| Size | Price | |
|---|---|---|
| 500mg | ||
| 1g | ||
| Other Sizes |
| Targets |
EGFRL858R (IC50 = 0.4 nM); EGFR (IC50 = 0.5 nM); EGFRL858R/T790M (IC50 = 10 nM); HER2 (IC50 = 14 nM); HER3
|
|---|---|
| ln Vitro |
Heregulin-stimulated HER3 phosphorylation can be prevented by afatinib oxalate at a concentration of 100 nM [1]. Effectively suppressing the anchorage-independent proliferation of NIH-3T3 cells ectopically expressing EGFR mutations as well as the cell proliferation of H1666, H3255, and NCI 1975 cells is achieved with the use of Afatinib oxalate (0-10000 nM) [1]. SLMT-1, EC-1, HKESC-1, and HKESC-2 cells show growth suppression in response to Afatinib oxalate (48–72 hours) [2]. In ESCC cell lines, afatinib oxalate (0–1 μM, 24-48 hours) suppresses the AKT and MAPK pathways as well as EGFR and AKT phosphorylation [2]. HKESC-2 and EC-1 experience G0/G1 cell cycle arrest when exposed to afatinib oxalate (0–1 μM) for 16–48 hours [2]. In HKESC-2 and EC-1, afatinib oxalate (0–1 μM, 24-48 hours) efficiently causes apoptosis [2].
|
| ln Vivo |
EGFR, HER2, HER3, and AKT phosphorylation were all significantly downregulated and tumor regression was observed when oral afatinib oxalate (0–20 mg/kg) was administered daily for 25 days [1]. Strongly inhibiting the growth of HKESC-2 tumors was afatinib oxalate (15 mg/kg), taken orally for 5 days, followed by 2 days off, for a duration of 2 weeks [2].
|
| Enzyme Assay |
EGFR kinase: 10 μL of inhibitor in 50% Me2SO, 20 μL of substrate solution (200 mM HEPES pH 7.4, 50 mM Mg-acetate, 2.5 mg/mL poly (EY), 5 μg/mL bio-pEY), and 20 µL enzyme preparation were included in each 100 µL enzyme reaction. The addition of 50 µL of a 100 µM ATP solution prepared in 10 mM MgCl2 initiates the enzymatic reaction. After 30 minutes of assaying at room temperature, 50 µL of stop solution (250 mM EDTA in 20 mM HEPES pH 7.4) is added to end the assay. 100 µL are added to a microtiterplate coated with streptavidin, and after 60 minutes of room temperature incubation, the plate is cleaned with 200 µL of wash solution (50 mM Tris, 0.05% Tween20). The wells are filled with a 100 µL aliquot of PY20H Anti-Ptyr:HRP, a 250 ng/mL HRPO-labeled anti-PY antibody. Following a 60-minute incubation period, the plate is three times cleaned using a 200 µL wash solution. Following that, 100µL of TMB Peroxidase Solution (A:B=1:1) is used to develop the samples. After ten minutes, the reaction is stopped. After the plate is placed in an ELISA reader, the extinction at OD450nm is calculated. The enzyme HER2-IC: The assay of enzyme activity is conducted in 50% Me2SO with or without serial inhibitor dilutions. Similar components as described for the EGFR kinase assay are included in each 100 µL reaction, along with the addition of 1000 µM Na3VO4. The addition of 50µL of a 500 µM ATP solution prepared in 10 mM magnesium acetate initiates the enzymatic reaction. The enzyme is diluted to the point where the amount of enzyme and the amount of time it takes for phosphate to be incorporated into bio-pEY are linear. The mixture of 20 mM HEPES pH 7.4, 130 mM NaCl, 0.05% Triton X-100, 1 mM DTT, and 10% glycerol is used to dilute the enzyme preparation. After 30 minutes of assaying at room temperature, 50 µL of stop solution is added to end the procedure. Src kinase assays: 10 µL of inhibitor in 50% Me2SO, 20 µL of enzyme preparation, and 20 µL of substrate solution enhanced with 1000 µM Na3VO4 were included in each 100 µL reaction. The addition of 50 µL of a 1000 µM ATP solution prepared in 10 mM Mg-acetate initiates the enzymatic reaction. Assay for BIRK kinase: 50 µL of a 2 mM ATP solution prepared in 8 mM MnCl2 and 20 mM Mg-acetate is added to 250 mM Tris pH 7.4, 10 mM DTT, 2.5 mg/mL poly(EY), and 5 mg/mL bio-pEY as the substrate solution to initiate the enzymatic reaction. HGFR kinase and VEGF2 assays: The assay is completed by adding 10 µL of 5% H3PO4 after it has been running at room temperature for 20 minutes. The precipitate is then collected using a 96 well filter mate universal harvester and trapped onto GF/B filters. The filter plate is thoroughly cleaned, dried for one hour at 50°C, sealed, and the radioactivity is measured using scintillation counting with either a TopCountTM or a Microbeta b counterTM.
