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Accessible (Haz class 3, 4, 5 or 8), International
Niflumic acid, a drug used for joint and muscular pain, affected Ca²⁺ signaling in different models. In MG63 cells, niflumic acid induced [Ca²⁺]i rises by evoking PLC-dependent (phospholipase C) Ca²⁺ release from the endoplasmic reticulum, and Ca²⁺ entry via PKC-sensitive (protein kinase C) store-operated Ca²⁺ entry. Niflumic acid also induced Ca²⁺-independent cell death[3]. Niflumic acid (10 and 30 mM) also inhibited the noradrenaline-induced increase in perfusion pressure and 30 mM niflumic acid reduced the pressor response to 1 nmol noradrenaline by 34 +/- 6%. The increases in perfusion elicited by 5-HT (0.3 and 3 nmol) were reduced by niflumic acid (10 and 30 mM) in a concentration-dependent manner and 30 mM niflumic acid inhibited responses to 0.3 and 3 nmol 5-HT by, respectively, 49 +/- 8% and 50 +/- 7%. Niflumic acid selectively reduces a component of noradrenaline- and 5-HT-induced pressor responses by inhibiting a mechanism which leads to the opening of voltage-gated calcium channels[4]. Niflumic acid restored core and associated symptoms of peripheral neuropathy by suppressing oxidative-nitrosative stress, inflammatory cytokines (TNF-α, IL-1β) and TRPV1 level in stavudine-induced neuropathic pain in rats. Pharmacological efficacy of niflumic acid (20 mg/kg) was equivalent to pregabalin (30 mg/kg) [5].
Niflumic Acid/氟尼酸 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Rat aortic smooth muscle cells
10 µM
10 min
Niflumic acid did not inhibit contractions induced by KCl (up to 120 mM), which were completely blocked by nifedipine.
Br J Pharmacol. 1996 Jun;118(4):1065-71
CHO cells
30, 100 µM
10 s
Niflumic acid inhibited glycine-induced currents mediated by α3 glycine receptors, with higher blocking potency at positive membrane potentials.
Front Mol Neurosci. 2017 May 16;10:125
CHO cells
10, 30, 100 µM
10 s
Niflumic acid showed stronger inhibition of glycine-induced currents mediated by α2 glycine receptors, with pronounced voltage dependence.
Front Mol Neurosci. 2017 May 16;10:125
CHO cells
30, 100, 300 µM
10 s
Niflumic acid inhibited glycine-induced currents mediated by α1 glycine receptors in a voltage-dependent manner, with higher blocking potency at positive membrane potentials.
Front Mol Neurosci. 2017 May 16;10:125
Rat skeletal muscle fibers
42 µM (IC50)
10–15 minutes
Niflumic acid inhibits chloride conductance of rat skeletal muscle by directly inhibiting the CLC-1 channel and by increasing intracellular calcium.
Br J Pharmacol. 2007 Jan;150(2):235-47
Hypoglossal motoneurons (HMs) in brainstem slices from mice
100 µM
1-3 minutes
NFA inhibited the amplitude and frequency of glycinergic synaptic currents, with stronger inhibition in the neonatal group
Front Mol Neurosci. 2018 Nov 13;11:416
Rat aortic smooth muscle cells
10 µM
15 min
In Ca-free conditions, niflumic acid did not inhibit the transient contraction induced by 1 μM NA, indicating it does not reduce calcium release from intracellular stores or the sensitivity of the contractile apparatus to calcium.
Br J Pharmacol. 1996 Jun;118(4):1065-71
Rat aortic smooth muscle cells
10 µM
15 min
Niflumic acid inhibited contractions induced by brief application of 1 μM NA by 55%.
Br J Pharmacol. 1996 Jun;118(4):1065-71
Rat mesenteric vascular bed smooth muscle cells
10 and 30 µM
15 minutes
Niflumic acid inhibited noradrenaline- and 5-HT-induced pressor responses, with 30 μM niflumic acid reducing the pressor response to 1 nmol noradrenaline by 34±6%.
Br J Pharmacol. 1997 Mar;120(5):813-8
Rat stomach fundus smooth muscle cells
1-30 µM
15 minutes
Niflumic acid concentration-dependently inhibited 5-HT-induced contractions, reducing to 15.5±6.0% of control at 30 μM.
Br J Pharmacol. 2000 Jun;130(3):678-84
Rat pulmonary artery smooth muscle cells
50 µM
2 minutes
NFA significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i.
