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Daunorubicin hydrochloride

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-D2022

  • Specification : 98%

  • CAS number : 23541-50-6

  • Formula : C27H29NO10.HCl

  • Molecular Weight : 563.99

  • PUBCHEM ID : 62770

  • Volume : 20mg

In stock

Quantity
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Catalogue Number

BF-D2022

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

563.99

Appearance

White crystal

Botanical Source

synthesis

Structure Type

Others

Category

Standards;Natural Pytochemical;API

SMILES

CC1C(C(CC(O1)OC2CC(CC3=C2C(=C4C(=C3O)C(=O)C5=C(C4=O)C(=CC=C5)OC)O)(C(=O)C)O)N)O.Cl

Synonyms

(8S,10S)-8-Acetyl-10-[(3-amino-2,3,6-trideoxy-a-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-5,12-naphthacenedione Hydrochloride/DAUNOBLASTINE/Daunorubicin hydrochloride/(1S,3S)-3-acetyl-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-α-L-lyxo-hexopyranoside hydrochloride/daunoblastin/(1S,3S)-3-Acetyl-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydro-1-tetracenyl 3-amino-2,3,6-trideoxy-α-L-lyxo-hexopyranoside hydrochloride (1:1)/Daunorubicin HCl/(1S,3S)-3-Acetyl-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-α-L-lyxo-hexopyranoside hydrochloride (1:1)/(8S-cis)-8-Acetyl-10-[(3-amino-2,3,6-trideoxy-a-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-5,12-naphthacenedione Hydrochloride/Daunorubicin (Hydrochloride)/(8S,10S)-8-acetyl-10-{[(2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyltetrahydro-2H-pyran-2-yl]oxy}-6,8,11-trihydroxy-1-methoxy-7,8,9,10-tetrahydrotetracene-5,12-dione hydrochloride/(8S,10S)-8-Acetyl-10-{[(2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyltetrahydro-2H-pyran-2-yl]oxy}-6,8,11-trihydroxy-1-methoxy-7,8,9,10-tetrahydrotetracen-5,12-dionhydrochlorid/Daunoblastina/(8S,10S)-8-acetyl-10-{[(2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyltetrahydro-2H-pyran-2-yl]oxy}-6,8,11-trihydroxy-1-methoxy-7,8,9,10-tetrahydrotetracene-5,12-dione chlorhydrate/Rubidomycin hydrochloride/Cerubidine/5,12-Naphthacenedione, 8-acetyl-10-[(3-amino-2,3,6-trideoxy-α-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-, (8S,10S)-, hydrochloride (1:1)/5,12-naphthacenedione, 8-acetyl-10-[(3-amino-2,3,6-trideoxy-α-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-, (8S,10S)-, hydrochloride/ndc0082-4155/Daunomycin, monohydrochloride/(1S,3S)-3-acetyl-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-a-L-lyxo-hexopyranoside hydrochloride/DAUNOMYCINE HCL/daunorubcin hydrochloride/Daunomycin hydrochloride/Dau hydrochloride/Daunorubicinol hydrochloride/Daunomycin HCl/WP900 HYDROCHLORIDE/Ondena/Hydroxydaunorubicin Hydrochloride/Daunorubicin.HCl

IUPAC Name

(7S,9S)-9-acetyl-7-[(2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyloxan-2-yl]oxy-6,9,11-trihydroxy-4-methoxy-8,10-dihydro-7H-tetracene-5,12-dione;hydrochloride

Density

Solubility

Flash Point

419.5ºC

Boiling Point

770ºC at 760 mmHg

Melting Point

188 - 190ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:23541-50-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

32027262

Abstract

OBJECTIVE:
To investigate the proliferation inhibition and pro-apoptosis effect of LY294002 (PI3K/AKT inhibtor) combined with daunorubicin (DNR) on the chronic myeloid leurenia cell line K562 and its possible mechanisms.

METHODS:
The effect of LY294002 and DNR on the proliferation of K562 cells in different treating time and concentration were measured by MTT assay. The cell cycle was determined by flow cytometry, the mRNA and protein expression of SKP2 , P27, BCL-2 and BAX were determined by RT-PCR and Western blot.

