Dopamine D1/D5 receptor

SKF 38393 氢溴酸也会引起细胞形状的类似改变，它也会提高培养基中的 cAMP 水平 [2]。在培养的 GC 细胞中，给予 10 μM SKF-38393 盐酸盐一小时，可诱导 Mr 32 kD (DARPP-32) 磷蛋白的 DA 和 cAMP 调节的苏氨酸磷酸化增加 [2]。 体外活性：SKF38393 (50-100 μM) 以蛋白质合成依赖性方式诱导持久的突触增强。在体外大鼠前额皮质神经元中，SKF 38393 模拟 DA 对 I(NaP) 的影响，并调节持续的钠电流。在听觉皮层中，SKF38393 通过激活下游效应器腺苷酸环化酶和磷脂酶 C 显着的蛋白质组改变来影响长期记忆的形成和巩固。激酶测定：SKF 38393 salthalide 是一种 D1 激动剂，IC50 为 110 nM。

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儿茶酚胺、去甲肾上腺素和多巴胺（DA）存在于人类卵巢中；特别是在卵泡液中。去甲肾上腺素激活卵巢α和β肾上腺素受体并调节卵巢类固醇生成，但卵巢DA的意义尚不清楚。我们检查了D1亚型（D1-R）的DA受体是否存在于人类卵巢和培养的人类颗粒黄体细胞（GC）中。使用RT-PCR，我们从成人卵巢和GC信使RNA中克隆了与人类D1-R序列相同的互补DNA。在卵巢切片中，在大窦卵泡的颗粒细胞、黄体细胞以及培养的GC中鉴定出D1-R蛋白（通过免疫组织化学）。在Western印迹中使用相同的抗血清在培养的黄素化GC中发现了约50000 Mr的免疫反应带。这些细胞中的D1-R是功能性的，因为DA单独或在β受体拮抗剂普萘洛尔存在的情况下会引起细胞收缩。选择性D1-R激动剂SKF-38393诱导了细胞形态的类似变化，并增加了培养基cAMP的水平。然而，SKF-38393未能在体外显著影响基础和hCG刺激的孕酮释放，表明D1-R的激活与人类GC的主要类固醇孕酮的合成没有直接联系。雌二醇的合成同样不受影响。使用RT-PCR和免疫组织化学，我们发现GC表达DA和cAMP调节的Mr 32000磷酸化蛋白（DARPP-32），这是一种通常与携带D1-R的神经元相关的蛋白。综上所述，DA和功能性DA受体以及DARPP-32的存在表明，人类卵巢中存在一种涉及DA的新的生理调节途径[2]。

SKF 38393 Hydrobromide (10 mg/kg; ip) 可阻断 1-甲基-4-苯基-1,2,3,6-四氢吡啶 (MPTP) 诱导的谷胱甘肽消耗 [3]。 SKF 38393 氢溴酸盐可减弱 MPTP 诱导的多巴胺消耗 [3]。 SKF 38393 氢溴酸可增强超氧化物歧化酶活性，从而模仿司来吉兰的作用 [3]。 SKF 38393 氢溴酸盐会增加抗河豚毒素的兴奋性突触后电流的频率，但不会增加其幅度，表明 D1 作用发生在突触前位点 [4]。 SKF 38393（6 mg/kg，腹腔注射）可防止东莨菪碱引起的 T 迷宫工作记忆任务表现受损。在成年雄性 NMRI 小鼠中，SKF38393（1 μg/小鼠）会损害情境依赖性恐惧学习。

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在这项研究中，研究人员检查了多巴胺能（D1）受体激动剂SKF-38393 HCl（SKF）对MPTP诱导的多巴胺能神经元损伤的可能神经保护作用。MPTP被单胺氧化酶-B（MAO-B）转化为其神经毒性代谢产物1-甲基-4-苯基吡啶鎓（MPP+），然后被多巴胺能神经元吸收。SKF-38393对纹状体中的总氧化酶或单胺氧化酶B均无影响。SKF-38393阻断了MPTP诱导的谷胱甘肽耗竭，并减轻了MPTP引起的多巴胺耗竭。此外，它增强了超氧化物歧化酶的活性，从而模拟了司来吉兰的作用。这些研究的结果被解释为表明，SKF-38393可能被证明是治疗帕金森病的一种有价值的药物。[3]

