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Icaritin

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-I2003

  • Specification : 98%

  • CAS number : 118525-40-9

  • Formula : C21H20O6

  • Molecular Weight : 368.38

  • PUBCHEM ID : 5318980

  • Volume : 20mg

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Quantity
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Catalogue Number

BF-I2003

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

368.38

Appearance

White crystalline powder

Botanical Source

Epimedium brevicornu,Fallopia multiflora

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

CC(=CCC1=C2C(=C(C=C1O)O)C(=O)C(=C(O2)C3=CC=C(C=C3)OC)O)C

Synonyms

3,5,7-Trihydroxy-2-(4-methoxyphenyl)-8-(3-methylbut-2-en-1-yl)-4H-chromen-4-one/Icaritin/3,5,7-Trihydroxy-2-(4-methoxyphenyl)-8-(3-methyl-2-buten-1-yl)-4H-chromen-4-one/BIDD:ER0021/4H-1-Benzopyran-4-one, 3,5,7-trihydroxy-2-(4-methoxyphenyl)-8-(3-methyl-2-buten-1-yl)-/3,7-dihydroxy-8-prenyl-4'-methoxychrysin/Anhydroicaritin

IUPAC Name

3,5,7-trihydroxy-2-(4-methoxyphenyl)-8-(3-methylbut-2-enyl)chromen-4-one

Density

1.4±0.1 g/cm3

Solubility

Methanol; Acetone

Flash Point

206.7±23.6 °C

Boiling Point

582.0±50.0 °C at 760 mmHg

Melting Point

239ºC

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#:118525-40-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

26568769

Abstract

Background
A large proportion of the tropical rain forests of central Africa undergo periodic selective logging for timber harvesting. The REDD+ mechanism could promote less intensive logging if revenue from the additional carbon stored in the forest compensates financially for the reduced timber yield.

Results
Carbon stocks, and timber yields, and their associated values, were predicted at the scale of a forest concession in Gabon over a project scenario of 40 yr with reduced logging intensity. Considering that the timber contribution margin (i.e. the selling price of timber minus its production costs) varies between 10 and US$40 m −3, the minimum price of carbon that enables carbon revenues to compensate forgone timber benefits ranges between US$4.4 and US$25.9/tCO 2 depending on the management scenario implemented.

Conclusions
Where multiple suppliers of emission reductions compete in a REDD+ carbon market, tropical timber companies are likely to change their management practices only if very favourable conditions are met, namely if the timber contribution margin remains low enough and if alternative management practices and associated incentives are appropriately chosen.

Electronic supplementary material
The online version of this article (doi:10.1186/s13021-014-0004-3) contains supplementary material, which is available to authorized users.

KEYWORDS

Break-even price, Carbon credit, Forest degradation, Forest management, REDD+, Tropical forest, Diameter cutting limit, Felling cycle, Forest dynamics

Title

Opportunity costs of carbon sequestration in a forest concession in central Africa

Author

Michel Ndjondo,1,6 Sylvie Gourlet-Fleury,2 Raphaël J Manlay,3 Nestor Laurier Engone Obiang,1 Alfred Ngomanda,1 Claudia Romero,4 Florian Claeys,2 and Nicolas Picardcorresponding author1,2,5

Publish date

2014 Jul 3

PMID

31591419

Abstract

Understanding the population composition and dynamics of migratory megafauna at key developmental habitats is critical for conservation and management. The present study investigated whether differential recovery of Caribbean green turtle (Chelonia mydas) rookeries influenced population composition at a major juvenile feeding ground in the southern Caribbean (Lac Bay, Bonaire, Caribbean Netherlands) using genetic and demographic analyses. Genetic divergence indicated a strong temporal shift in population composition between 2006-2007 and 2015-2016 (ϕST = 0.101, P < 0.001). Juvenile recruitment (<75.0 cm straight carapace length; SCL) from the north-western Caribbean increased from 12% to 38% while recruitment from the eastern Caribbean region decreased from 46% to 20% between 2006-2007 and 2015-2016. Furthermore, the product of the population growth rate and adult female abundance was a significant predictor for population composition in 2015-2016. Our results may reflect early warning signals of declining reproductive output at eastern Caribbean rookeries, potential displacement effects of smaller rookeries by larger rookeries, and advocate for genetic monitoring as a useful method for monitoring trends in juvenile megafauna. Furthermore, these findings underline the need for adequate conservation of juvenile developmental habitats and a deeper understanding of the interactions between megafaunal population dynamics in different habitats.

