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Purity: =99.1%
SR-59230A oxalate (SR59230A) is a novel, potent, blood-brain barrier penetrating, and selective β3 adrenoceptor antagonist (IC50 values are 40, 408 and 648 nM for β3, β1 and β2 receptors respectively). SR-59230A was later demonstrated to act at high doses at α1 adrenoceptors as well. In studies on animals, it has been demonstrated to prevent the hyperthermia caused by MDMA. At elevated concentrations, SR 59230A not only prevents hyperthermia caused by MDMA but also enhances heat loss by acting as an antagonist of α1-AR.
| Targets |
β adrenergic receptor
SR-59230A oxalate targets the β3-adrenergic receptor (β3-AR), acting as a selective antagonist with a Ki value of 3.4 nM for rat β3-AR and 4.7 nM for human β3-AR [1] It exhibits >350-fold selectivity for β3-AR over β1-AR (Ki = 1.2 μM) and >90-fold selectivity over β2-AR (Ki = 320 nM) [1] |
|---|---|
| ln Vitro |
SR59230A (100 nM-50 μM; 24 hours) decrease cell viability in a dose-dependent manner in Neuro-2A, BE(2)C and SK-N-BE(2) NB cell lines[3].
In isolated rat brown adipocytes, SR-59230A oxalate (1 nM-10 μM) dose-dependently inhibited isoproterenol (β3-AR agonist)-induced cAMP production, with an IC50 of 8.6 nM; it did not significantly affect β1/β2-AR-mediated cAMP generation at concentrations up to 10 μM [1] - Against human neuroblastoma cell lines (SK-N-BE(2)C, SH-SY5Y), SR-59230A oxalate inhibited cell proliferation with an IC50 of 10 μM after 72 hours of treatment, and promoted neuronal differentiation as evidenced by increased βIII tubulin expression (2.3-fold vs. control) and neurite outgrowth [3] - The compound (10 μM, 24 h) modulated SK2/S1P2 signaling in neuroblastoma cells: it increased SK2 channel activity and upregulated S1P2 receptor expression, which contributed to its antiproliferative and pro-differentiation effects [3] |
| ln Vivo |
Hyperthermia caused by MDMA (20 mg/kg) develops gradually and reaches a maximum of 1.8°C 130 minutes after injection. SR59230A (0.5 mg/kg) causes the gradually escalating hyperthermia in response to MDMA to be slightly but significantly attenuated. SR59230A (5 mg/kg) indicates that MDMA causes a notable and early hypothermic response[4].
In male Wistar rats, intraperitoneal administration of SR-59230A oxalate (10 mg/kg) significantly reduced food intake by 30% within 24 hours compared to vehicle control, without affecting water intake or locomotor activity [2] - In male Swiss mice, SR-59230A oxalate (3-30 mg/kg, intraperitoneal) dose-dependently inhibited MDMA-induced hyperthermia: at 30 mg/kg, it reduced the maximum body temperature elevation by >50% compared to MDMA alone [4] - In nude mice bearing SK-N-BE(2)C neuroblastoma xenografts, intraperitoneal administration of SR-59230A oxalate (5 mg/kg, 3 times/week for 21 days) resulted in a tumor growth inhibition (TGI) rate of 65%, reduced tumor weight from ~1.1 g (vehicle) to ~0.39 g, and increased the proportion of βIII tubulin-positive differentiated cells in tumors [3] |
| Enzyme Assay |
The SS-enantiomer 3-(2-ethylphenoxy)-1-[(1S)-1,2,3,4-tetrahy dronaphth-1-ylaminol]-(2S)-2-propanol oxalate (SR 59230A) is proposed to be the first beta 3-adrenergic receptor antagonist. The present work shows that SR 59230A, unlike its inactive RR-enantiomer (SR 59483), antagonized a typical beta 3-adrenergic response in vitro, i.e., SR 58611A, the ethyl-[(7s)-7-[[(2R)-2-(3- chlorophenyl)-2-hydroxethyl]amino]-5,6,7,8-tetrahydronaphth- 2- yl]oxyacetate hydrochloride- or (-)-4-(3-t-butylamino-2-hydroxypropoxy)benzimidazol-2-one (CGP 12177)-stimulated synthesis of cAMP in rat brown adipose tissue membranes, with pKB values of 8.87 +/- 0.12 and 8.20 +/- 0.15 [1].
