Quin-2 (potassium salt)
(Synonyms: 2-[(2-氨基-5-甲基苯氧基)甲基]-6-甲氧基-8-氨基喹啉-N,N,N',N'-四乙酸四钾) 目录号 : GC44796
A high-affinity fluorescent calcium indicator
Cas No.:73630-23-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Quin-2 is a high-affinity fluorescent calcium indicator (Kd = 115 nM for calcium). It displays high selectivity for calcium, as it is not affected by sodium gradients, membrane potential, or intracellular pH. High affinity probes like quin-2 are ideal for monitoring low levels of calcium, as are found in resting cells. Loadings of up to 2 mM quin-2 are without serious toxic effects, so quin-2 may be used to buffer intracellular calcium transients. Excitation/emission maxima for quin-2 are 339 and 492 nm, respectively.
| Cas No. | 73630-23-6 | SDF | |
| 别名 | 2-[(2-氨基-5-甲基苯氧基)甲基]-6-甲氧基-8-氨基喹啉-N,N,N',N'-四乙酸四钾 | ||
| Canonical SMILES | O=C([O-])CN(CC([O-])=O)C1=C2C(C=CC(COC3=C(N(CC([O-])=O)CC([O-])=O)C=CC(C)=C3)=N2)=CC(OC)=C1.[K+].[K+].[K+].[K+] | ||
| 分子式 | C26H23N3O10•4K | 分子量 | 693.9 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.4411 mL | 7.2056 mL | 14.4113 mL |
| 5 mM | 0.2882 mL | 1.4411 mL | 2.8823 mL |
| 10 mM | 0.1441 mL | 0.7206 mL | 1.4411 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Measurement of free Ca2+ changes and total Ca2+ release in a single striated muscle fibre using the fluorescent indicator quin 2
Biochem Biophys Res Commun 1985 May 16;128(3):1180-9.PMID:4004856DOI:10.1016/0006-291x(85)91065-4.
The fluorescent Ca2+ indicator, quin 2, has been used in isolated striated muscle fibres. There is a distinct quin 2 fluorescence peak at lambda 500 nm upon excitation at lambda 339 nm after axial injection of the potassium salt of quin 2, pH 7.1. Single voltage-clamp or current clamp electrical stimulation resulted in a distinct transient change in the fluorescence at lambda 500 nm which was not observed at lambda 400 nm, the peak of the fibre autofluorescence. Ca2+ buffering is marked at high quin 2 concentrations (greater than or equal to 400 microM) producing a slow decay of force and fluorescence. At lower concentrations (8-30 microM) of quin, the decay of force is within the range observed in non-injected control fibres. A Kd of 457 nM at 5 mM free Mg2+ suggests an upper resting free Ca2+ concentration of 310 nM at 12 degrees C.
Differential release of [3H]acetylcholine from the rat phrenic nerve-hemidiaphragm preparation by electrical nerve stimulation and by high potassium
Neuroscience 1987 Jul;22(1):289-99.PMID:2442663DOI:10.1016/0306-4522(87)90219-3.
Neuronal transmitter stores of the phrenic nerve were labelled under different conditions. Subsequently, transmitter release evoked by electrical nerve stimulation and by a high potassium-low sodium solution was studied. Incubation of the end-plate preparation with [3H]choline at rest led to the synthesis of [3H]acetylcholine which could not be released by electrical nerve stimulation but it was released by high potassium-low sodium solution, independent of the presence of extracellular calcium. When the end-plate preparation was labelled during stimulation at 1 Hz, prolonged periods of electrical nerve stimulation released 83% of the total releasable [3H]transmitter pool in a completely calcium-dependent manner. After exhaustion of the electrically releasable pool, high potassium-low sodium solution still caused a significant outflow. Without a preceding exhaustion of the [3H]acetylcholine pool, high potassium-low sodium solution released a similar amount in the absence of extracellular calcium or after pretreatment with the intracellular calcium chelating substance, Quin-2. When evoked transmitter release was studied at different temperatures (36, 26 and 16 degrees C) Q 10 values of 1.6 and 1.0 were found for the release caused by electrical nerve stimulation and high potassium-low sodium solution (calcium-independent effect), respectively. After labelling during a short interval (2 min) but at a high stimulation rate (50 Hz), only 72% of the releasable [3H]transmitter could be released by electrical nerve stimulation, whereas the outflow due to the calcium-independent effect of high potassium-low sodium solution increased from 17 (labelling during stimulation at 1 Hz) to 28%. It is suggested that the calcium-independent effect of high potassium-low sodium solution reflects the release of acetylcholine from the cytoplasmic compartment, as this outflow occurred after labelling at rest and increased when cytoplasmic synthesis was enhanced by a high loading stimulation. In contrast to high potassium-low sodium solution, propagated nerve activity cannot release acetylcholine synthesized at rest (presumed to be cytoplasmic), but only [3H]acetylcholine synthesized during quantal release (presumed to be vesicular). The absolute requirement of extracellular calcium for electrically stimulated release suggests an exocytotic release mechanism. The low Q 10 value of 1.6 does not fit into the concept of a carrier- or channel-operated release mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)
Quinapril treatment and arterial smooth muscle responses in spontaneously hypertensive rats
Br J Pharmacol 1993 Apr;108(4):980-90.PMID:8485636DOI:10.1111/j.1476-5381.1993.tb13495.x.
