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| 500μg |
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Purity: ≥98%
Aviptadil (Vasoactive Intestinal Peptide) is a novel analog of vasoactive intestinal polypeptide (VIP) with the potential for the treatment of erectile dysfunction. Aviptadil in combination with phentolamine and sexual stimulation, is expected to provide a new and effective alternative for erectile dysfunction (ED) patients that is essentially free of the troublesome side effects and cumbersome delivery methods which limit the use of other pharmacologic preparations.
| Targets |
VIP/vasoactive intestinal polypeptide; vasodilatory
Aviptadil, a synthetic form of Human Vasoactive Intestinal Polypeptide (VIP) has been awarded FDA Orphan Drug Designation for the treatment of ARDS and admitted to the FDA CoronaVirus Technology Accelerator Program. VIP binds to VPAC1 receptors on the pulmonary Alveolar Type II (ATII) cell. ATII cells comprise only 5% of lung epithelial cells but are critical for oxygen transfer, surfactant production, and maintenance of Alveolar Type 1 cells. 70% of VIP binds to this receptor. The Type II cell is also the cell selectively attacked by the SARS-CoV-2 virus via the ACE2 surface receptor. [1] |
|---|---|
| ln Vitro |
Aviptadil, a synthetic form of Human Vasoactive Intestinal Polypeptide (VIP) has been awarded FDA Orphan Drug Designation for the treatment of ARDS and admitted to the FDA CoronaVirus Technology Accelerator Program.
VIP binds to VPAC1 receptors on the pulmonary Alveolar Type II (ATII) cell. ATII cells comprise only 5% of lung epithelial cells but are critical for oxygen transfer, surfactant production, and maintenance of Alveolar Type 1 cells. 70% of VIP binds to this receptor. The Type II cell is also the cell selectively attacked by the SARS-CoV-2 virus via the ACE2 surface receptor. [1]
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| ln Vivo |
Pulmonary hypertension (PH) leads to an increased right ventricular workload, cardiac failure and death. In idiopathic pulmonary arterial hypertension (PAH) the vasodilating vasoactive intestinal peptide (aviptadil) is deficient. The aim of the present study was to test the acute effects on haemodynamics and blood gases, and the safety, of a single dose of inhaled aviptadil in chronic PH. A total of 20 patients with PH (PAH in nine, PH in lung disease in eight and chronic thromboembolic PH in three) inhaled a single 100-microg dose of aviptadil during right-heart catheterisation. Haemodynamics and blood gases were measured. Aviptadil aerosol caused a small and temporary but significant selective pulmonary vasodilation, an improved stroke volume and mixed venous oxygen saturation. Overall, six patients experienced a pulmonary vascular resistance reduction of >20%. In patients with significant lung disease, aviptadil tended to improve oxygenation. The pulmonary vasodilating effect of aviptadil aerosol was modest and short-lived, did not cause any side-effects and led to a reduced workload of the right ventricle without affecting systemic blood pressure. Aviptadil inhalation tended to improve oxygenation in patients with significant lung disease. Further studies are needed to evaluate the full therapeutic potential of aviptadil aerosol, including higher doses and chronic treatment. [5]
Vasoactive Intestinal Peptide (VIP) completely prevented the development of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) when treatment began on the same day as MCT injection, as evidenced by normalized hemodynamics, pulmonary vascular morphology, and 100% survival over 45 days.[3] Vasoactive Intestinal Peptide (VIP) significantly reversed established MCT-induced PAH when treatment began 3 weeks after MCT, reducing RV systolic pressure, medial area/luminal area ratio, and lung inflammation, and reducing mortality from 100% to 29%.[3] Vasoactive Intestinal Peptide (VIP) combined with bosentan fully reversed established MCT-induced PAH, normalizing RV systolic pressure, vascular remodeling, RV hypertrophy, inflammation, and achieving 100% survival over 45 days.[3] |
| Animal Protocol |
Acute Lung Injury, which triggers Critical COVID-19 is a known lethal complication of Corona Virus (SARS-CoV-2) infection. Conventional medical therapy, including intensive care and respiratory support is associated with an 80% mortality. Aviptadil, a synthetic form of Human Vasoactive Intestinal Polypeptide (VIP) has been awarded FDA Orphan Drug Designation for the treatment of ARDS and admitted to the FDA CoronaVirus Technology Accelerator Program.