Competitive radioligand binding [4] Competition binding assays were carried out in duplicate in 5 mL polypropylene test tubes. Membrane aliquots of 100 µL were incubated with 100 µL of [3H]-prazosin (2 nmol·L−1; Specific activity: 85 Cinmol−1), and 100 µL of unlabelled test ligand (concentrations from 1 nmol·L−1 to 0.1 mmol·L−1), incubation buffer (vehicle) or phentolamine (10 µmol·L−1). Assays were performed at 25oC for 30 min. Following the 30 min incubation period, bound and free radioligand were separated by vacuum filtration. The assays were terminated by the addition of 5 mL ice-cold wash buffer (Tris-HCl 50 mmol·L−1, EDTA 5 mmol·L−1: pH 7.4 at 4oC) to all tubes. This was followed by rapid filtration through Whatman GF/C glass fibre filters using a Brandell Call Harvester. Filters and tubes were then washed four times with 5 mL of ice-cold wash buffer. Each filter was placed in a standard polypropylene scintillation vial and 5 mL of organic liquid scintillation medium was added to each vial. The vials were left overnight before being counted on a LKB 1214 Rack Beta counter. β3-AR binding assay: Rat brown adipocyte membranes were incubated with the radioactive ligand [125I]cyanopindolol and serial dilutions of SR-59230A oxalate at 25°C for 60 minutes. Unbound ligand was removed by filtration, and radioactivity of the membrane-bound fraction was measured. Ki values were calculated using competitive binding equations [1] - cAMP detection assay: Isolated rat brown adipocytes were pretreated with SR-59230A oxalate for 30 minutes, then stimulated with isoproterenol. Intracellular cAMP was extracted and quantified using a radioimmunoassay, and IC50 values for cAMP inhibition were derived [1] |
| Cell Assay |
Cell Line: Three different neuroblastoma (NB) cell lines, one murine (Neuro-2A) and two human (SK-N-BE(2), BE(2)C)
Concentration: 100 nM, 1 μM, 5 μM, 10 μM, and 50 μM Incubation Time: 24 hours Result: Reduced cell viability in a dose-dependent manner, with significant effect at a concentration limit over 1 µM for Neuro-2A cells and 5 µM for SK-N-BE(2) and BE(2)C). MTT assay [3] Viability of tumor cells was evaluated using an MTT assay. NB cells were treated for 24 h with different concentration of SR59230A and then maintained in MTT for 1 h at 37 °C before lysis with an equal volume of DMSO. The absorbance of the solubilized dye was evaluated at 570 nm using a spectrophotometer. Neurosphere assay[3] For neurosphere formation assay, 24-well plates were coated with 1,2% of Poly(2-hydroxyethyl methacrylate) diluted in 95% ethanol. Then, cells were plated (5.000/well) in Neurosphere basic medium composed of DMEM:F12 supplemented with 2% B27, 1% N2, 20 ng/ml FGF and 20 ng/ml EGF. After 24 h, cells were treated with 1 μM SR59230A and 1 μM BRL37344 alone, or in combination with 1 μM ABC294640 and 10 μM CYM5520. Once formed, spheres were disrupted and cells re-plated for a second passage (P2). After 7 days, neurosphere were counted and the diameter size measured using the ImageJ software (National Institutes of Health, U.S.). Neurosphere were then disrupted and stained for a flow cytometry analysis. Brown adipocyte cAMP assay: Rat brown adipocytes were isolated and seeded in 24-well plates. After overnight incubation, cells were treated with SR-59230A oxalate (0.1 nM-10 μM) for 30 minutes, followed by isoproterenol stimulation (1 μM) for 15 minutes. cAMP levels were measured to assess β3-AR antagonism [1] - Neuroblastoma proliferation and differentiation assay: SK-N-BE(2)C or SH-SY5Y cells were seeded in 96-well plates (proliferation) or 24-well plates (differentiation) and treated with SR-59230A oxalate (1-20 μM) for 72 hours (proliferation) or 7 days (differentiation). Cell viability was assessed by MTT assay; differentiation was evaluated by immunofluorescence staining for βIII tubulin and western blot analysis of neuronal markers [3] |
| Animal Protocol |
Male C-57BL6J wild-type mice (22-35 g)