|
| Cell Assay |
Cell proliferation assay [1]
Cell Types: NIH-3T3 cells, H1666, H3255 and NCI 1975 Cell Tested Concentrations: 0, 1, 10, 100, 1000, 10000 nM Incubation Duration: Experimental Results: Effective inhibition of NIH- anchorage-dependent proliferation 3T3 Cells ectopically express EGFR mutants. It inhibits the anchorage-independent cell proliferation of multiple lung cancer cell lines (H1666, H3255 and NCI 1975 cells) with IC50 values of 60 nM, 0.7 nM and 99 nM respectively. Cell viability assay[2] Cell Types: HKESC-1, HKESC-2, SLMT-1 and EC-1 Cell Line Tested Concentrations: Incubation Duration: 48 and 72 hrs (hours) Experimental Results: More than 95% growth inhibition was observed. Respective IC50 concentrations at 48 hrs (hours) (HKESC-1=0.078 μM, HKESC-2=0.115 μM, KYSE510=3.182 μM, SLMT-1=4.625 μM and EC-1=1.489 μM) and 72 hrs (hours) (HKESC-1=0.002) μM, HKESC-2=0.002 μM, KYSE510=1.090 μM, SLMT-1=1.161 μM and EC-1=0.109 μM) are all in the lower micromolar range. Western Blot Analysis[2] Cell Types: HKESC-2 cells and EC-1 cells Tested Concentrations: 0, 0.01 a |
| Animal Protocol |
Animal/Disease Models: Athymic NMRI-nu/nu female mice (21–31 g, 5 to 6 weeks old, transgenic mouse lung cancer model and xenograft model) [1]
Doses: 15 mg/kg, 20 mg/kg given Medication: Orally administered daily for 25 days Experimental Results: In a standard xenograft model of the epidermoid cancer cell line A431, tumors Dramatically regressed with a cumulative treatment/control tumor volume ratio (T/C ratio) of 2%, and EGFR and AKT downregulates phosphorylation. Induced regression of large tumors in this HER2-driven model and effectively controlled xenograft tumor formation in the NCIH1975 cell line expressing EGFR L858R/T790M, with a T/C value of 12% at a dose of 20 mg/kg. After 4 weeks of treatment, the tumor was diminished by more than 50%. Downregulates EGFR, HER2 and HER3 phosphorylation. Animal/Disease Models: Sixweeks old female athymic nude mice (nu/nu) (16-20 g)[2] Doses: 15 mg/kg Route of Administration: po (oral gavage), according to a schedule of 5 days plus 2 days of rest , lasted for two weeks. Experimental Results: Str |
| References |
|
| Additional Infomation |
Afatinib is a quinazoline compound having a 3-chloro-4-fluoroanilino group at the 4-position, a 4-dimethylamino-trans-but-2-enamido group at the 6-position, and an (S)-tetrahydrofuran-3-yloxy group at the 7-position. Used (as its dimaleate salt) for the first-line treatment of patients with metastatic non-small cell lung cancer. It has a role as a tyrosine kinase inhibitor and an antineoplastic agent. It is a member of quinazolines, a member of furans, an organofluorine compound, an enamide, an aromatic ether, a tertiary amino compound, a member of monochlorobenzenes and a secondary carboxamide.