VIP binds to VPAC1 receptors on the pulmonary Alveolar Type II (ATII) cell. ATII cells comprise only 5% of lung epithelial cells but are critical for oxygen transfer, surfactant production, and maintenance of Alveolar Type 1 cells. 70% of VIP binds to this receptor. The Type II cell is also the cell selectively attacked by the SARS-CoV-2 virus via the ACE2 surface receptor.
Nonclinical studies demonstrate that VIP is highly concentrated in the lung and specifically bound to the ATII cell, where it prevents NMDA-induced caspase-3 activation in the lung, inhibits IL6 and TNFa production, protects against HCl-induced pulmonary edema, and upregulates surfactant production, These and other effects have been observed in numerous animal model systems of lung injury in mice, rats, guinea pigs, sheep, swine, and dogs. In these models, Aviptadil restores barrier function at the endothelial/alveolar interface and thereby protects the lung and other organs from failure.
Aviptadil ihas a demonstrated 20 year history of safety in phase 2 trials for Sarcoid, Pulmonary Fibrosis, Bronchospasm, and a phase I trial in ARDS. In that phase I trial, 8 patients with severe ARDS on mechanical ventilation were treated with ascending doses of VIP. Seven of the 8 patients were successfully extubated and were alive at the five day timepoint. Six left the hospital and one died of an unrelated cardiac event.
Five phase 2 trials of aviptadil have been conducted under European regulatory authority. Numerous healthy volunteer studies have shown that i.v. infusion of Aviptadil is well tolerated with few adverse effects including alterations in blood pressure, heart rate, or ECG. In addition to published studies of human use, Aviptadil has been used on a compounded basis in certain ICUs for many years in the belief that it preserves life and restores function in pulmonary hypertension, ARDS, and Acute Lung Injury (ALI).
In this study, patients who are hospitalized for Critical COVID-19 infection with respiratory failure will be randomly allocated to Aviptadil administered by intravenous infusion in addition to maximal intensive care vs. maximal intensive care alone. Primary endpoints will be improvement in blood oxygenation and mortality. [1]
Sprague Dawley rats (200-230 g) received a single subcutaneous injection of monocrotaline (MCT, 60 mg/kg) to induce PAH. For prevention study: Vasoactive Intestinal Peptide (VIP) (500 µg/kg) was administered intraperitoneally every other day for 3 weeks, starting on the same day as MCT injection.[3] For reversal study: Vasoactive Intestinal Peptide (VIP) (500 µg/kg) was administered intraperitoneally every other day for 3 weeks, starting 3 weeks after MCT injection.[3] For combination therapy: Vasoactive Intestinal Peptide (VIP) (500 µg/kg, i.p., every other day) and bosentan (300 mg/kg/day, as food admix) were administered for 3 weeks, starting 3 weeks after MCT injection.[3] Hemodynamic measurements (RV systolic pressure) were taken via right ventricular catheterization. Histological and morphometric analyses were performed on lung sections. RV hypertrophy was assessed by weighing RV and LV+septum. Lung inflammation was graded semi-quantitatively. Survival was monitored for 45 days.[3] |
| Toxicity/Toxicokinetics |
Of the 20 patients, 19 tolerated a single 100 μg dose of aviptadil well (tolerance score of 1-4, with 1 representing excellent tolerability). No side effects were observed in any of these patients. [4] One patient withdrew from the study due to anxiety during inhalation. This patient had a history of recurrent panic attacks since 1999, and the event was assessed to be unrelated to aviptadil. [4]
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| References | |
| Additional Infomation |
Avicardil is a synthetic vasoactive intestinal peptide (VIP) with potential anti-cytokine, anti-inflammatory, and immunomodulatory activities. After administration, avicardil mimics the effects of endogenous VIP. In the lungs, avicardil may inhibit N-methyl-D-aspartate (NMDA)-induced caspase-3 activation, suppress the production of certain pro-inflammatory mediators such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and may protect the lungs from cytokine storms and inflammation. Since cytokines cause alveoli to fill with water, making them impermeable to oxygen, avicardil may help prevent pulmonary edema and restore the barrier function of the endothelial/alveolar interface. This may improve blood oxygenation, alleviate respiratory distress, and prevent lung injury. VIP is a naturally occurring synthetic peptide hormone that is highly enriched in the lungs.
