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Millipore

Fractogel® EMD SO3⁻ (S) Resin

Synonym(s):

Fractogel® EMD SO₃⁻ (S)

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About This Item

UNSPSC Code:
41115711

ligand

(Sulfoisobutyl)

Quality Level

100
400

description

strong cation exchanger, suspension in 20% ethanol and 150 mM NaCl (20-40 µm)

sterility

sterile (Caustic Stable)

assay

≥90% (HPLC)

form

resin

manufacturer/tradename

Calbiochem®

parameter

8 bar max. pressure
80 cm/hr flow rate

matrix active group

methacrylate

mean particle size

20-40 um μm

capacity

150 mg binding capacity (lysozyme/ml of resin)

transition temp

flash point 35 °C (Does not sustain combustion.)

density

1.43 g/cm3 at 20 °C

bulk density

1000 kg/m3

separation technique

strong cation exchange

shipped in

ambient

storage temp.

2-8°C

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Packaging

  • 1.16882.0100: Fractogel® EMD SO3- (S) Resin 100ml
  • 1.16882.0010: Fractogel® EMD SO3- (S) Resin 10ml
  • 1.16882.0500: Fractogel® EMD SO3- (S) Resin 500ml
  • 1.16882.5000: Fractogel® EMD SO3- (S) Resin 5L

Warning

Toxicity: Standard Handling (A)

Analysis Note

Appearance: Milky turbid suspension, free from impurities (foreign particles)
Microscopic evaluation: Uniform spherical particles,no agglomerates,no fines
Extractable matter (water): ≤ 0.05 %
Cerium: ≤ 10 µg/g
Pressure drop(column: ID=1.6 cm, L=10 cm at 5 ml/min): ≤ 5.0 bar
Particle size (d10): 20 - 28 µm
Particle size (d50): 24 - 34 µm
Particle size (d90): 28 - 38 µm
Colony forming units (TAMC + TYMC): ≤ 100 CFU/ml
Endotoxins: ≤ 1.00 EU/ml
Protein binding capacity (lysozyme): 120 - 180 mg/ml
Functional test (c:d): ≤ 0.15
Functional test (b:a): ≤ 0.15
Functional test: Separation chymotrypsinogen A, cytochrom C and lysozyme

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
FRACTOGEL is a registered trademark of Merck KGaA, Darmstadt, Germany

pictograms

Flame
GHS02

signalword

Warning

hcodes

H226

Hazard Classifications

Flam. Liq. 3

Storage Class

3 - Flammable liquids

wgk_germany

WGK 1

flash_point_f

95.0 °F

flash_point_c

35 °C

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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D L Boyle et al.
The Journal of pharmacology and experimental therapeutics, 296(2), 495-500 (2001-02-13)
Adenosine (ADO) is a homeostatic inhibitory autocoid that is released at sites of inflammation and tissue injury, and exerts anti-inflammatory effects via multiple interactions at ADO receptor subtypes. Inhibition of ADO kinase (AK) increases extracellular ADO concentrations and AK inhibitors
R Suzuki et al.
British journal of pharmacology, 132(7), 1615-1623 (2001-03-27)
1. Adenosine (ADO) receptor activation modulates sensory transmission in the dorsal horn. Little is known about the circumstances underlying release of the purine. The present study was conducted to investigate the effect of a novel and potent non-nucleoside adenosine kinase
Jean De Vry et al.
European journal of pharmacology, 491(2-3), 137-148 (2004-05-14)
The chronic constriction injury model is a rat model of neuropathic pain based on a unilateral loose ligation of the sciatic nerve. The aim of the present study was to test its sensitivity to various clinically validated and experimental drugs.
M F Jarvis et al.
The Journal of pharmacology and experimental therapeutics, 295(3), 1156-1164 (2000-11-18)
Adenosine (ADO) is an inhibitory neuromodulator that can increase nociceptive thresholds in response to noxious stimulation. Inhibition of the ADO-metabolizing enzyme adenosine kinase (AK) increases extracellular ADO concentrations at sites of tissue trauma and AK inhibitors may have therapeutic potential
E A Kowaluk et al.
The Journal of pharmacology and experimental therapeutics, 295(3), 1165-1174 (2000-11-18)
Adenosine kinase (AK; EC 2.7.1.20) is a key intracellular enzyme regulating intra-and extracellular concentrations of adenosine (ADO), an endogenous neuromodulator, antinociceptive, and anti-inflammatory autocoid. AK inhibition provides a means of potentiating local tissue concentrations of endogenous ADO, and AK inhibitors

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