FOSINOPRIL SODIUM tablet

Land: Vereinigte Staaten

Sprache: Englisch

Quelle: NLM (National Library of Medicine)

Wirkstoff:

FOSINOPRIL SODIUM (UNII: NW2RTH6T2N) (FOSINOPRILAT - UNII:S312EY6ZT8)

Verfügbar ab:

St Marys Medical Park Pharmacy

INN (Internationale Bezeichnung):

FOSINOPRIL SODIUM

Zusammensetzung:

FOSINOPRIL SODIUM 40 mg

Verschreibungstyp:

PRESCRIPTION DRUG

Berechtigungsstatus:

Abbreviated New Drug Application

Fachinformation

FOSINOPRIL SODIUM - FOSINOPRIL SODIUM TABLET
ST MARYS MEDICAL PARK PHARMACY
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FOSINOPRIL SODIUM TABLETS USP 40 MG
7224
RX ONLY
USE IN PREGNANCY
WHEN USED IN PREGNANCY DURING THE SECOND AND THIRD TRIMESTERS, ACE
INHIBITORS CAN CAUSE
INJURY AND EVEN DEATH TO THE DEVELOPING FETUS. When pregnancy is
detected, fosinopril sodium
tablets should be discontinued as soon as possible. See WARNINGS,
FETAL/NEONATAL MORBIDITY
AND MORTALITY.
DESCRIPTION
Fosinopril sodium is the sodium salt of fosinopril, the ester prodrug
of an angiotensin-converting
enzyme (ACE) inhibitor, fosinoprilat. It contains a phosphinate group
capable of specific binding to the
active site of angiotensin-converting enzyme. Fosinopril sodium is
designated chemically as: L-proline,
4-cyclohexyl-1-[[[2-methyl-1-(1-oxopropoxy) propoxy] (4-phenylbutyl)
phosphinyl] acetyl]-, sodium
salt, _trans-_.
Fosinopril sodium is a white to off-white crystalline powder. It is
soluble in water (100 mg/mL),
methanol, and ethanol and slightly soluble in hexane.
Its structural formula is:
C
H NNaO P M.W. 585.65
Fosinopril sodium is available for oral administration as 10 mg, 20
mg, and 40 mg tablets. Inactive
ingredients include: crospovidone, glyceryl behenate, isopropyl
alcohol, lactose anhydrous, NF,
microcrystalline cellulose, povidone, and sodium lauryl sulfate.
CLINICAL PHARMACOLOGY
MECHANISM OF ACTION
In animals and humans, fosinopril sodium is hydrolyzed by esterases to
the pharmacologically active
form, fosinoprilat, a specific competitive inhibitor of
angiotensin-converting enzyme (ACE).
ACE is a peptidyl dipeptidase that catalyzes the conversion of
angiotensin I to the vasoconstrictor
30
45
7
substance, angiotensin II. Angiotensin II also stimulates aldosterone
secretion by the adrenal cortex.
Inhibition of ACE results in decreased plasma angiotensin II, which
leads to decreased vasopressor
activity and to decreased aldosterone secretion. The latter decrease
may result in a small increase of
serum potassium.
In 647 hypertensive patients treated with fosi