AVIPTADIL is a protein drug that has completed Phase III clinical trials (covering all indications) and has four investigational indications. Advances in biomedicine over the past decade have revealed the central role of proliferating pulmonary artery smooth muscle cells (PASMCs) in the development of pulmonary hypertension (PH). Furthermore, research has identified factors promoting PASMC and endothelial cell proliferation and anti-apoptosis, such as aberrant signaling pathways involving growth factors, G protein-coupled receptors, kinases, and microRNAs. Based on these findings, PH is now classified into different subtypes according to underlying pathology, allowing for more targeted treatments. PH is characterized by dysplastic PASMC proliferation, local inflammation, and endothelial cell anti-apoptosis, all of which ultimately lead to vascular wall remodeling. Several promising targets have been identified to assess the relative contributions of these factors. This review discusses new targets for PH treatment developed in recent years based on these advances, which are currently in preclinical and clinical trial phases (e.g., imatinib [Phase III]; nilotinib, AT-877ER, rituximab, tacrolimus, paroxetine, sertraline, fluoxetine, bardoxolone methyl ester [Phase II]; and sorafenib, FK506, avipadil, endothelial progenitor cells (EPCs) [Phase I]). Despite significant progress in targeting key molecular pathways in recent years, pulmonary arterial hypertension (PH) remains incurable. These novel therapies provide an important conceptual framework for classifying patients based on molecular phenotypes to achieve effective treatment of the disease. [2] Background: Treatment of pulmonary arterial hypertension (PAH) remains challenging, and more effective drugs and drug combinations are still being explored. We recently reported that deletion of the vasoactive intestinal peptide (VIP) gene leads to spontaneous expression of the PH phenotype, which VIP can completely correct. This study aims to answer the following questions: 1) Can VIP prevent PH in other experimental models? 2) Does the combined use of vasoactive intestinal peptide (VIP) and the endothelin (ET) receptor antagonist bosentan enhance its efficacy? Methods: Pulmonary hypertension (PAH) was induced in Sprague Dawley rats within 3 weeks following a single subcutaneous injection of monoclonal antibody (MCT), characterized by pulmonary vascular remodeling, pulmonary inflammation, and right ventricular hypertrophy, leading to death within the next 2 weeks. Animals in the MCT injection group received one of the following treatments: no treatment, oral bosentan alone, intraperitoneal VIP alone, or a combination therapy. This combination therapy was chosen because VIP downregulates endothelin receptor expression, while bosentan further inhibits endothelin receptor expression. Hemodynamics, pulmonary vascular pathology, and survival rates were compared among the treatment groups. Results: VIP treatment, initiated on the same day as the MCT injection and administered every other day for 3 weeks, almost completely halted the pathological progression of PAH and eliminated deaths within 45 days. However, VIP treatment initiated 3 weeks after MCT treatment, while more effective than bosentan, only partially reversed the pathological changes of PAH. The combined treatment of the two drugs completely reversed the pathological changes and prevented death for at least 45 days. Conclusions: 1) VIP can completely prevent and significantly reverse MCT-induced PAH; 2) VIP is more effective than bosentan, possibly