   Nalidixic acid Steptococcus
Mycoplasma
Aerobic Gram +
Phototoxicity
Achilles tendon rupture
Impaired fracture healing
2nd generation Ciprofloxacin
Norfloxacin
Enoxacin
Ofloxacin
Levofloxacin
As Above +Pseudomonas as above
3rd generation Gatifloxacin As above + Gram-positives as above
4th generation Moxifloxacin
Gemifloxacin
As above + Gram-positives + anaerobes as above
Other DNA Inhibitors
Metronidazole
(bacteridical: metabolic biproducts disrupt DNA)
Metronidazole (Flagyl) Anaerobics Seizures
Crebelar dysfunction
ETOH disulfram reaction
RNA Synthesis Inhibitors
Rifampin
(bactericidal: inhibits RNA transcription by inhibiting RNA polymerase)
Rifampin Staphylococcus
Mycobacterium 
(TB)
Body fluid discoloration
Hepatoxicity (with INH)
Mycolic Acids Synthesis Inhibitors
Isoniazid Isoniazidz TB
Latent TB
Folic acid Synthesis Inhibitors
Trimethoprim/Sulfonamides
(bacteriostatic: inhibition with PABA)
Trimethoprim/Sulfamethoxazole (SMX)
Sulfisoxazole
Sulfadiazine
UTI organisms
Proteus
Enterobacter
Thrombocytopenia
Avoid in third trimester of pregnancy
Pyrimethamine Pyrimethamine Malaria
T. gondii

 

Gram Postive Cocci
Staphylococcus Staph. aureus
MSSA
MRSA
Staph. epidermis
Staph saprophyticus
Streptococcus Strep pneumoniae
Strep pyogenes (Group A)
Strep agalacticae (Group B)
Strep viridans
Strep Bovis (Group D)
Enterococci E. faecalis (Group D strep)
Gram Positive Bacilli
Spore Forming Bacillus anthracis
Bacillus cereus
Clostridium tetani
Clostridium botulinum
Clostridium perfringens
Clostridium difficile
Non-Spore Forming Corynebacterium diphtheriae
Listeria monocytogenes
Gram Negative Cocci
Neisseria Neisseria meningitidis
Neisseria gonorrhoeae
Gram Negative Bacilli
Enterics Escherichia coli
Salmonella typhi
Salmonella enteridis
Shigella dysenteriae
Klebsiella pneumoniae
Serratia
Proteus
Campylobacter jejuni
Vibrio cholerae
Vibrio parahaemolyticus/vulnificus
Helicobacter pylori
Pseudomonas aeruginosa
Bacteroides fragilis
Respiratory bacilli Haemophilus influenzae
Haemophilius ducreyi
Bordatella pertussis
Zoonotic bacilli Yersinia enterocolitica
Yersinia pestis
Brucella
Francisella tularensis
Pasteurella multocida
Bartonella henselae
Other Gardnerella vaginalis
Other Bacteria
Mycobacteria Mycobacterium tuberculosis
Mycobacterium leprae
MOTTS
Spirochetes Borrelia burgdorferi
Leptospira interrogans
Treponema pallidum
Chlamydiaceae Chlamydia trachomatis
Chlamydophila
Rickettsia
Ehrlichia
Mycoplasmataceae Mycoplasma pneumoniae
Ureaplasma urealyticum
Fungus-like Bacteria Actinomyces israelii
Nocardia

 

References

Mechanism of action

 

 

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