We Offer Worldwide Shipping
Login Wishlist

2‘,6’-Dihydroxypinobanksin

$1,120

  • Brand : BIOFRON

  • Catalogue Number : BN-O1572

  • Specification : 98%(HPLC)

  • CAS number : 80366-15-0

  • Formula : C15H12O7

  • Molecular Weight : 304.3

  • PUBCHEM ID : 71307292

  • Volume : 5mg

Available on backorder

Quantity
Checkout Bulk Order?

Catalogue Number

BN-O1572

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

304.3

Appearance

Powder

Botanical Source

This product is isolated and purified from the roots of Scutellaria baicalensis Georgi

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=C(C(=C1)O)C2C(C(=O)C3=C(C=C(C=C3O2)O)O)O)O

Synonyms

2-(2,6-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydro-4H-chromen-4-one/(2R,3R)-2-(2,6-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydro-4H-chromen-4-one/4H-1-Benzopyran-4-one, 2-(2,6-dihydroxyphenyl)-2,3-dihydro-3,5,7-trihydroxy-/4H-1-Benzopyran-4-one, 2-(2,6-dihydroxyphenyl)-2,3-dihydro-3,5,7-trihydroxy-, (2R,3R)-

IUPAC Name

2-(2,6-dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydrochromen-4-one

Density

1.7±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

273.8±26.4 °C

Boiling Point

713.4±60.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

NBQYBZYBTNQEQG-LSDHHAIUSA-N

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#:80366-15-0) 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

27845856

Abstract

Context:
The classic androgen synthesis pathway proceeds via dehydroepiandrosterone, androstenedione, and testosterone to 5α-dihydrotestosterone. However, 5α-dihydrotestosterone synthesis can also be achieved by an alternative pathway originating from 17α-hydroxyprogesterone (17OHP), which accumulates in congenital adrenal hyperplasia (CAH). Similarly, recent work has highlighted androstenedione-derived 11-oxygenated 19-carbon steroids as active androgens, and in CAH, androstenedione is generated directly from 17OHP. The exact contribution of alternative pathway activity to androgen excess in CAH and its response to glucocorticoid (GC) therapy is unknown.

Objective:
We sought to quantify classic and alternative pathway-mediated androgen synthesis in CAH, their diurnal variation, and their response to conventional GC therapy and modified-release hydrocortisone.

Methods:
We used urinary steroid metabolome profiling by gas chromatography-mass spectrometry for 24-hour steroid excretion analysis, studying the impact of conventional GCs (hydrocortisone, prednisolone, and dexamethasone) in 55 adults with CAH and 60 controls. We studied diurnal variation in steroid excretion by comparing 8-hourly collections (23:00-7:00, 7:00-15:00, and 15:00-23:00) in 16 patients with CAH taking conventional GCs and during 6 months of treatment with modified-release hydrocortisone, Chronocort.

Results:
Patients with CAH taking conventional GCs showed low excretion of classic pathway androgen metabolites but excess excretion of the alternative pathway signature metabolites 3α,5α-17-hydroxypregnanolone and 11β-hydroxyandrosterone. Chronocort reduced 17OHP and alternative pathway metabolite excretion to near-normal levels more consistently than other GC preparations.

Conclusions:
Alternative pathway-mediated androgen synthesis significantly contributes to androgen excess in CAH. Chronocort therapy appears superior to conventional GC therapy in controlling androgen synthesis via alternative pathways through attenuation of their major substrate, 17OHP.

Title

Modified-Release and Conventional Glucocorticoids and Diurnal Androgen Excretion in Congenital Adrenal Hyperplasia

Author

Christopher M. Jones,1 Ashwini Mallappa,2 Nicole Reisch,3 Nikolaos Nikolaou,1,4 Nils Krone,1,5 Beverly A. Hughes,1 Donna M. O’Neil,1 Martin J. Whitaker,5,6 Jeremy W. Tomlinson,4 Karl-Heinz Storbeck,7 Deborah P. Merke,2 Richard J. Ross,5,6 and Wiebke Arltcorresponding author1,8

Publish date

2017 Jun 1;

PMID

10447743

Abstract

1999 Jun;

Title

Induction of abortive and productive proliferation in resting human T lymphocytes via CD3 and CD28

Author

Y Muller,* H Wolf,*‡ E Wierenga,† and G Jung*

Publish date

1999 Jun;

PMID

10803412

Abstract

Ocular pursuit in monkeys, elicited by sinusoidal and triangular (constant velocity) stimuli, was studied before and after lesions of the nucleus of the optic tract (NOT). Before NOT lesions, pursuit gains (eye velocity/target velocity) were close to unity for sinusoidal and constant-velocity stimuli at frequencies up to 1 Hz. In this range, retinal slip was less than 2°. Electrode tracks made to identify the location of NOT caused deficits in ipsilateral pursuit, which later recovered. Small electrolytic lesions of NOT reduced ipsilateral pursuit gains to below 0.5 in all tested conditions. Pursuit was better, however, when the eyes moved from the contra-lateral side toward the center (centripetal pursuit) than from the center ipsilaterally (centrifugal pursuit), although the eyes remained in close proximity to the target with saccadic tracking. Effects of lesions on ipsilateral pursuit were not permanent, and pursuit gains had generally recovered to 60-80% of baseline after about 2 weeks. One animal had bilateral NOT lesions and lost pursuit for 4 days. Thereafter, it had a centrifugal pursuit deficit that lasted for more than 2 months. Vertical pursuit and visually guided saccades were not affected by the bilateral NOT lesions in this animal. We also compared effects of these and similar NOT lesions on opto-kinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN). Correlation of functional deficits with NOT lesions from this and previous studies showed that rostral lesions of NOT in and around the pretectal oli-vary nucleus, which interrupted cortical input through the brachium of the superior colliculus (BSC), affected both smooth pursuit and OKN. In two animals in which it was tested, NOT lesions that caused a deficit in pursuit also decreased the rapid and slow components of OKN slow-phase velocity and affected OKAN. It was previously shown that slightly more caudal NOT lesions were more effective in altering gain adaptation of the angular vestibulo-ocular relfex (aVOR). The present findings suggest that cortical pathways through rostral NOT play an important role in maintenance of ipsilateral ocular pursuit. Since lesions that affected ocular pursuit had similar effects on ipsilateral OKN, processing for these two functions is probably closely linked in NOT, as it is elsewhere.

KEYWORDS

Monkey, Smooth pursuit, Optokinetic nystagmus, Nucleus of the optic tract (NOT), Eye movemen

Title

Functions of the nucleus of the optic tract (NOT): II. Control of ocular pursuit

Author

Sergei B. Yakushin, Martin Gizzi, Harvey Reisine, Theodore Raphan, Jean Buttner-Ennever, Bernard Cohen

Publish date

2007 Oct 9.


Description :

Empty ...