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Warfarin sodium

Catalog No.: GC39731Purity:>98.00%
Warfarin sodium is an orally active vitamin K antagonist.

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Warfarin sodium
Cas No.: 129-06-6
500mgIn Stock
$25.00
1

Citations

1 publicationsPublications from researchers using this product

Description

Warfarin sodium is an orally active vitamin K antagonist. Warfarin sodium inhibits VKORC1 to reduce the synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X, exerting anticoagulant effects. Warfarin sodium prolongs coagulation time by inhibiting the maturation of protein C and protein S. Warfarin sodium can be used in research on venous thromboembolism, pulmonary embolism, stroke prevention in atrial fibrillation, and anticoagulation for heart valve replacement[1-4].

In vitro, K562 and HL-60 cells were treated with 5-200μM Warfarin sodium for 72 hours. Warfarin sodium reduced cell proliferation, induced apoptosis, and increased cytosolic cytochrome C levels and DNA fragmentation[5]. Stable FIXgla-PC-expressing HEK293 and AV12 cells were co-treated with 2μM Warfarin sodium and 5μM vitamin K epoxide for 48 hours. Warfarin sodium abolished vitamin K epoxide-supported FIXgla-PC carboxylation and secretion[6]. Rat C6 glioma cells were treated with 1mM and 10mM Warfarin sodium for 5 days. Warfarin sodium inhibited cell growth and increased cell detachment from culture plates. Rat C6 glioma cells were treated with 1mM Warfarin sodium for 3 hours. Warfarin sodium mildly reduced the thymidine deoxyribonucleoside cytosolic pool[7].

In vivo, C57BL/6J mouse models of cortical traumatic brain injury received a single oral dose of 0.70mg/kg Warfarin sodium via drinking water. Warfarin sodium increased PT-INR values and enlarged hemorrhage volume in the injured cerebral hemisphere[8]. C57BL/6 mice that underwent 5/6 nephrectomy received daily oral administration of 3mg/kg Warfarin sodium for 16 weeks. Warfarin sodium induced extensive calcification of the ascending and descending aorta, aortic media calcification, increased aortic calcium content, and decreased left ventricular ejection fraction[9]. C57BL/6 pregnant mice received daily intraperitoneal injections of 2-4mg/kg/day Warfarin sodium from gestational days 3 to 11. Warfarin sodium caused placental hemorrhage and subsequent fetal loss. On gestational day 10, a single intraperitoneal injection of 4mg/kg Warfarin sodium increased fetal death and resorption rates and mildly increased minor malformations such as cleft lip/cleft palate[10].

References:
[1] Dimitrokalli E, Fertaki S, Lykouras M, et al. Warfarin Sodium Stability in Oral Formulations. Molecules. 2021 Nov 1;26(21):6631.
[2] Bernard JM, Black JR, Kokseng CU, et al. Warfarin sodium. Practitioner beware. J Am Podiatr Med Assoc. 1992 Jul;82(7):345-51.
[3] O'Reilly RA. Sodium warfarin. Pharmacology. 1972;8(1):181-90.
[4] Beirne OR, Koehler JR. Surgical management of patients on warfarin sodium. J Oral Maxillofac Surg. 1996 Sep;54(9):1115-8.
[5] Onaran I, Sencan S, Demirtas H, et al. Toxic-dose warfarin-induced apoptosis and its enhancement by gamma ionizing radiation in leukemia K562 and HL-60 cells is not mediated by induction of oxidative stress. Naunyn Schmiedebergs Arch Pharmacol. 2008;378(5):471-81.
[6] Tie J, Jin D, Straight D, et al. Functional study of the vitamin K cycle in mammalian cells. Blood. 2011 Mar 10;117(10):2967-74.
[7] McNiel N, Morgan L, et al. Effects of sodium warfarin and sodium heparin plus anticancer agents on growth of rat C6 glioma cells. JNCI. 1984 Jul;73(1):169-76.
[8] Tatara Y, Nakao K, Shimada R, et al. Mechanism of exacerbation of traumatic brain injury under warfarin anticoagulation in male mice. PLoS ONE. 2024 Dec 5;19(12):e0314765.
[9] Tsai M, Chen Y, Chang W, et al. Warfarin accelerated vascular calcification and worsened cardiac dysfunction in remnant kidney mice. Journal of the Chinese Medical Association. 2018;81(4):324-30.
[10] Kronick J, Phelps NE, McCallion DJ, et al. Effects of sodium warfarin administered during pregnancy in mice. Am J Obstet Gynecol. 1974 Mar 15;118(6):819-23.