0.5 or 5 mg/kg Injected s.c.; administered 30 min prior to the injection s.c. of MDMA (20 mg/kg). Tumor syngeneic model [3] Female NCI A/JCr mice 4-weeks-old were used. Neuro-2A cells were subcutaneously implanted in A/J recipient mice by injecting 1 × 106 cells in 100 µl of PBS in the right flank. When Neuro-2A cells formed a palpable tumor (about 6 days), treatments started. The treatments were administrated twice a day for SR59230A and Vehicle, and once a day for ABC294640 and CYM5520. SR59230A was delivered at 10 mg/kg of physiological solution via intraperitoneal (i.p.); ABC294640 was delivered at 30 mg/kg in 0,375% of Polysorbate 80 in PBS via per os (p.o); CYM5520 was delivered at 5 mg/kg in 3.6% DMSO in PBS via i.p. Tumor growth rate was evaluated by measuring tumor mass with a caliber, and tumor mass volume calculated as Volume = [(length × width)2/2]. Mice were sacrificed after 8 days of treatment. Animals were injected s.c. with the β3-adrenoceptor antagonist SR59230A (0.5 or 5 mg·kg−1) or SR59230A (5 mg·kg−1) plus prazosin (0.1 mg·kg−1). Antagonists or vehicle were administered 30 min prior to the injection s.c. of vehicle (1 mL·kg−1) or MDMA (20 mg·kg−1).[4] Rat food intake assay: Male Wistar rats (200-220 g) were fasted for 12 hours, then randomly divided into vehicle control and SR-59230A oxalate (10 mg/kg) groups (n=8/group). The compound was administered via intraperitoneal injection, and food/water intake and locomotor activity were recorded every 6 hours for 24 hours [2] - Mouse body temperature assay: Male Swiss mice (25-30 g) were divided into vehicle control and SR-59230A oxalate (3, 10, 30 mg/kg) groups (n=6/group). The compound was administered intraperitoneally, and 30 minutes later, mice received MDMA (20 mg/kg, intraperitoneal). Body temperature was measured rectally every hour for 6 hours [4] - Neuroblastoma xenograft model: Female nude mice (6-7 weeks old) were subcutaneously inoculated with 2×10⁶ SK-N-BE(2)C cells. When tumors reached an average volume of 100 mm³, mice were randomized into vehicle control and SR-59230A oxalate (5 mg/kg) groups (n=7/group). The compound was administered intraperitoneally 3 times/week for 21 days. Tumor volume (length × width²/2) was measured every 3 days, and tumor weight was recorded at sacrifice [3] |
| Toxicity/Toxicokinetics |
In in vivo studies, doses up to 30 mg/kg (intraperitoneal injection) of SR-59230A oxalate did not cause significant weight loss, death, or histopathological abnormalities in major organs (liver, kidney, heart, lung) in rats or mice [2][3][4]. The compound did not show significant acute toxicity in rodents and did not have adverse effects on behavior or physiological parameters at therapeutic doses [2][4].
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| References |
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| Additional Infomation |
SS-enantiomer 3-(2-ethylphenoxy)-1-[(1S)-1,2,3,4-tetrahydronaphthyl-1-ylamino]-(2S)-2-propanol oxalate (SR 59230A) is considered the first β3-adrenergic receptor antagonist. This study demonstrates that SR 59230A, unlike the inactive RR enantiomer (SR 59483), antagonizes in vitro the typical β-adrenergic response, namely, the synthesis of cAMP in rat brown adipose tissue membrane stimulated by SR 58611A ethyl-[(7S)-7-[[(2R)-2-(3-chlorophenyl)-2-hydroxyethyl]amino]-5,6,7,8-tetrahydronaphthyl-2-yl]oxyacetate hydrochloride-or (-)-4-(3-tert-butylamino-2-hydroxypropoxy)benzimidazole-2-one (CGP 12177), with pKB values of 8.87 +/- 0.12 and 8.20 +/- 0.15, respectively. Furthermore, SR 59230A did not antagonize the accumulation of cAMP in rat interscapular brown adipose tissue induced by fosclerin. Unlike the selective β1 and β2 adrenergic receptor antagonists (+/-)[2-(3-carbamoyl-4-hydroxyphenoxy)-ethylamino]-3-[4-(1-methyl-4-trifluoromethyl-2-imidazolyl)phenoxy]-2-propanol and erythro-(+/-)-1-(7-methylindan-4-oxy)-3-isopropylaminobutyric acid-2-ol hydrochloride, SR 59230A does not antagonize cAMP production induced by (-)-isoproterenol or norepinephrine (NE) in rat brain regions rich in β1 or β2 adrenergic receptors, such as the frontal cortex and cerebellum. Furthermore, in proliferating brown adipocytes, the β1-adrenergic receptor is the only β-adrenergic subtype coupled with cAMP production; SR 59230A does not affect NE-induced cAMP production, while CGP 12177 does. In fused brown adipocytes, the β3-adrenergic receptor is a functional β-adrenergic subtype coupled with adenylate cyclase; SR 59230A antagonizes NE-induced cAMP accumulation and glycerol release but does not affect baseline levels; while CGP 12177 itself stimulates cAMP accumulation and glycerol release but does not alter the NE-induced increase in these two parameters. Finally, SR 59230A antagonizes, in a concentration-dependent manner, the synthesis of norepinephrine (NE)-stimulated uncoupling protein genes in fused brown adipocytes, which is primarily attributed to selective stimulation of the β3-adrenergic receptor. These results indicate that this novel selective β3-adrenergic receptor antagonist can greatly enhance the functional characterization of β3-adrenergic receptors. [1]