1 The effects of long-term angiotensin-converting enzyme inhibition with quinapril on arterial function were studied in spontaneously hypertensive rats, Wistar-Kyoto rats serving as normotensive controls. 2 Adult hypertensive animals were treated with quinapril (10 mg kg-1 day-1) for 15 weeks, which reduced their blood pressure and the concentrations of atrial natriuretic peptide in plasma and ventricular tissue to a level comparable with that in normotensive rats. 3 Responses of mesenteric arterial rings in vitro were examined at the end of the study. Compared with normotensive and untreated hypertensive rats, responses to noradrenaline were attenuated in hypertensive animals on quinapril, both force of contraction and sensitivity being reduced. Quinapril also attenuated maximal contractions but not sensitivity to potassium chloride. Nifedipine less effectively inhibited vascular contractions in normotensive and quinapril-treated than in untreated hypertensive rats. 4 Arterial relaxation responses by endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitrite, isoprenaline) mechanisms were similar in normotensive and quinapril-treated rats and more pronounced than in untreated hypertensive rats. 5 Cell membrane permeability to ions was evaluated by means of potassium-free solution-induced contractions of endothelium-denuded denervated arterial rings. These responses were comparable in normotensive and quinapril-treated rats and less marked than in untreated hypertensive rats. 6 Intracellular free calcium concentrations in platelets and lymphocytes, measured by the fluorescent indicator Quin-2, were similar in normotensive and quinapril-treated rats and lower than in untreated hypertensive rats. 7 In conclusion, quinapril treatment improved relaxation responses and attenuated contractions in arterial smooth muscle of hypertensive rats. These changes may be explained by diminished cytosolic free calcium concentration, reduced cell membrane permeability, and alterations in dihydropyridine-sensitive calcium channels following long-term angiotensin-converting enzyme inhibition.
Ouabain and low extracellular potassium inhibit PTH secretion from bovine parathyroid cells by a mechanism that does not involve increases in the cytosolic calcium concentration
Metabolism 1987 Jan;36(1):36-42.PMID:3025550DOI:10.1016/0026-0495(87)90060-6.
We have previously found that high extracellular calcium (Ca++) concentrations inhibit PTH release in association with a threefold to fourfold rise in cytosolic Ca++ concentration. Recent data have also shown that low extracellular potassium (K+) concentration or ouabain also inhibits PTH release to an extent comparable to that seen with high Ca++ and produce a marked rise in the intracellular sodium (Na+) content. These results suggested that low K+ and ouabain might modulate PTH release through increases in cytosolic Ca++ related to alterations in Na+-Ca++-exchange. In the present studies, we have examined further the mechanism(s) by which inhibition of the Na+-K+-ATPase regulates PTH release. Exposure of cells loaded with the Ca++-sensitive dye Quin-2 to low K+ produced a 10% to 17% increase in cytosolic Ca++ at 0.5 to 1.0 mmol/L extracellular Ca++, which was statistically significant only at 0.75 mmol/L Ca++. In contrast, low K+ caused a statistically significant decrease in cytosolic Ca++ at 1.5 to 2 mmol/L Ca++, while ouabain lowered cytosolic Ca++ significantly by 23% to 46% at all Ca++ concentrations examined (0.5 to 2 mmol/L). Low K+ or ouabain had no effect on cellular levels of ATP or GTP or intracellular pH measured using the pH-sensitive dye BCECF [2', 7'-bis(carboxyethyl)-5,6-carboxyfluorescein]. The inhibition of secretion by low K+ or ouabain, unlike that due to high extracellular Ca++, was not reversed by TPA (12-O-tetradecanoyl phorbol 13-acetate), an activator of protein kinase C. Low K+ did produce a modest (30% to 40%) lowering of agonist-stimulated but not basal cAMP content.(ABSTRACT TRUNCATED AT 250 WORDS)
PTH release stimulated by high extracellular potassium is associated with a decrease in cytosolic calcium in bovine parathyroid cells
Biochem Biophys Res Commun 1984 Sep 17;123(2):684-90.PMID:6487306DOI:10.1016/0006-291x(84)90283-3.
We employed the calcium (Ca++)-sensitive, intracellular dye Quin-2 to examine the role of cytosolic Ca++ in the stimulation of PTH release by high extracellular potassium (K+) concentrations. Addition of 55 mM KC1 to cells incubated with 115 mM NaC1 and 5 mM KC1 lowered cytosolic Ca++ at either low (0.5 mM) extracellular Ca++ (from 194 +/- 14 to 159 +/- 9 nM, p less than .01, N = 6) or high (1.5 mM) extracellular calcium (from 465 +/- 38 to 293 +/- 20 nM, p less than .01, N = 10). This reduction in cytosolic Ca++ was due to high K+ per se and not to changes in tonicity since addition of 55 mM NaC1 was without effect while a similar decrease in cytosolic Ca++ occurred when cells were resuspended in 60 mM NaC1 and 60 mM KC1. PTH release was significantly (p less than .01) greater at 0.5 and 1.5 mM Ca++ in QUIN-2-loaded cells incubated with 60 mM NaC1 and 60 mM KC1 than in those exposed to 115 mM NaC1 and 5 mM KC1. In contrast to most secretory cells, therefore, stimulation of PTH release by high K+ is associated with a decrease rather than an increase in cytosolic Ca++.