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Merck

SML2263

Sigma-Aldrich

Ladostigil tartrate

≥98% (HPLC)

Synonym(e):

(3R)-(N-Propargylaminoindan-5-yl)-ethyl methyl carbamate tartrate (2:1), TV-3326, TV3326

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5 MG
CHF 85.90
25 MG
CHF 346.00

CHF 85.90


Voraussichtliches Versanddatum30. Mai 2025


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5 MG
CHF 85.90
25 MG
CHF 346.00

About This Item

Empirische Formel (Hill-System):
C16H20N2O2 · 0.5C4H6O6
CAS-Nummer:
Molekulargewicht:
347.39
MDL-Nummer:
UNSPSC-Code:
12352200

CHF 85.90


Voraussichtliches Versanddatum30. Mai 2025


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Assay

≥98% (HPLC)

Form

powder

Lagerbedingungen

desiccated

Farbe

white to beige

Löslichkeit

H2O: 2 mg/mL, clear

Lagertemp.

2-8°C

SMILES String

N([C@@H]3CCc4c3cc(cc4)OC(=O)N(CC)C)CC#C.N([C@@H]1CCc2c1cc(cc2)OC(=O)N(CC)C)CC#C.O[C@H]([C@@H](O)C(=O)O)C(=O)O

InChI

1S/2C16H20N2O2.C4H6O6/c2*1-4-10-17-15-9-7-12-6-8-13(11-14(12)15)20-16(19)18(3)5-2;5-1(3(7)8)2(6)4(9)10/h2*1,6,8,11,15,17H,5,7,9-10H2,2-3H3;1-2,5-6H,(H,7,8)(H,9,10)/t2*15-;1-,2-/m111/s1

InChIKey

PRLVBVAJMQZMJN-OGOSNNLPSA-N

Biochem./physiol. Wirkung

Ladostigil, a carbamate is also a butyryl cholinesterase (BuChE) inhibitor.[1] It possesses anti-inflammatory property and effectively reduces the levels of tumor necrosis factor α (TNF-α) in lipopolysaccharide (LPS)-activated macrophages.[1] It provides protection to cardiomyocytes.[2] Ladostigil has neuroprotective functionality and has the potential to treat mild cognitive impairment (MCI) and spatial memory deficits development.[3] It also exhibits protective effects during oxidative and nitrative stress.[3]
Multifunctional drug designed to treat Alzhemier′s disease by combining in a single molecule the neuroprotective/neurorestorative effects of the (MAO)-B inhibitor rasagiline with the cholinesterase (ChE) inhibitory activity of rivastigmine.
Multifunctional drug designed to treat Alzhemier′s disease by combining in a single molecule the neuroprotective/neurorestorative effects of the (MAO)-B inhibitor rasagiline with the cholinesterase (ChE) inhibitory activity of rivastigmine.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

Moussa B H Youdim
Experimental neurobiology, 22(1), 1-10 (2013-04-16)
Present anti-PD and -AD drugs have limited symptomatic activity and devoid of neuroprotective and neurorestorative property that is needed for disease modifying action. The complex pathology of PD and AD led us to develop several multi-target neuroprotective and neurorestorative drugs
Rony Panarsky et al.
Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 7(2), 488-498 (2012-03-29)
Impaired mitochondrial function accompanied by microglial activation and the release of nitric oxide (NO) and pro-inflammatory cytokines has been reported in Alzheimer's disease, its prodromal phase of Mild Cognitive Impairment (MCI) and in aged rats. The present study showed that
Inessa Yanovsky et al.
Journal of medicinal chemistry, 55(23), 10700-10715 (2012-11-16)
The cascade of events that occurs in Alzheimer's disease involving oxidative stress and the reduction in cholinergic transmission can be better addressed by multifunctional drugs than cholinesterase inhibitors alone. For this purpose, we prepared a large number of derivatives of
John P M Finberg et al.
Frontiers in pharmacology, 7, 340-340 (2016-11-03)
Inhibitors of MAO-A and MAO-B are in clinical use for the treatment of psychiatric and neurological disorders respectively. Elucidation of the molecular structure of the active sites of the enzymes has enabled a precise determination of the way in which
Orly Weinreb et al.
British journal of pharmacology, 173(13), 2080-2094 (2015-09-04)
Alzheimer's disease (AD) is accepted nowadays as a complex neurodegenerative disorder with multifaceted cerebral pathologies, including extracellular deposition of amyloid β peptide-containing plaques, intracellular neurofibrillary tangles, progressive loss of cholinergic neurons, metal dyshomeostasis, mitochondrial dysfunction, neuroinflammation, glutamate excitoxicity, oxidative stress

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