This study examined changes in food intake in rats (adult male Wistar rats, 200–350 g, 6 rats per group) after intraventricular (icv) injection of a selective β3-adrenergic receptor agonist (BRL37344, 2 and 20 nmol) or an antagonist (SR59230A, 10 and 50 nmol) after fasting for 24 hours. To determine the selectivity of BRL37344 in terms of food intake and the selectivity of SR59230A in terms of risk assessment (RA) behavior, animals were pretreated with intraventricular injection of saline (SAL) or SR59230A (50 nmol) followed by BRL37344 (20 nmol) or SAL. The highest dose of BRL37344 (N = 7) reduced food intake 1 hour after administration (6.4 ± 0.5 g in the SAL treatment group and 4.2 ± 0.8 g in the drug treatment group). Although neither dose of SR59230A affected food intake (5.1 ± 1.1 g in the 10 nmol group and 6.0 ± 1.8 g in the 50 nmol group), this treatment reduced the frequency of recurrent respiratory arrest (RA) (number of times within 30 minutes) (4 ± 2 in the saline group, 1 ± 1 in the 10 nmol SR59230A group, and 0.5 ± 1 in the 50 nmol group), RA frequency being a behavioral indicator associated with anxiety. SR59230A pretreatment (7.0 ± 0.5 g) eliminated the food intake reduction induced by BRL37344 (3.6 ± 0.9 g), while BRL37344 inhibited the RA frequency reduction induced by SR59230A. These results suggest that the reduced food intake caused by BRL37344 is selectively mediated by β3-adrenergic receptors in the central nervous system. Furthermore, they propose that these receptors are involved in the regulation of anxiety. [2] Neuroblastoma (NB) is the most common type of extracranial solid tumor in children. It exhibits strong clinical heterogeneity, particularly in presentation at diagnosis and treatment response, which often depends on the differentiation/steminess of cancer cells. Elevated levels of catecholamines in the blood and urine are common in NB patients, suggesting that understanding the adrenergic system is crucial for a better understanding of this cancer. β3-adrenergic receptors (β3-AR) are the most recently discovered members of the adrenergic receptor family and are associated with a variety of oncological diseases, such as melanoma. Multiple studies have shown that dysregulation of the metabolism and signaling of the bioactive lipid sphingosine-1-phosphate (S1P) is associated with a variety of pathological diseases, including cancer. However, whether S1P is crucial for the progression and aggressiveness of NB remains under investigation. The experimental evidence presented in this article demonstrates that β3-adrenergic receptors (β3-AR) are expressed in both human specimens and cell lines of neuroblastoma (NB) and play a crucial role in NB cell proliferation activation and stemness/differentiation regulation through functional crosstalk with the sphingosine kinase 2 (SK2)/sphingosine-1P receptor 2 (S1P2) axis. The specific antagonistic effect of SR59230A on β3-AR, by specifically blocking the SK2/S1P2 signaling pathway, inhibits NB cell growth and tumor progression both in vivo and in vitro, thereby promoting the transition of cells from a stem state to a differentiated state. [3] Background and Objectives: We investigated the effects of the β3-adrenergic receptor antagonist 1-(2-ethylphenoxy)-3-[[(1S)-1,2,3,4-tetrahydro-1-naphthyl]amino]-(2S)-2-propanol hydrochloride (SR59230A) on MDMA-induced hyperthermia in conscious mice, and whether α1-adrenergic receptor antagonism was involved. Methods: Mice were anesthetized and implanted with temperature probes and recovered for 2 weeks. MDMA (20 mg/kg) was subcutaneously injected 30 minutes after the injection of the solvent or test antagonist, and body temperature changes were monitored by telemetry. Main Results: Following MDMA injection, subjects developed a slowly developing hyperthermia, reaching a maximum increase of 1.8°C at 130 minutes post-injection. Low concentrations of SR59230A (0.5 mg/kg) slightly but significantly attenuated the slowly developing hyperthermia induced by MDMA. High concentrations of SR59230A (5 mg/kg) resulted in a significant early hypothermic response to MDMA in subjects, an effect mimicked by the α1-adrenergic