Br J Pharmacol. 2003 Dec;140(8):1442-50
Xenopus oocytes
100 µM
2 to 5 min
NFA increased Kv1.1 current amplitudes by enhancing the channel open probability, causing a hyperpolarizing shift in the voltage dependence of both channel opening and gating charge movement, slowing the OFF-gating current decay.
Proc Natl Acad Sci U S A. 2023 Aug;120(31):e2207978120
HEK293 cells
50 µM
24 hours
Niflumic acid (NFA) acted as a pharmacological chaperone, restoring chloride current density of A531V and V947E mutants to levels similar to WT without altering voltage dependence.
Front Pharmacol. 2022 Aug 11;13:958196
Rat aortic smooth muscle cells
3 µM and 10 µM
30 min
Niflumic acid reversibly and concentration-dependently inhibited noradrenaline (NA)-induced contractions, with 10 μM niflumic acid inhibiting the maximal contraction by 38%.
Br J Pharmacol. 1996 Jun;118(4):1065-71
BALB/3T3 clone A31 (mouse normal fibroblasts)
158.8 ± 33.0 µM (IC50)
72 hours
Evaluation of antiproliferative activity of niflumic acid alone, IC50 value was 158.8 ± 33.0 µM
Int J Mol Sci. 2024 Oct 13;25(20):11015
A172 (glioblastoma)
143.2 ± 6.5 µM (IC50)
72 hours
Evaluation of antiproliferative activity of niflumic acid alone, IC50 value was 143.2 ± 6.5 µM
Int J Mol Sci. 2024 Oct 13;25(20):11015
MCC13 (Merkel cell cancer)
175.4 ± 6.9 µM (IC50)
72 hours
Evaluation of antiproliferative activity of niflumic acid alone, IC50 value was 175.4 ± 6.9 µM
Int J Mol Sci. 2024 Oct 13;25(20):11015
SK-MEL-3 (melanoma)
167.1 ± 4.4 µM (IC50)
72 hours
Evaluation of antiproliferative activity of niflumic acid alone, IC50 value was 167.1 ± 4.4 µM
Int J Mol Sci. 2024 Oct 13;25(20):11015
UM-SCC-17A (head and neck squamous carcinoma)
310.3 ± 32.6 µM (IC50)
72 hours
Evaluation of antiproliferative activity of niflumic acid alone, IC50 value was 310.3 ± 32.6 µM
Int J Mol Sci. 2024 Oct 13;25(20):11015
A-431 (epidermoid carcinoma)
153.3 ± 43.1 µM (IC50)
72 hours
Evaluation of antiproliferative activity of niflumic acid alone, IC50 value was 153.3 ± 43.1 µM
Int J Mol Sci. 2024 Oct 13;25(20):11015
5637 (urinary bladder carcinoma)
103.5 ± 17.1 µM (IC50)
72 hours
Evaluation of antiproliferative activity of niflumic acid alone, IC50 value was 103.5 ± 17.1 µM
Int J Mol Sci. 2024 Oct 13;25(20):11015
Niflumic Acid/氟尼酸 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Rat
Isolated mesenteric vascular bed
Perfusion
10 and 30 μM
15 minutes pre-exposure
Niflumic acid selectively inhibited noradrenaline- and 5-HT-induced pressor responses but did not affect KCl-induced pressor responses.
Br J Pharmacol. 1997 Mar;120(5):813-8
Mice
Kv1.1V408A/+ mouse model
Intraperitoneal injection
10 mg/kg
Single administration
NFA ameliorated the motor performance of Kv1.1V408A/+ mice, significantly reducing foot slips and missteps on both narrow beam and horizontal ladder tasks.
Proc Natl Acad Sci U S A. 2023 Aug;120(31):e2207978120
Mice
Kir6.2−/− mice
Pancreas perfusion
100 µM
Single administration
Niflumic acid almost completely blocked cAMP-induced glucose-stimulated insulin secretion
Diabetologia. 2009 May;52(5):863-72
Rats
Chronic hypoxia model
Lung perfusion
30 μM
Single administration
To evaluate the role of Cl? channels in NS1619-induced pulmonary vasodilation
Lung. 2014 Oct;192(5):811-7
Zebrafish
Zebrafish embryos
Bath application
500 µM
30 minutes
Niflumic acid treatment caused bilateral muscle contractions in response to tactile stimulation
Sci Rep. 2020 Aug 19;10(1):13999
Sprague Dawley rats
Steroid-induced Pneumocystis pneumonia model
Intraperitoneal injection
6 mg/kg/day
Once daily for 4 weeks
NFA caused a significant decrease in total mucus, MUC5AC and mCLCA3 and also, in Pneumocystis-associated inflammation. Most relevant, NFA treatment improved survival at 8 weeks of steroids.
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