because it targets a wider range of pro-remodeling pathways; 3) VIP combined with bosentan is more effective than either drug alone, possibly because the two drugs synergistically inhibit the ET-ET receptor pathway. [3] Background: Vasoactive intestinal peptide (VIP) has been reported to have some protective properties against lung damage. In addition, its protective effect in cold preservation of donor lungs has been confirmed. We used an in vivo rat lung transplantation model to study the effects of VIP and the timing of its administration. Methods: All lungs were flushed with low-potassium dextran-1% glucose solution and orthotopically transplanted with the left lung. Rats were divided into four groups (n=6). The first group did not undergo any preservation treatment. The transplanted lungs in the second, third and fourth groups were preserved at 4°C for 18 hours. The second group did not receive VIP treatment. The third group received VIP (0.1 g/ml) via flushing solution. Recipients in group IV received an intravenous injection of VIP (3 μg/kg) immediately after reperfusion. Twenty-four hours post-transplantation, the right pulmonary artery and right bronchus were ligated, and the recipients were ventilated with 100% oxygen for 5 minutes. Mean pulmonary artery pressure, peak airway pressure, blood gas analysis, serum lipid peroxidation levels, tissue myeloperoxidase activity, and wet/dry weight ratio were measured. Results: The partial pressure of oxygen in groups III and IV was better than that in group II (Groups II, III, and IV: 147.4±71.4, 402.1±64.8, 373.4±81.0 mmHg; p<0.05). The peak airway pressure in groups III and IV was lower than that in group II (Groups II, III, and IV: 19.7±0.8, 16.7±0.9, and 16.3±1.0 mmHg; p<0.05). The mean pulmonary artery pressure in group III was lower than that in group II (groups II and III: 36.3±3.0 and 22.1±2.2 mmHg, respectively; p<0.01). The wet weight/dry weight ratio in group III was lower than that in groups II and IV (groups II, III, and IV: 5.2±0.2, 4.4±0.2, and 5.2±0.3, respectively; p<0.05 between groups II and III, and p<0.01 between groups III and IV). The serum lipid peroxide levels in groups III and IV were significantly lower than those in other groups (groups II, III, and IV: 2.643±0.913, 0.455±0.147, and 0.325±0.124 nmol/ml, respectively; p<0.01). Conclusion: VIP can improve reperfusion injury in an in vivo rat lung transplantation model. Systemic administration of vasoactive intestinal peptide (VIP) via flushing fluid or immediately after reperfusion can improve lung function. [4] Vasoactive intestinal peptide (VIP) is a neuropeptide with pulmonary vasodilatory, antiproliferative, and broad-spectrum anti-inflammatory properties. [3] Vasoactive intestinal peptide (VIP) has been tested in clinical trials for pulmonary arterial hypertension (PAH), but with mixed results: one trial showed significant efficacy, while another reported negative results. [3] Vasoactive intestinal peptide (VIP) may be more effective when used in combination with bosentan, as the two synergistically inhibit the endothelin pathway and have complementary anti-inflammatory and anti-remodeling effects. [3] VIP gene deletion in mice leads to spontaneous PAH, and VIP treatment can reverse this PAH. [3] |
| Molecular Formula |
C147H238N44O42S
|
|---|---|
| Molecular Weight |
3325.80
|
| Exact Mass |
3323.756
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| Elemental Analysis |
C, 52.19; H, 7.15; N, 16.89; O, 22.87; S, 0.90
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| CAS # |
40077-57-4
|
| Related CAS # |