SKF 38393 saltloride 是 D1 的激动剂，IC50 为 110 nM。 使用定量放射自显影检查碘化SCH 23390、125I-SCH 23982（杜邦NEN）在大鼠脑切片中与多巴胺D1受体结合的效力、选择性以及解剖和神经元定位。125I-SCH 23982以非常高的亲和力（Kd值为55-125pM）、特异性（70-85%的结合被5微摩尔顺式氟戊噻醇取代）和可饱和的方式（Bmax值为65-176fmol/mg蛋白）结合基底节中的D1位点。选择性D1拮抗剂SCH 23390（IC50=90 pM）和顺式氟戊噻醇（IC50=200 pM）以及D1激动剂SKF 38393（IC50=110 nM）取代了特异性125I-SCH 23982结合，但D2选择性配体（I-舒必利，LY 171555）或S2拮抗剂西那塞林没有取代。与3H-SCH 23390相比，125I-SCH 23882对D1位点的亲和力提高了5到10倍，比放射性提高了50倍，使其成为标记D1受体的优秀放射性配体。D1位点的浓度在内侧黑质中最高，超过外侧黑质、尾壳核、伏隔核、嗅结节和内脚核中D1位点浓度的50%以上。较低浓度的D1位点存在于内囊、背内侧额叶皮层、屏状核和新皮层第6层。腹侧被盖区缺失D1位点。纹状体注射保留轴突的神经毒素喹啉酸，分别使同侧尾壳核和黑质内侧和中央网状部可移位D1位点的浓度减少87%和46-58%。黑质外侧未见D1位点丢失。用6-羟基多巴胺破坏高达94%的中脑多巴胺能投射并没有减少D1结合，也没有增加纹状体或黑质D1受体浓度，只有一个例外。125I-SCH 23982以皮摩尔亲和力选择性标记纹状体神经元上的D1结合位点，这些神经元包含大鼠大脑中的大部分D1位点[1]。

蛋白质印迹分析[2]
细胞类型： GC 细胞
测试浓度： 10 μM
孵育时间： 1小时
实验结果：在培养的 GC 细胞中诱导 DARPP-32 苏氨酸磷酸化增加。

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蛋白质印迹[2]
如前所述进行蛋白质印迹，但稍作修改。简而言之，收集细胞，冷冻、解冻，在含有10%蔗糖和2%SDS的62.5 mmol/L Tris-HCl缓冲液（pH 6.8）中均质化，超声处理，并在10%巯基乙醇存在下加热（95℃5分钟）。样品（15μg/泳道）在10%或12.5%SDS-聚丙烯酰胺凝胶（SDS-PAGE）上进行电泳分离。将蛋白质转移到硝化纤维膜上，并用用于免疫组织化学的相同D1-R抗血清（1:1000稀释，在4℃下孵育过夜）进行检测。

此外，使用特征明确的单克隆磷酸-DARPP-32特异性抗体（1:500）检测用DA（1和10μmol/L）或SKF-38393（1和1μmol/L，RBI，Biotrend，Cologne，Germany，稀释于无血清培养基中）处理GC（1小时，2例，24小时）是否改变了DARPP-32的磷酸化。为了控制目的，将β受体拮抗剂普萘洛尔（10μmol/L）或D1-R拮抗剂SCH-23390（10μmol/L，RBI）添加到用DA或SKF-38393（在1μm处使用）处理的细胞中。监测并记录细胞形态。如所述，使用过氧化物酶标记的抗血清（1:3000）和增强化学发光检测免疫反应性。在某些情况下，印迹被数字化，并使用NIH Image程序的编辑版本确定条带的积分光密度，如前所述。