Protocol

Cell experiment [1]:

Cell lines

K562 cells (chronic human myelogenous leukemic cell line) and HL-60 cells (promyelocytic leukemic cell line)

Preparation Method

K562 and HL-60 cells were maintained in RPMI-1640 supplemented with 10% heat-inactivated FBS at 37°C, 5% CO2. K562 and HL-60 cells were treated with Warfarin sodium at 5-200μM for 72 hours, with part of cells irradiated at 6 Gy before Warfarin sodium treatment, and detections of cell viability, proliferation, protein carbonyl, DNA fragmentation and cytosolic cytochrome C were performed.

Reaction Conditions

5-200μM; 72h

Applications

Warfarin sodium reduced K562 and HL-60 cell proliferation in a dose-dependent manner and produced apoptosis with increased DNA fragmentation and cytosolic cytochrome C at ≥50μM. Warfarin sodium increased DCF fluorescence at 50-200μM. Warfarin sodium at >5μM enhanced radiation-mediated growth inhibition and apoptosis.
Animal experiment [2]:

Animal models

C57BL/6 male mice

Preparation Method

Mice were fed a vitamin K-deficient diet for 1 week before and throughout the experiment. Mice received oral Warfarin sodium via drinking water at low dose (0.35mg/kg/24h) or high dose (0.70mg/kg/24h) for 24 hours. After 24 hours of Warfarin sodium pretreatment, traumatic brain injury was induced by controlled cortical impact (CCI) surgery, or sham procedures (scalp incision or scalp incision plus bone window formation) were performed. Mice were sacrificed at post-injury hours 2, 24, and 72 for measurement of PT-INR, brain hemorrhage volume, blood Warfarin sodium and 7-hydroxywarfarin levels, and liver CYP2C9 protein expression.

Dosage form

0.35-0.70mg/kg/24h; p.o.; single treatment

Applications

Warfarin sodium increased PT-INR values and brain hemorrhage volume in the injured hemisphere at post-injury, increased blood Warfarin sodium and 7-hydroxywarfarin levels at post-injury hour 24 in high-dose groups. Warfarin sodium did not change liver CYP2C9 protein expression.

References:
[1] Onaran I, Sencan S, Demirtas H, et al. Toxic-dose warfarin-induced apoptosis and its enhancement by gamma ionizing radiation in leukemia K562 and HL-60 cells is not mediated by induction of oxidative stress. Naunyn Schmiedebergs Arch Pharmacol. 2008;378(5):471-81.
[2] Tatara Y, Nakao K, Shimada R, et al. Mechanism of exacerbation of traumatic brain injury under warfarin anticoagulation in male mice. PLoS ONE. 2024 Dec 5;19(12):e0314765.

Product Documents

Purity:>98.00%Appearance:A solid

Chemical Properties

CAS No.
129-06-6
SMILES
O=C1C(C(C2=CC=CC=C2)CC(C)=O)=C([O-])C3=CC=CC=C3O1.[Na+]
Molecular Formula
C19H15NaO4
Molecular Weight
330.31
Solubility
Soluble in DMSO
Storage
Store at RT
General tips
Select a suitable solvent according to the product solubility data. Once prepared, aliquot the stock solution to avoid repeated freeze-thaw cycles.
Use stock solutions within 6 months when stored at -80°C or within 1 month when stored at -20°C.
To improve solubility, warm the tube to 37°C and sonicate it for an appropriate period.
Shipping Condition
Evaluation samples are shipped with blue ice. Other available sizes are shipped at room temperature or with blue ice upon request.

CalculatorsMolarity / Dilution / Molecular Weight / Unit Conversion / In Vivo Formulation / Solubility

g/mol

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