| Identification | Back Directory | [Name]
Nebivolol | [CAS]
118457-14-0 | [Synonyms]
R065824
R-065824
R 065824
NEBIVOLOL
dl-Nebivolol
Unii-030Y90569u
Nebivolol USP/EP/BP
Nebivolol (R 065824)
Nebivolol, racemic mixture
NEBILET; BYSTOLIC; R 065824; R065824; R-065824
2H-1-Benzopyran-2-methanol, α,α'-[iminobis(methylene)]bis[6-fluoro-3,4-dihydro-, (αR,α'R,2R,2'S)-rel-
[2R*[R*[R*(S*)]]]-alpha,alpha'-[Iminobis(methylene)]bis[6-fluoro-3,4-dihydro-2H-1-benzopyran-2-methanol
(1S)-1-[(2R)-6-fluoro-3,4-dihydro-2H-chromen-2-yl]-2-[[(2S)-2-[(2S)-6-fluoro-3,4-dihydro-2H-chromen-2-yl]-2-hydroxyethyl]amino]ethanol
Nebivolol D4Q: What is
Nebivolol D4 Q: What is the CAS Number of
Nebivolol D4 Q: What is the storage condition of
Nebivolol D4 Q: What are the applications of
Nebivolol D4 | [EINECS(EC#)]
601-527-4 | [Molecular Formula]
C8H11NO4 | [MDL Number]
MFCD09910531 | [MOL File]
118457-14-0.mol | [Molecular Weight]
185.178 |
| Chemical Properties | Back Directory | [Melting point ]
155-156°C | [Boiling point ]
600.5±55.0 °C(Predicted) | [density ]
1.309 | [storage temp. ]
-20°C Freezer | [solubility ]
DMSO (Slightly), Methanol (Slightly, Heated) | [form ]
Solid | [pka]
pKa 8.22(H2O,t =25±1,Iundefined,Ar) (Uncertain) | [color ]
White to Off-White |
| Hazard Information | Back Directory | [History]
The development of nebivolol began in the early 1980s, led by a research team at Janssen Pharmaceutica in Belgium. The design goal was to develop a novel cardiovascular drug with high β1-adrenergic receptor selectivity. The compound was successfully synthesized in the early 1990s, and its unique pharmacological characteristics lie in its dual mechanism of action: it is not only a highly potent third-generation β-blocker, but also promotes nitric oxide (NO)-mediated vasodilation by activating endothelial nitric oxide synthase (eNOS). This innovative mechanism of action was elucidated in the work of early researchers such as P. M. Vanhoutte. After systematic preclinical and clinical development, nebivolol received its first regulatory approval in Germany in 1997 for the treatment of essential hypertension. Subsequent extensive studies further established its clinical advantages in improving endothelial function and exhibiting better tolerability, distinguishing it from traditional β-blockers as a modern antihypertensive drug with vasodilatory properties. | [Uses]
Antihypertensive (β-blocker). | [Definition]
ChEBI: (R,S,S,S)-nebivolol is a 2,2'-iminobis[1-(6-fluoro-3,4-dihydro-2H-chromen-2-yl)ethanol] that has (1S,1'S,2R,2'S)-configuration. It is a conjugate base of a (R,S,S,S)-nebivolol(1+). It is an enantiomer of a (S,R,R,R)-nebivolol. | [Clinical Use]
Beta-adrenoceptor blocker:
Essential hypertension
Adjunct in heart failure | [Drug interactions]
Potentially hazardous interactions with other drugs
Anaesthetics: enhanced hypotensive effect.
Analgesics: NSAIDs antagonise hypotensive effect.
Anti-arrhythmics: increased risk of myocardial
depression and bradycardia; increased risk of
bradycardia, myocardial depression and AV block
with amiodarone; increased risk of myocardial
depression and bradycardia with flecainide.
Antidepressants: enhanced hypotensive effect with
MAOIs.
Antihypertensives; enhanced hypotensive effect;
increased risk of withdrawal hypertension with
clonidine; increased risk of first dose hypotensive effect
with post-synaptic alpha-blockers such as prazosin.
Antimalarials: increased risk of bradycardia with
mefloquine.
Antipsychotics enhanced hypotensive effect with
phenothiazines.
Calcium-channel blockers: increased risk of
bradycardia and AV block with diltiazem;
hypotension and heart failure possible with
nifedipine and nisoldipine; asystole, severe
hypotension and heart failure with verapamil.
Cytotoxics: possible increased risk of bradycardia
with crizotinib.
Diuretics: enhanced hypotensive effect.
Fingolimod: possibly increased risk of bradycardia.
Moxisylyte: possible severe postural hypotension.
Sympathomimetics: severe hypertension with
adrenaline and noradrenaline and possibly with
dobutamine. | [Metabolism]
Nebivolol is extensively metabolised in the liver by
acyclic and aromatic hydroxylation, N-dealkylation,
and glucuronidation. Hydroxylation is by cytochrome
P450 isoenzyme CYP2D6, partly to active
hydroxy-metabolites.
It is excreted in the urine and faeces, almost entirely as
metabolites. |
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J S LABS
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+91-7330612784 |
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www.jslaboratories.com |
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