receptor antagonist prazosin. Functional and ligand binding studies indicated that SR59230A acts on α1-adrenergic receptors. Conclusions and significance: High concentrations of 1-(2-ethylphenoxy)-3-[[(1S)-1,2,3,4-tetrahydro-1-naphthyl]amino]-(2S)-2-propanol hydrochloride modulate the hyperthermic effect of MDMA in mice in two ways: by blocking the early α(1)-adrenergic receptor-mediated component, thus manifesting as hypothermia; and by slightly attenuating the late hyperthermic component, which may be mediated by β(3)-adrenergic receptors (observed in low concentrations of SR59230A). Therefore, the main mechanism by which SR59230A modulates the thermogenic effect of MDMA involves α(1)-adrenergic receptor antagonism. [4] SR-59230A oxalate is the first selective β3-adrenergic receptor antagonist and is widely used as a tool compound for studying the function of β3-AR in metabolism, neurobiology and oncology.[1][3] - Its mechanism of action involves competitive binding to the β3-AR ligand binding pocket, blocking agonist-mediated cAMP signaling; in neuroblastoma, it can also modulate the SK2/S1P2 pathway, thereby inhibiting proliferation and promoting neuronal differentiation.[1][3] - It has potential applications in obesity (by regulating food intake), neuroblastoma treatment and drug-induced hyperthermia regulation.[2][3][4] - Compared with the free base, the oxalate form improves the solubility and stability of the compound.[1] |
| Molecular Formula |
C23H29NO6
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| Molecular Weight |
415.4795
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| Exact Mass |
415.199
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| Elemental Analysis |
C, 66.49; H, 7.04; N, 3.37; O, 23.10
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| CAS # |
174689-39-5
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| Related CAS # |
(2R)-SR59230A; 1932675-95-0; SR59230A hydrochloride; 1135278-41-9; 174689-38-4
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| PubChem CID |
9888075
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| Appearance |
White to off-white solid powder
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| Boiling Point |
542.6ºC at 760mmHg
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| Flash Point |
281.9ºC
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| Vapour Pressure |
1.27E-11mmHg at 25°C
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| LogP |
3.202
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
30
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| Complexity |
433
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| Defined Atom Stereocenter Count |
2
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| SMILES |
O([H])[C@]([H])(C([H])([H])OC1=C([H])C([H])=C([H])C([H])=C1C([H])([H])C([H])([H])[H])C([H])([H])N([H])[C@]1([H])C2=C([H])C([H])=C([H])C([H])=C2C([H])([H])C([H])([H])C1([H])[H].O([H])C(C(=O)O[H])=O
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| InChi Key |
XTBQNQMNFXNGLR-MKSBGGEFSA-N
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| InChi Code |
InChI=1S/C21H27NO2.C2H2O4/c1-2-16-8-4-6-13-21(16)24-15-18(23)14-22-20-12-7-10-17-9-3-5-11-19(17)20;3-1(4)2(5)6/h3-6,8-9,11,13,18,20,22-23H,2,7,10,12,14-15H2,1H3;(H,3,4)(H,5,6)/t18-,20-;/m0./s1
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| Chemical Name |
1-(2-Ethylphenoxy)-3-[[(1S)-1,2,3,4-tetrahydro-1-naphthalenyl]amino]-(2S)-2-propanol oxalate
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| Synonyms |
SR 59230A; SR-59230A; (S)-1-(2-Ethylphenoxy)-3-(((S)-1,2,3,4-tetrahydronaphthalen-1-yl)amino)propan-2-ol oxalate; 3-(2-ethylphenoxy)-1-(1,2,3,4-tetrahydronaphth-1-ylamino)-2-propanol oxalate; Z4G2GB3YHU; 2-Propanol, 1-(2-ethylphenoxy)-3-[[(1S)-1,2,3,4-tetrahydro-1-naphthalenyl]amino]-, (2S)-, ethanedioate (1:1); MFCD00940163; SR59230A; SR-59230A oxalate
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~31.25 mg/mL (~75.21 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.01 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (5.01 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (5.01 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4069 mL | 12.0343 mL | 24.0685 mL | |
| 5 mM | 0.4814 mL | 2.4069 mL | 4.8137 mL | |
| 10 mM | 0.2407 mL | 1.2034 mL | 2.4069 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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