RESULTS:
LY294002 and DNR were able to inhibit the growth of K562 cells and promote apoptosis in time- and concentration-dependent manner (P<0.05), both the cell proliferation-inhibiting rate and apoptosis rate in combination therapy group were higher than that in DNR-monotherapy group (P<0.05). After K562 cells treated by LY294002 combined DNR for 36 h, the cells were statistically significantly reduced in G2/M phase (P<0.05), as compared with control group and DNR group. Compared with DNR group, the cell level of G0/G1 phase rased (P<0.05) and cell level of S phase decreased (P>0.05). Compared with DNR group, the expresson of SKP2 and BCL-2 mRNA decreased, and the expression of P27 mRNA increased in the combination therapy group (P<0.05). The expression of BAX mRNA was not significantly different between different groups. The same result was found in the protein expression.

CONCLUSION:
LY294002 has the sensibilizative effect on DNR chemotherapy, which may be relative with blocking the cell cycle and inducing cell apoptosis.

Title

[LY294002 Enhaces Chemosensitivity of K562 Cells to Daunorubicin].

Author

Geng YH1, Wu WJ2, Li J3, Zhou LL3, Yang YL3.

Publish date

2020 Feb;

PMID

31992692

Abstract

Since the discovery of metal nanoparticles (NPs) in the 1960s, unknown toxicity, cost and the ethical hurdles of research in humans have hindered the translation of these NPs to clinical use. In this work, we demonstrate that Pt NPs with protein coronas are generated in vivo in human blood when a patient is treated with cisplatin. These self-assembled Pt NPs form rapidly, accumulate in tumors, and remain in the body for an extended period of time. Additionally, the Pt NPs are safe for use in humans and can act as anti-cancer agents to inhibit chemotherapy-resistant tumor growth by consuming intracellular glutathione and activating apoptosis. The tumor inhibitory activity is greatly amplified when the Pt NPs are loaded in vitro with the chemotherapeutic drug, daunorubicin, and the formulation is effective even in daunorubicin-resistant models. These in vivo-generated metal NPs represent a biocompatible drug delivery platform for chemotherapy resistant tumor treatment.

Title

Blood-triggered generation of platinum nanoparticle functions as an anti-cancer agent.

Author

Zeng X1,2, Sun J3, Li S4,5, Shi J6, Gao H7, Sun Leong W8, Wu Y2, Li M2, Liu C2, Li P1, Kong J8, Wu YZ9, Nie G10,11,12, Fu Y13,14, Zhang G15.

Publish date

2020 Jan 28

PMID

31887299

Abstract

PURPOSE:
In acute myeloid leukemia (AML), complete remission can be achieved in parts of patients using cytarabine/anthracycline combination-based chemotherapy, however, drug resistance-related recurrence is still a common cause of treatment failure, leading to high mortality among patients. In our research, we revealed the molecular mechanisms that were sufficient to improve sensitivity of AML cells to the anthracycline daunorubicin (DNR).

METHODS:
We evaluated the effects of autophagy and apoptosis induced by DNR using two AML cell lines HL60 and U937.Western blot was preformed to analyze the apoptotic pathway protein expression and flow cytometric analysis was used to detect the level of apoptosis in AML cells. The levels of autophagy-related proteins were detected by western blotting and autophagic vesicles were observed by electron microscopy.

RESULTS:
DNR effectively induced autophagy in two AML cell lines HL60 and U937 confirming by upregulation of LC3-II lipidation, formation of autophagosomes. Inhibition of autophagy by pharmacologic inhibitor HCQ promoted apoptosis induced by DNR, suggesting that autophagy played a vital role in pro-survival in AML. Furthermore, ULK1 inhibition by a highly selective kinase inhibitor SBI-0206965 and shRNA enhanced cytotoxicity of DNR against AML cells. Independent of mTOR -ULK1 signaling pathway, activation of autophagy of DNR was proved to be mediated by AMPK (pThr172)/ULK1 pathway.

CONCLUSIONS:
These results revealed that pro-survival autophagy induced by ULK1 activation was one of the potential mechanisms of AML resistance to DNR. Targeting ULK1 selectively could be a promising therapeutic strategy to enhance sensitivity of DNR for AML therapy.

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

KEYWORDS

Acute myeloid leukemia; Autophagy; Daunorubicin; Drug resistance; ULK1

Title

Targeted inhibition of ULK1 enhances daunorubicin sensitivity in acute myeloid leukemia.

Author

Qiu L1, Zhou G2, Cao S3.

Publish date

2020 Feb 15


Description :

Daunorubicin hydrochloride is a topoisomerase II inhibitor with potent antineoplastic activities.