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免疫沉淀实验[2]
进行免疫沉淀实验，以检查SKF-38393（100μmol/L，在无血清培养基中稀释）处理培养的GC（分离后1天）1小时是否会增加DARPP-32的苏氨酸磷酸化。移除培养基，将细胞溶解在含有10 mmol/L NaH2PO4、150 mmol/L NaCl、2 mmol/L EDTA、1%Triton X-100、0.25%SDS、1%脱氧胆酸钠和2 mmol/L苯基甲磺酰氟的缓冲液中。为了进行免疫沉淀，我们使用了标记有抗鼠IgG的磁珠和磁分离。首先将珠子与正常小鼠血清（5%在含有10 mmol/L EGTA、250 mmol/L蔗糖和0.1%BSA的PBS中）一起孵育，然后用2μL特征明确的针对牛DARPP-32的单克隆抗体标记，该抗体可识别灵长类动物DARPP-32，也用于免疫细胞化学。随后，将珠子与150μL GC细胞裂解液在室温下孵育1小时，然后在4℃下孵育30分钟。磁铁分离后，将小球洗涤几次并用于SDS-PAGE，如所述。使用抗磷酸苏氨酸的单克隆抗体（1:100）进行印迹；在某些情况下，它们是通过密度测定法进行评估的。

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孕酮和雌二醇测量[2]
在hCG（10IU/mL）存在或不存在的情况下，通过GC与SKF-38393（10μmol/L）一起孵育6小时，使用三个孔对每种处理（n=3）检测孕酮和雌二醇在培养基中的释放情况。按照制造商的说明，使用商业酶免疫测定法对样品进行分析。批内变异系数在5-8%之间，批间变异系数不超过10%。所有孵育和移液步骤以及激素浓度的计算都在全自动免疫诊断分析仪中进行。对细胞蛋白的微小变化进行了校正。方差分析和t检验用于评估结果。

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cAMP的测定[2]
在磷酸二酯酶抑制剂异丁甲基黄嘌呤（1 mmol/L）的存在下，用SKF-38393（1-100μmol/L）孵育3或6小时后，检测分离后1天GC培养基中cAMP的水平。在一项初步研究中，SKF-38393（浓度为1μmol/L）导致cAMP小幅但无统计学意义的增加（比基础水平高20%）。因此，对于三个独立的附加实验，使用了更高的SKF-38393浓度（100μmol/L）。根据制造商的说明，这些样品是使用酶免疫测定法（R&D Systems）测量的。该测定的灵敏度为0.5 pmol/mL，批内变异系数小于10%。为了校正细胞密度的微小差异，每微克细胞蛋白表达cAMP结果。学生t检验用于评估数据。

Animal/Disease Models: balb/c (Bagg ALBino) mouse (20-25 g) [3]
Doses: 5 mg/kg, 10 mg/kg
Route of Administration: intraperitoneal (ip) injection
Experimental Results: Blocks MPTP-induced glutathione depletion and attenuates MPTP Induced dopamine depletion.

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Balb/c mice were injected intraperitoneally with 5 or 10 mg/kg of SKF-38393 every 16 h with a final dose administered 30 min prior to administration of MPTP. Saline-injected but otherwise identically treated mice served as the control group. Animals were euthanized by decapitation in the morning in order to avoid diurnal variations of the endogenous levels of biogenic amines, enzymes, and antioxidant molecules. SN and NCP were micropunched and homogenized in 0.1 M phosphate buffer, pH 7.8, using a glass-teflon homogenizer. Tissue homogenates were centrifuged at 10 000×g for 60 min at 4°C. The supernatant obtained was assayed for GSH content and the activities of SOD and CAT.[3]

[1]. Picomolar affinity of 125I-SCH 23982 for D1 receptors in brain demonstrated with digital subtraction auto radiography. J Neurosci. 1987 Jan;7(1):213-222.

[2]. Functional Dopamine-1 Receptors and DARPP-32 Are Expressed in Human Ovary and Granulosa Luteal Cells in Vitro. J Clin Endocrinol Metab. 1999 Jan;84(1):257-64.

