We Offer Worldwide Shipping
Login Wishlist

2-Chloromethyl-3-methyl-4-(2,2,2-trifluoroethoxy)pyridine hydrochloride

$58

Brand : BIOFRON
Catalogue Number : BN-O1231
Specification : 98%(HPLC)
CAS number : 127337-60-4
Formula : C9H10Cl2F3NO
Molecular Weight : 276.08
PUBCHEM ID : 16217647
Volume : 5mg

Available on backorder

Quantity
Checkout Bulk Order?

Catalogue Number

BN-O1231

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

276.08

Appearance

Botanical Source

Structure Type

Category

SMILES

CC1=C(C=CN=C1CCl)OCC(F)(F)F.Cl

Synonyms

2-(Chloromethyl)-3-methyl-4-(2,2,2-trifluoroethoxy)pyridine hydrochloride/Pyridine, 2-(chloromethyl)-3-methyl-4-(2,2,2-trifluoroethoxy)-, hydrochloride (1:1)/2-(Chloromethyl)-3-methyl-4-(2,2,2-trifluoroethoxy)pyridine hydrochloride (1:1)/2-(Chlormethyl)-3-methyl-4-(2,2,2-trifluorethoxy)pyridinhydrochlorid/2-(chloromethyl)-3-methyl-4-(2,2,2-trifluoroethoxy)pyridine,hydrochloride/Lansoprazole Impurity 17

IUPAC Name

2-(chloromethyl)-3-methyl-4-(2,2,2-trifluoroethoxy)pyridine;hydrochloride

Density

Solubility

Flash Point

132.5ºC

Boiling Point

295.4ºC at 760 mmHg

Melting Point

208-214 °C

InChl

InChl Key

CMZBQUWICURDCD-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#:127337-60-4) 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

31148919

Abstract

Detailed morphological study of more than 2600 North East Atlantic (NEA) sphaerodorids (SphaerodoridaeAnnelida) and phylogenetic analyses of DNA sequences of representatives of several identified morphospecies enforced changing the current systematic classification within the family allowed the discovery of new species provided new information about the morphological and genetic characterisation of members of this group and increased the species occurrence data to better infer their geographic and bathymetric distribution ranges. Phylogenetic analyses of nuclear (18S rRNA and 28S rRNA) and mitochondrial sequences (COI and 16S rRNA) of NEA short-bodied sphaerodorids revealed outstanding results including paraphyly of the genera SphaerodoropsisSphaerodoridium, and Sphaerephesia. The number of longitudinal and transverse rows of dorsal macrotubercles is proposed as potential synapomorphies for the main clades and are consequently herein used for the genera delimitation. The new classification proposed here implies nomenclatural changes and the erection of a new genus Geminofilumgen. n. to accommodate the species previously considered as Sphaerodoropsis with two transverse rows of dorsal macrotubercles per segment. Four species are being described herein: Euritmianordica Capa & Bakken sp. n.Sphaerephesiamultichaeta Capa Moreira & Parapar sp. n.Sphaerephesiaponsi Capa Parapar & Moreira sp. n. and Sphaerodoridiumceliae Moreira Capa & Parapar sp. n. Characterisation of the other 21 species including updated iconography and an identification key to all NEA short-bodied sphaerodorids are provided.

KEYWORDS

16S rRNA, 18S rRNA, 28S rRNA, classification, COI, identification key, integrative taxonomy, morphology, new genus, new species, phylogeny, systematics

Title

Systematic re-structure and new species of Sphaerodoridae (Annelida) after morphological revision and molecular phylogenetic analyses of the North East Atlantic fauna

Author

Maria Capa,corresponding author1,2 Arne Nygren,3 Julio Parapar,4 Torkild Bakken,2 Karin Meißner,5 and Juan Moreira6

Publish date

2019;

PMID

30470303

Abstract

MYC is one of the most important oncogenes in cancer. Indeed, MYC is upregulated in 50-60% of all tumors. MYC overexpression can be achieved through a variety of mechanisms, including gene duplications, chromosomal translocations or somatic mutations leading to increased MYC stability. However, recent studies have identified numerous tissue-specific non-coding enhancers of MYC that play major roles in cancer, highlighting long-range transcriptional regulation of MYC as a critical novel mechanism leading to MYC hyperactivation and as a potential target for new therapeutic strategies in the near future. Here, we summarize the regions and mechanisms involved in the long-range transcriptional regulation of MYC, underscoring the relevance of MYC enhancers both in normal physiological development and in MYC-driven cancer initiation and progression.

KEYWORDS

MYC, Enhancer, long-range transcriptional regulation, cancer, SNP

Title

The MYC enhancer-ome: Long-range transcriptional regulation of MYC

Author

Olga Lancho1 and Daniel Herranz1,2

Publish date

2019 Dec 1.

PMID

26455377

Abstract

A major problem in patients with multiple myeloma is chemotherapy resistance, which develops in myeloma cells upon interaction with bone marrow stromal cells. However, few studies have determined the role of bone marrow adipocytes, a major component of stromal cells in the bone marrow, in myeloma chemotherapy resistance. We reveal that mature human adipocytes activate autophagy and upregulate the expression of autophagic proteins, thereby suppressing chemotherapy-induced caspase cleavage and apoptosis in myeloma cells. We found that adipocytes secreted known and novel adipokines, such as leptin and adipsin. The addition of these adipokines enhanced the expression of autophagic proteins and reduced apoptosis in myeloma cells. In vivo studies further demonstrated the importance of bone marrow-derived adipocytes in the reduced response of myeloma cells to chemotherapy. Our findings suggest that adipocytes, adipocyte-secreted adipokines, and adipocyte-activated autophagy are novel targets for combatting chemotherapy resistance and enhancing treatment efficacy in myeloma patients.

KEYWORDS

multiple myeloma, adipocytes, autophagy, apoptosis, chemotherapy resistance

Title

Mature adipocytes in bone marrow protect myeloma cells against chemotherapy through autophagy activation

Author

Zhiqiang Liu,#1 Jingda Xu,#1 Jin He,1 Huan Liu,1 Pei Lin,2 Xinhai Wan,3 Nora M. Navone,3 Qiang Tong,4 Larry W. Kwak,1 Robert Z. Orlowski,1 and Jing Yang1

Publish date

2015 Oct 27;