The Mechanism of Action of First

8/12/2019 The Mechanism of Action of First

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Mechanismof action of dapsone

As anantibacterial,dapsone inhibitsbacterialsynthesis ofdihydrofolic acid,via competition

withpara-aminobenzoatefor the active site of dihydropteroate synthetase.[9]Though structurally

distinct from dapsone, the sulfonamide group of antibacterial drugs also work in this way.

When used for the treatment of skin conditions in which bacteria do not have a role, the

mechanism or action of dapsone is not well understood. Dapsone hasanti-inflammatoryand

immunomodulatory effects,[10]which are thought to come from the drug's blockade

ofmyeloperoxidase.This is thought to be its mechanism of action in treatingdermatitis

herpetiformis.[11]

As part of therespiratory burstthatneutrophilsuse to kill bacteria, myeloperoxidase converts

hydrogen peroxide (H2O2) into hypochlorous acid (HOCl). HOCl is the most potent oxidant

generated by neutrophils, and can cause significant tissue damage during inflammation.

Dapsone arrests myeloperoxidase in an inactive intermediate form, reversibly inhibiting theenzyme. This prevents accumulation of hypochlorous acid, and reduces tissue damage during

inflammation.[12][13][14][15][16]

Myeloperoxidase inhibition has also been suggested as a neuron-sparing mechanism for

reducing inflammation in neurodegenerative diseases such asAlzheimer's diseaseand

stroke.[17]

Though dapsone is an anti-inflammatory agent and not a steroid, it does not fit the usual

definition of anNSAID.By definition, NSAIDs blockcyclo-oxygenaseas their primary

mechanism of action, which dapsone does not do.

Mechanism of Actionof reserpine

Reserpine irreversibly blocks the vesicular monoamine transporter(VMAT).[4]

This normally transports

free intracellularnorepinephrine,serotonin,anddopaminein the presynaptic nerve terminal into

presynaptic vesicles for subsequent release into thesynaptic cleft("exocytosis"). Unprotected

neurotransmitters are metabolized byMAO(as well as byCOMT)in the cytoplasm and consequently

never excite the post-synaptic cell.

It may take the body days to weeks to replenish the depleted VMAT, so reserpine's effects are long-

lasting.

As the result of above, reserpine can cause drug-induced Parkinson's Disease.[5]

Mechanism of Action flurazepam

EFFECTS OF FLURAZEPAM ON EEG DIFFER FROM THOSE OF BARBITURATES IN

THAT FAST ACTIVITY SEEMS TO BE INCREASED ONLY IN FRONTAL LOBE & DOES

NOT SPREAD TO OCCIPITAL LOBE. IN DOSES UP TO 30 MG IT NEITHER AFFECTS

REM SLEEP NOR CAUSES A REBOUND AFTER WITHDRAWAL, BUT DOSES OF 60 MG

SUPPRESS REM SLEEP WITHOUT REBOUND. FLURAZEPAM DECREASES SLEEP
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minobenzoic_acidhttp://en.wikipedia.org/wiki/Dihydrofolic_acidhttp://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Antibacterial


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LATENCY, TIME IN STAGE 4, & WAKE TIME, & INCREASES TOTAL SLEEP TIME FOR

AS LONG AS 22 NIGHTS OF USE. /FLURAZEPAM DIHYDROCHLORIDE/

Mechanism of action of minoxidil]

Themechanismby which minoxidil promotes hair growth is not fully understood. Minoxidilcontains thenitric oxidechemicalmoietyand may act as a nitric oxide agonist. Similarly,

minoxidil is apotassium channel opener,causinghyperpolarizationof cell membranes. Minoxidil

is less effective when there is a large area of hair loss. In addition, its effectiveness has largely

been demonstrated in younger men who have experienced hair loss for less than 5 years.

Minoxidil use is indicated for central (vertex)hair loss only.[4]Minoxidil is also

avasodilator.[5]Hypothetically, by widening blood vessels and opening potassium channels, it

allows more oxygen, blood, and nutrients to the follicle. This may cause follicles in the telogen

phaseto shed, which are then replaced by thicker hairs in a newanagen phase.

Rifampin: mechanisms of action

Rifampin specifically inhibits bacterial RNA polymerase, the enzyme responsible for DNA

transcription, by forming a stable drug-enzyme complex with a binding constant of 10(-9) M at

37 C. The corresponding mammalian enzymes are not affected by rifampin. Bacterial resistance

to rifampin is caused by mutations leading to a change in the structure of the beta subunit of

RNA polymerase. Such resistance is not an all-or-nothing phenomenon; rather, a large number

of RNA polymerases with various degrees of sensitivity to rifampin have been found. No strict

correlation exists between enzyme sensitivity and MIC values, since inhibition of RNA synthesis

does not always show up to the same extent in the two different test systems used for the

determination of these values.

Mechanismgriseofulvan

The drug binds totubulin,interfering withmicrotubulefunction, thus inhibitingmitosis.