Subject terms: Conservation biology, Population dynamics, Population genetics

Title

Population recovery changes population composition at a major southern Caribbean juvenile developmental habitat for the green turtle, Chelonia mydas

Author

Jurjan P. van der Zee,corresponding author1,2 Marjolijn J. A. Christianen,1,3 Mabel Nava,4 Ximena Velez-Zuazo,4,5 Wensi Hao,1 Martine Berube,1,6 Hanneke van Lavieren,7 Michael Hiwat,7 Rachel Berzins,8 Johan Chevalier,9 Damien Chevallier,10 Marie-Clelia Lankester,9 Karen A. Bjorndal,11 Alan B. Bolten,11 Leontine E. Becking,2,12 and Per J. Palsbøll1,6

Publish date

2019 Oct 7

PMID

20653960

Abstract

Background
The evolution of drug resistance in malaria parasites highlights a need to identify and evaluate strategies that could extend the useful therapeutic life of anti-malarial drugs. Such strategies are deployed to best effect before resistance has emerged, under conditions of great uncertainty.

Methods
Here, the emergence and spread of resistance was modelled using a hybrid framework to evaluate prospective strategies, estimate the time to drug failure, and weigh uncertainty. The waiting time to appearance was estimated as the product of low mutation rates, drug pressure, and parasite population sizes during treatment. Stochastic persistence and the waiting time to establishment were simulated as an evolving branching process. The subsequent spread of resistance was simulated in simple epidemiological models.

Results
Using this framework, the waiting time to the failure of artemisinin combination therapy (ACT) for malaria was estimated, and a policy of multiple first-line therapies (MFTs) was evaluated. The models quantify the effects of reducing drug pressure in delaying appearance, reducing the chances of establishment, and slowing spread. By using two first-line therapies in a population, it is possible to reduce drug pressure while still treating the full complement of cases.

Conclusions
At a global scale, because of uncertainty about the time to the emergence of ACT resistance, there was a strong case for MFTs to guard against early failure. Our study recommends developing operationally feasible strategies for implementing MFTs, such as distributing different ACTs at the clinic and for home-based care, or formulating different ACTs for children and adults.

Title

Prospective strategies to delay the evolution of anti-malarial drug resistance: weighing the uncertainty

Author

David L Smith,corresponding author1 Eili Y Klein,2,3 F Ellis McKenzie,5 and Ramanan Laxminarayan2,4

Publish date

2010 Jul 23


Description :

Icaritin(Anhydroicaritin) is a component of Epimedium flavonoid isolated from Herba Epimedii; enhances osteoblastic differentiation of mesenchymal stem cells (MSCs) while it inhibits adipogenic differentiation of MSCs by inhibiting PPAR-g pathway.IC50 value:Target: in vitro: Icaritin was unable to promote proliferation, migration and tube like structure formation by human umbilical vein endothelial cells (HUVECs) in vitro [1]. Icaritin potently inhibited proliferation of K562 cells (IC50 was 8 μM) and primary CML cells (IC50 was 13.4 μM for CML-CP and 18 μM for CML-BC), induced CML cells apoptosis and promoted the erythroid differentiation of K562 cells with time-dependent manner. Furthermore, Icaritin was able to suppress the growth of primary CD34+ leukemia cells (CML) and Imatinib-resistant cells, and to induce apoptosis [2]. icaritin strongly inhibited the growth of breast cancer MDA-MB-453 and MCF7 cells. At concentrations of 2-3 μM, icaritin induced cell cycle arrest at the G(2)/M phase accompanied by a down-regulation of the expression levels of the G(2)/M regulatory proteins such as cyclinB, cdc2 and cdc25C. Icaritin at concentrations of 4-5 μM, however, induced apoptotic cell death characterized by the accumulation of the annexin V- and propidium iodide-positive cells, cleavage of poly ADP-ribose polymerase (PARP) and down-regulation of the Bcl-2 expression [3].in vivo: In mouse leukemia model, Icaritin could prolong lifespan of NOD-SCID nude mice inoculated with K562 cells as effective as Imatinib without suppression of bone marrow. Icaritin could up-regulate phospho-JNK or phospho-C-Jun and down-regulate phospho-ERK, phospho-P-38, Jak-2, phospho-Stat3 and phospho-Akt expression with dose- or time-dependent manner [2].