[3]. SKF-38393, a dopamine receptor agonist, attenuates 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity. Brain Res. 2001 Feb 23;892(2):241-7.

[4]. The D1 dopamine receptor agonist SKF-38393 stimulates the release of glutamate in the hippocampus. Neuroscience. 1999;94(4):1063-70.

The catecholamines norepinephrine and dopamine (DA) are present in the human ovary; in particular, in follicular fluid. Norepinephrine activates ovarian alpha- and beta-adrenergic receptors and modulates ovarian steroidogenesis, but the significance of ovarian DA is unclear. We examined whether a DA receptor of the D1-subtype (D1-R) is present in human ovary and in cultured human granulosa luteal cells (GC). Using RT-PCR, we cloned complementary DNAs from adult human ovarian and GC messenger RNAs, which are identical to the human D1-R sequence. In ovarian sections, D1-R protein was identified (by immunohistochemistry) in granulosa cells of large antral follicles, cells of the corpus luteum, as well as in cultured GC. An immunoreactive band of approximately Mr 50,000 was found in cultured luteinized GC using the same antiserum in Western blots. The D1-R in these cells was functional, because DA, alone or in the presence of the beta-receptor antagonist propranolol, caused cellular contraction. The selective D1-R agonist SKF-38393 induced a similar change in cytomorphology and increased the levels of media cAMP. SKF-38393 failed, however, to significantly affect basal and hCG-stimulated progesterone release in vitro, indicating that the activation of the D1-R was not directly linked to synthesis of progesterone, the major steroid of human GC. Estradiol synthesis likewise was not affected. Using RT-PCR and immunohistochemistry, we found that GC express DA- and cAMP-regulated phosphoprotein of Mr 32,000 (DARPP-32), a protein typically associated with neurons bearing the D1-R. In cultured GC, DA and SKF-38393 induced increased threonine-phosphorylation of DARPP-32, even in the presence of propranolol but not in the presence of D1-R antagonist SCH-23390. Taken together, the presence of DA and a functional DA receptor and DARPP-32 indicate that a novel, physiological regulatory pathway involving DA exists in the human ovary.[2]

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The present study was undertaken to better assess the role of dopamine on exocytosis. Since direct activation of adenylate cyclase (e.g., with forskolin) enhances neurotransmitter release it was of interest to see whether the activation of D1-type dopamine receptors, which are positively coupled to adenylate cyclase, could also modulate the molecular machinery underlying the fusion of synaptic vesicles and the release of neurotransmitter. To answer this question we have looked at the effect of the D1-type dopamine receptor agonist SKF-38393 on the spontaneous release of glutamate from cultured rat hippocampal neurons. SKF-38393 enhanced the frequency but not the amplitude of tetrodotoxin-resistant excitatory postsynaptic currents which argues for a presynaptic locus of D1 action. This effect was blocked by the D1-dopaminergic receptor antagonist SCH-23390 and the protein kinase A inhibitors H-7 and Rp-cAMP whereas pertussis toxin failed to affect the dopaminergic response. In addition, carbachol and Ruthenium Red also stimulated exocytosis but did not occlude the SKF-38393-induced modulation. These results indicate that SKF-38393 presynaptically enhances the release of glutamate via a pertussis toxin-insensitive and protein kinase A-dependent mechanism, which most likely involves D1-type dopamine receptors. Our results underline the importance of protein kinase A as potent modulator of synaptic transmission and suggest that high concentrations of dopamine can greatly enhance the release of glutamate in the hippocampus.[4] .

