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Amoxapine

$92

  • Brand : BIOFRON

  • Catalogue Number : BN-O1190

  • Specification : 98%(HPLC)

  • CAS number : 14028-44-5

  • Formula : C17H16ClN3O

  • Molecular Weight : 313.8

  • PUBCHEM ID : 2170

  • Volume : 5mg

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Catalogue Number

BN-O1190

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

313.8

Appearance

Botanical Source

Structure Type

Category

SMILES

C1CN(CCN1)C2=NC3=CC=CC=C3OC4=C2C=C(C=C4)Cl

Synonyms

Asendis/Demolox/N-desmethylloxapine/Defanyl/2-Chloro-11-(1-piperazinyl)dibenz[b,f][1,4]oxazepine/2-Chlor-11-(1-piperazinyl)dibenz<1.4>oxazepin/Moxadil/2-Chloro-11-(1-piperazinyl)dibenzo[b,f][1,4]oxazepine/Amoxapine/Amoxapinum/Asendin/8-chloro-6-piperazin-1-ylbenzo[b][1,4]benzoxazepine/Amoxapina/Amoxan/Amoxepine

IUPAC Name

8-chloro-6-piperazin-1-ylbenzo[b][1,4]benzoxazepine

Density

1.37g/cm3

Solubility

Flash Point

238ºC

Boiling Point

469.9ºC at 760mmHg

Melting Point

175-1760C

InChl

InChl Key

QWGDMFLQWFTERH-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:14028-44-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

30000242

Title

Amoxapine

Publish date

2019 Feb 7.

PMID

29109161

Abstract

Earlier, we reported that three Food and Drug Administration-approved drugs, trifluoperazine (TFP; an antipsychotic), amoxapine (AXPN; an antidepressant), and doxapram (DXP; a breathing stimulant), identified from an in vitro murine macrophage cytotoxicity screen, provided mice with 40 to 60% protection against pneumonic plague when administered at the time of infection for 1 to 3 days. In the present study, the therapeutic potential of these drugs against pneumonic plague in mice was further evaluated when they were administered at up to 48 h postinfection. While the efficacy of TFP was somewhat diminished as treatment was delayed to 24 h, the protection of mice with AXPN and DXP increased as treatment was progressively delayed to 24 h. At 48 h postinfection, these drugs provided the animals with significant protection (up to 100%) against challenge with the agent of pneumonic or bubonic plague when they were administered in combination with levofloxacin. Likewise, when they were used in combination with vancomycin, all three drugs provided mice with 80 to 100% protection from fatal oral Clostridium difficile infection when they were administered at 24 h postinfection. Furthermore, AXPN provided 40 to 60% protection against respiratory infection with Klebsiella pneumoniae when it was administered at the time of infection or at 24 h postinfection. Using the same in vitro cytotoxicity assay, we identified an additional 76/780 nonantibiotic drugs effective against K. pneumoniae For Acinetobacter baumannii, 121 nonantibiotic drugs were identified to inhibit bacterium-induced cytotoxicity in murine macrophages. Of these 121 drugs, 13 inhibited the macrophage cytotoxicity induced by two additional multiple-antibiotic-resistant strains. Six of these drugs decreased the intracellular survival of all three A. baumannii strains in macrophages. These results provided further evidence of the broad applicability and utilization of drug repurposing screening to identify new therapeutics to combat multidrug-resistant pathogens of public health concern.

KEYWORDS

Acinetobacter baumannii; Clostridium difficile; Klebsiella pneumoniae; Yersinia pestis; bubonic plague; in vitro assays; mouse models; new therapeutics; pneumonic plague.

Title

Combating Multidrug-Resistant Pathogens With Host-Directed Nonantibiotic Therapeutics

Author

Jourdan A Andersson 1, Jian Sha 2 3, Michelle L Kirtley 2, Emily Reyes 2, Eric C Fitts 2, Sara M Dann 1 2 3 4 5, Ashok K Chopra 6 2 3 7 5

Publish date

2017 Dec 21

PMID

30185102

Abstract

GM3 synthase deficiency is due to biallelic pathogenic variants in ST3GAL5, which encodes a sialyltransferase that synthesizes ganglioside GM3. Key features of this rare autosomal recessive condition include profound intellectual disability, failure to thrive and infantile onset epilepsy. We expand the phenotypic spectrum with 3 siblings who were found by whole exome sequencing to have a homozygous pathogenic variant in ST3GAL5, and we compare these cases to those previously described in the literature. The siblings had normal birth history, subsequent developmental stagnation, profound intellectual disability, choreoathetosis, failure to thrive, and visual and hearing impairment. Ichthyosis and self-injurious behavior are newly described in our patients and may influence clinical management. We conclude that GM3 synthase deficiency is a neurodevelopmental disorder with consistent features of profound intellectual disability, choreoathetosis, and deafness. Other phenotypic features have variable expressivity, including failure to thrive, epilepsy, regression, vision impairment, and skin findings. Our analysis demonstrates a broader phenotypic range of this potentially under-recognized disorder.

KEYWORDS

GM3 synthase; ST3GAL5; cerebral palsy; gangliosides; intellectual disability.

Title

ST3GAL5-Related Disorders: A Deficiency in Ganglioside Metabolism and a Genetic Cause of Intellectual Disability and Choreoathetosis

Author

Eliza Gordon-Lipkin 1 2 3, Julie S Cohen 4, Siddharth Srivastava 5, Bruno P Soares 6, Eric Levey 1 3, Ali Fatemi 1 2 3 4

Publish date

Nov-18


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