It binds tokeratinin keratin precursor cells and makes them resistant to fungal infections. It is

only when hair or skin is replaced by the keratin-griseofulvin complex that the drug reaches its

site of action. Griseofulvin will then enter thedermatophytethrough energy dependent transport

processes and bind to fungalmicrotubules.This alters the processing for mitosis and also

underlying information for deposition of fungal cell walls.

Mechanism of actionimipramine

Imipramine,tertiary amine,affects numerous neurotransmitter systems known to be involved in

the etiology of depression, anxiety,ADHD,enuresis and numerous other mental and physical

conditions. Imipramine is similar in structure to some muscle relaxants, and has a significant

analgesic effect and, thus, is very useful in some pain conditions.
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Mechanism of action of isosorbide dinitrate

Similar to other nitrites and organic nitrates, isosorbide dinitrate is converted to nitric oxide

(NO), an active intermediate compound which activates the enzyme guanylate cyclase

(atrial natriuretic peptide receptor A). This stimulates the synthesis of cyclic guanosine 3',5'-

monophosphate (cGMP) which then activates a series of protein kinase-dependentphosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation

of the myosin light chain of the smooth muscle fiber. The subsequent release of calcium

ions results in the relaxation of the smooth muscle cells and vasodilation

Mechanism of action of tolbutamide

Sulfonylureas lower blood glucose in patients with NIDDM by directly stimulating the acute

release of insulin from functioning beta cells of pancreatic islet tissue by an unknown

process that involves a sulfonylurea receptor (receptor 1) on the beta cell. Sulfonylureas

inhibit the ATP-potassium channels on the beta cell membrane and potassium efflux, which

results in depolarization and calcium influx, calcium-calmodulin binding, kinase activation,and release of insulin-containing granules by exocytosis, an effect similar to that of glucose

Mechanism of action of ranitidine

The H2 antagonists are competitive inhibitors of histamine at the parietal cell H2 receptor.

They suppress the normal secretion of acid by parietal cells and the meal-stimulated

secretion of acid. They accomplish this by two mechanisms: histamine released by ECL

cells in the stomach is blocked from binding on parietal cell H2 receptors which stimulate

acid secretion, and other substances that promote acid secretion (such as gastrin and

acetylcholine) have a reduced effect on parietal cells when the H2 receptors are blocked.

Definitions: Optical Isomers

Optical isomersare molecules that differ three-dimensionally by the placement of substituents aroundone or more atoms in a molecule. Optical isomerswere given their name because they were first able tobe distinguished by how they rotated plane-polarized light. These molecules are not necessarily lockedinto their positions, but cannot be converted into one another, even by a rotation around a single bond.

For example, consider the following two molecules.

In the molecule on the left, the chlorine is oriented upward, and in the molecule on the right, the chlorineis oriented downward. (These molecules are presented in Wedge-Dash Notation, which will be covered inmore detail in a later section in the tutorial. To learn about this notation now, clickhere.To navigate back
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to th ispage from the Wedge-Dash information page, use the Back button in the browser, not within thetutorial.)

These structures can be viewed from a different angle, using Newman Projections, as shown below.(Converting between two different types of structural representations is complicated and will be coveredin detail in a later section. For now, simply note that in the above structures, the chlorines were oppositesin the sense of being "up" and "down," and now they are opposites in the sense of being "left" and"right.")

Geometric Isomerism

Geometric Isomerism results most commonly from Carbon-Carbon double bonds.The important property which introduces the feature is the inability of the Carbon

atoms to rotate relative to one another about the double bond. This is due specifically

to the Pi bond but I won't discuss this part of the subject further on this site.

The lack of rotation means the same groups can be attached in different ways to

achieve diastereomers. The molecules have identical connectivity so can't be

described as structural isomers.

Conformational isomerism

Inchemistry,conformational isomerismis a form ofstereoisomerismin which theisomerscan

be interconverted exclusively by rotations about formally single bonds (refer to figure on single

bond rotation).[1]Such isomers are generally referred to as conformational

isomersor conformersand, specifically, as rotamers.[2]Rotations about single bonds are

restricted by a rotational energy barrier which must be overcome to interconvert one conformer

to another. Conformational isomerism arises when the rotation about a single bond is relatively

unhindered. That is, theenergy barriermust be small enough for the interconversion to occur.

Conformational isomers are thus distinct from the other classes ofstereoisomers(i.

e.configurationalisomers) where interconversion necessarily involves breaking and reforming

of chemical bonds.[3]For example, L- & D and R- & S- configurations of organic molecules have

different handedness and optical activities, and can only be interconverted by breaking one or

more bonds connected to thechiralatom and reforming a similar bond in a different direction or

spatial orientation.
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The study of the energetics between different rotamers is referred to as conformational

analysis.[4]It is useful for understanding the stability of different isomers, for example, by taking

into account the spatial orientation and through-space interactions of substituents. In addition,

conformational analysis can be used to predict and explain product(s) selectivity, mechanisms,

and rates of reactions
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The Mechanism of Action of First