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Merck

HT90132

Crystal Violet Solution

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About This Item

Empirical Formula (Hill Notation):
C25H30ClN3
CAS Number:
Molecular Weight:
407.98
UNSPSC Code:
12171500
NACRES:
NA.47
PubChem Substance ID:
MDL number:
Beilstein/REAXYS Number:
3580948
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form

solution

Quality Level

shelf life

Expiry date on the label

IVD

for in vitro diagnostic use

concentration

2.3%

technique(s)

microbe id | staining: suitable

pH

4.6

application(s)

hematology
histology

storage temp.

room temp

SMILES string

[Cl-].CN(C)c1ccc(cc1)\C(c2ccc(cc2)N(C)C)=C3/C=C\C(C=C3)=[N+](/C)C

InChI

1S/C25H30N3.ClH/c1-26(2)22-13-7-19(8-14-22)25(20-9-15-23(16-10-20)27(3)4)21-11-17-24(18-12-21)28(5)6;/h7-18H,1-6H3;1H/q+1;/p-1

InChI key

ZXJXZNDDNMQXFV-UHFFFAOYSA-M

Application

Intended for use in the Gram Stain Procedure No. HT90.

Other Notes

Contains 2.3% certified crystal violet, 0.1% ammonium oxalate and 20% ethyl alcohol, SD3A.


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signalword

Warning

Hazard Classifications

Aquatic Chronic 3 - Carc. 2 - Eye Irrit. 2 - Flam. Liq. 3

Storage Class

3 - Flammable liquids

wgk

WGK 2

flash_point_f

100.0 °F - closed cup

flash_point_c

37.8 °C - closed cup

ppe

Eyeshields, Faceshields, Gloves, type ABEK (EN14387) respirator filter



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Journal of biomedical science, 27(1), 42-42 (2020-03-15)
The underlying mechanism involved in ovarian cancer stemness and chemoresistance remains largely unknown. Here, we explored whether the regulation of c-Kit and plasma membrane prohibitin (PHB) affects ovarian cancer stemness and chemotherapy resistance. Mass spectrum analysis and an in vitro
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Mechanistic target of rapamycin complex 1 (mTORC1) is a master modulator of cellular growth, and its aberrant regulation is recurrently documented within breast cancer. While the small GTPase Rheb1 is the canonical activator of mTORC1, Rheb1-independent mechanisms of mTORC1 activation
Chao Wan et al.
Science advances, 6(13), eaay9789-eaay9789 (2020-04-02)
Radiotherapy (RT) is routinely used in cancer treatment, but expansion of its clinical indications remains challenging. The mechanism underlying the radiation-induced bystander effect (RIBE) is not understood and not therapeutically exploited. We suggest that the RIBE is predominantly mediated by