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Iodinated SCH 23390, 125I-SCH 23982 (DuPont-NEN), was examined using quantitative autoradiography for its potency, selectivity, and anatomical and neuronal localization of binding to the dopamine D1 receptor in rat brain sections. 125I-SCH 23982 bound to D1 sites in the basal ganglia with very high affinity (Kd values of 55-125 pM), specificity (70-85% of binding was displaced by 5 microM cis-flupenthixol), and in a saturable manner (Bmax values of 65-176 fmol/mg protein). Specific 125I-SCH 23982 binding was displaced by the selective D1 antagonists SCH 23390 (IC50 = 90 pM) and cis-flupenthixol (IC50 = 200 pM) and the D1 agonist SKF-38393 (IC50 = 110 nM) but not by D2-selective ligands (I-sulpiride, LY 171555) or the S2 antagonist cinanserin. Compared with 3H-SCH 23390, the 5- to 10-fold greater affinity for the D1 site and 50-fold greater specific radioactivity of 125I-SCH 23982 makes it an excellent radioligand for labeling the D1 receptor. The concentrations of D1 sites were greatest in the medial substantia nigra and exceeded by over 50% the concentration of D1 sites in the lateral substantia nigra, caudoputamen, nucleus accumbens, olfactory tubercle, and entopeduncular nucleus. Lower concentrations of D1 sites were present in the internal capsule, dorsomedial frontal cortex, claustrum, and layer 6 of the neocortex. D1 sites were absent in the ventral tegmental area. Intrastriatal injections of the axon-sparing neurotoxin, quinolinic acid, depleted by 87% and by 46-58% the concentrations of displaceable D1 sites in the ipsilateral caudoputamen and medial and central pars reticulata of the substantia nigra, respectively. No D1 sites were lost in the lateral substantia nigra. Destruction of up to 94% of the mesostriatal dopaminergic projection with 6-hydroxydopamine did not reduce D1 binding nor, with one exception, increase striatal or nigral D1 receptor concentrations. 125I-SCH 23982 selectively labels D1 binding sites on striatonigral neurons with picomolar affinity, and these neurons contain the majority of D1 sites in rat brain. [1]

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Parkinson's disease (PD) is characterized by progressive degeneration of nigrostriatal dopaminergic neurons. Several factors such as inhibition of the mitochondrial respiration, generation of hydroxyl radicals and reduced free radical defense mechanisms causing oxidative stress, have been postulated to contribute to the degeneration of dopaminergic neurons. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated animals is a useful experimental model of PD, exhibiting most of the clinical features, as well as the main biochemical and pathologic symptoms of the disease. In the present study, we have examined a dopaminergic (D1) receptor agonist, SKF-38393 HCl (SKF) for its possible neuroprotective action against MPTP-induced insults on dopaminergic neurons. MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-pyridinium (MPP+), which is then taken up into the dopaminergic neurons. SKF-38393 had no effects either on total or monoamine oxidase B in the striatum. SKF-38393 blocked the MPTP-induced depletion of glutathione and attenuated MPTP-induced depletion of dopamine. Furthermore, it enhanced the activity of superoxide dismutase and hence mimicked the action of selegiline. The results of these studies are interpreted to suggest that SKF-38393 may prove a valuable drug in the treatment of Parkinson's disease. [3]

C16H18BRNO2

336.229

335.052

C, 57.16; H, 5.40; Br, 23.76; N, 4.17; O, 9.52

20012-10-6

SKF 38393 hydrochloride;62717-42-4; 67287-49-4, 81702-42-3 (R-isomer HCl), 62751-59-1 (R-isomer), 20012-10-6 (HBr)

12928470

Solid powder

3.662

52.49

4

3

1

20

291

0

C1=CC=C(C=C1)C2CNCCC3=CC(=C(C=C32)O)O.Br

INNWVRBZMBCEJI-UHFFFAOYSA-N

InChI=1S/C16H17NO2.BrH/c18-15-8-12-6-7-17-10-14(13(12)9-16(15)19)11-4-2-1-3-5-11;/h1-5,8-9,14,17-19H,6-7,10H2;1H

1-phenyl-2,3,4,5-tetrahydro-1H-benzo[d]azepine-7,8-diol hydrobromide

SKF 38393 hydrobromide; 20012-10-6; SKF 38393 hydrobromide - Bio-X; SKF 38393 (hydrobromide); SKF-38393 HBr; CHEMBL505308; 5-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol;hydrobromide; 1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diolhydrobromide;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。