Aviptadil acetate;1444827-29-5
|
| PubChem CID |
16132300
|
| Sequence |
HSDAVFTDNYTRLRKQMAVKKYLNSILN-NH2
H-His-Ser-Asp-Ala-Val-Phe-Thr-Asp-Asn-Tyr-Thr-Arg-Leu-Arg-Lys-Gln-Met-Ala-Val-Lys-Lys-Tyr-Leu-Asn-Ser-Ile-Leu-Asn-OH |
| SequenceShortening |
HSDAVFTDNYTRLRKQMAVKKYLNSILN
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| Appearance |
White to off-white solid powder
|
| Density |
1.5±0.1 g/cm3
|
| Index of Refraction |
1.660
|
| LogP |
-5.39
|
| SMILES |
CC[C@@H]([C@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](N)CC1=CN=CN1)=O)CO)=O)CC(O)=O)=O)C)=O)C(C)C)=O)CC2=CC=CC=C2)=O)[C@H](O)C)=O)CC(O)=O)=O)CC(N)=O)=O)CC3=CC=C(O)C=C3)=O)[C@H](O)C)=O)CCCNC(N)=N)=O)CC(C)C)=O)CCCNC(N)=N)=O)CCCCN)=O)CCC(N)=O)=O)CCSC)=O)C)=O)C(C)C)=O)CCCCN)=O)CCCCN)=O)CC4=CC=C(O)C=C4)=O)CC(C)C)=O)CC(N)=O)=O)CO)=O)C(N[C@H](C(N[C@H](C(N)=O)CC(N)=O)=O)CC(C)C)=O)C
|
| InChi Key |
CBTPBFFYMHBLFP-KQVGQEDNSA-N
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| InChi Code |
InChI=1S/C147H237N43O43S.4C2H4O2/c1-18-75(12)115(142(229)180-96(56-72(6)7)131(218)183-104(145(232)233)63-110(155)200)188-139(226)106(68-192)185-134(221)101(62-109(154)199)177-130(217)95(55-71(4)5)174-132(219)97(58-81-37-41-84(195)42-38-81)175-125(212)88(33-23-26-49-149)167-123(210)89(34-24-27-50-150)171-140(227)113(73(8)9)186-118(205)76(13)164-121(208)93(47-53-234-17)170-127(214)92(45-46-107(152)197)169-122(209)87(32-22-25-48-148)166-124(211)90(35-28-51-161-146(156)157)168-129(216)94(54-70(2)3)173-126(213)91(36-29-52-162-147(158)159)172-143(230)116(78(15)193)189-136(223)98(59-82-39-43-85(196)44-40-82)176-133(220)100(61-108(153)198)178-135(222)103(65-112(203)204)182-144(231)117(79(16)194)190-137(224)99(57-80-30-20-19-21-31-80)181-141(228)114(74(10)11)187-119(206)77(14)165-128(215)102(64-111(201)202)179-138(225)105(67-191)184-120(207)86(151)60-83-66-160-69-163-83;4*1-2(3)4/h19-21,30-31,37-44,66,69-79,86-106,113-117,191-196H,18,22-29,32-36,45-65,67-68,148-151H2,1-17H3,(H2,152,197)(H2,153,198)(H2,154,199)(H2,155,200)(H,160,163)(H,164,208)(H,165,215)(H,166,211)(H,167,210)(H,168,216)(H,169,209)(H,170,214)(H,171,227)(H,172,230)(H,173,213)(H,174,219)(H,175,212)(H,176,220)(H,177,217)(H,178,222)(H,179,225)(H,180,229)(H,181,228)(H,182,231)(H,183,218)(H,184,207)(H,185,221)(H,186,205)(H,187,206)(H,188,226)(H,189,223)(H,190,224)(H,201,202)(H,203,204)(H,232,233)(H4,156,157,161)(H4,158,159,162);4*1H3,
|
| Chemical Name |
H-His-Ser-Asp-Ala-Val-Phe-Thr-Asp-Asn-Tyr-Thr-Arg-Leu-Arg-Lys-Gln-Met-Ala-Val-Lys-Lys-Tyr-Leu-Asn-Ser-Ile-Leu-Asn-NH2 tetraacetic acid.
|
| Synonyms |
Aviptadil Acetate; VIP; Invicorp; Aviptadil; 40077-57-4; (2S)-4-amino-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-5-amino-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]propanoyl]amino]-3-methylbutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-carboxypropanoyl]amino]-4-oxobutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxybutanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]hexanoyl]amino]-5-oxopentanoyl]amino]-4-methylsulfanylbutanoyl]amino]propanoyl]amino]-3-methylbutanoyl]amino]hexanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]
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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) |
H2O : ~100 mg/mL (~30.07 mM)
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|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.3007 mL | 1.5034 mL | 3.0068 mL | |
| 5 mM | 0.0601 mL | 0.3007 mL | 0.6014 mL | |
| 10 mM | 0.0301 mL | 0.1503 mL | 0.3007 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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