Afatinib is a 4-anilinoquinazoline tyrosine kinase inhibitor in the form of a dimaleate salt available as Boehringer Ingelheim's brand name Gilotrif. For oral use, afatinib tablets are a first-line (initial) treatment for patients with metastatic non-small cell lung cancer (NSCLC) with common epidermal growth factor receptor (EGFR) mutations as detected by an FDA-approved test. Gilotrif (afatinib) is the first FDA-approved oncology product from Boehringer Ingelheim. Afatinib is a Kinase Inhibitor. The mechanism of action of afatinib is as a Protein Kinase Inhibitor. Afatinib is a tyrosine kinase receptor inhibitor that is used in the therapy of selected forms of metastatic non-small cell lung cancer. Afatinib is associated with transient elevations in serum aminotransferase levels during therapy and has been reported to cause clinically apparent acute liver injury and rare instances of death. Afatinib is an orally bioavailable anilino-quinazoline derivative and inhibitor of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (ErbB; EGFR) family, with antineoplastic activity. Upon administration, afatinib selectively and irreversibly binds to and inhibits the epidermal growth factor receptors 1 (ErbB1; EGFR), 2 (ErbB2; HER2), and 4 (ErbB4; HER4), and certain EGFR mutants, including those caused by EGFR exon 19 deletion mutations or exon 21 (L858R) mutations. This may result in the inhibition of tumor growth and angiogenesis in tumor cells overexpressing these RTKs. Additionally, afatinib inhibits the EGFR T790M gatekeeper mutation which is resistant to treatment with first-generation EGFR inhibitors. EGFR, HER2 and HER4 are RTKs that belong to the EGFR superfamily; they play major roles in both tumor cell proliferation and tumor vascularization and are overexpressed in many cancer cell types. A quinazoline and butenamide derivative that acts as a tyrosine kinase inhibitor of epidermal growth factor receptors (ERBB RECEPTORS) and is used in the treatment of metastatic NON-SMALL CELL LUNG CANCER. View More
Drug Indication Pharmacodynamics Aberrant ErbB signaling triggered by receptor mutations, and/or amplification, and/or receptor ligand overexpression contributes to the malignant phenotype. Mutation in EGFR defines a distinct molecular subtype of lung cancer. In non-clinical disease models with ErbB pathway deregulation, afatinib as a single agent effectively blocks ErbB receptor signaling resulting in tumor growth inhibition or tumor regression. NSCLC tumors with common activating EGFR mutations (Del 19, L858R) and several less common EGFR mutations in exon 18 (G719X) and exon 21 (L861Q) are particularly sensitive to afatinib treatment in non-clinical and clinical settings. Limited non-clinical and/or clinical activity was observed in NSCLC tumors with insertion mutations in exon 20. The acquisition of a secondary T790M mutation is a major mechanism of acquired resistance to afatinib and gene dosage of the T790M-containing allele correlates with the degree of resistance in vitro. The T790M mutation is found in approximately 50% of patients' tumors upon disease progression on afatinib, for which T790M targeted EGFR TKIs may be considered as a next line treatment option. Other potential mechanisms of resistance to afatinib have been suggested preclinically and MET gene amplification has been observed clinically. At the same time, the effect of multiple doses of afatinib (50 mg once daily) on cardiac electrophysiology and the QTc interval was evaluated in an open-label, single-arm study in patients with relapsed or refractory solid tumors. Ultimately, no large changes in the mean QTc interval (i.e., >20 ms) were detected in the study. Absorption Following oral administration, time to peak plasma concentration (Tmax) is 2 to 5 hours. Maximum concentration (Cmax) and area under the concentration-time curve from time zero to infinity (AUC0-∞) values increased slightly more than dose proportional in the range of 20 to 50 mg. The geometric mean relative bioavailability of 20 mg tablets was 92% as compared to an oral solution. Additionally, systemic exposure to afatinib is decreased by 50% (Cmax) and 39% (AUC0-∞), when administered with a high-fat meal compared to administration in the fasted state. Based on population pharmacokinetic data derived from clinical trials in various tumor types, an average decrease of 26% in AUCss was observed when food was consumed within 3 hours before or 1 hour after taking afatinib. Route of Elimination In humans, excretion of afatinib is primarily via the feces. Following administration of an oral solution of 15 mg afatinib, 85.4% of the dose was recovered in the feces and 4.3% in urine. The parent compound afatinib accounted for 88% of the recovered dose. Volume of Distribution The volume of distribution of afatinib recorded in healthy male volunteers is documented as 4500 L. Such a high volume of distribution in plasma suggests a potentially high tissue distribution. Clearance The apparent total body clearance of afatinib as recorded in healthy male volunteers is documented as being a high geometric mean of 1530 mL/min. Metabolism / Metabolites Enzyme-catalyzed metabolic reactions play a negligible role for afatinib in vivo. Covalent adducts to proteins were the major circulating metabolites of afatinib. Biological Half-Life Afatinib is eliminated with an effective half-life of approximately 37 hours. Thus, steady-state plasma concentrations of afatinib were achieved within 8 days of multiple dosing of afatinib resulting in an accumulation of 2.77-fold (AUC0-∞) and 2.11-fold (Cmax). In patients treated with afatinib for more than 6 months, a terminal half-life of 344 h was estimated. Protein Binding In vitro binding of afatinib to human plasma proteins is approximately 95%. Afatinib binds to proteins both non-covalently (traditional protein binding) and covalently. Mechanism of Action Afatinib is a potent and selective, irreversible ErbB family blocker. Afatinib covalently binds to and irreversibly blocks signaling from all homo and heterodimers formed by the ErbB family members EGFR (ErbB1), HER2 (ErbB2), ErbB3 and ErbB4. In particular, afatinib covalently binds to the kinase domains of EGFR (ErbB1), HER2 (ErbB2), and HER4 (ErbB4) and irreversibly inhibits tyrosine kinase autophosphorylation, resulting in downregulation of ErbB signaling. Certain mutations in EGFR, including non-resistant mutations in its kinase domain, can result in increased autophosphorylation of the receptor, leading to receptor activation, sometimes in the absence of ligand binding, and can support cell proliferation in NSCLC. Non-resistant mutations are defined as those occurring in exons constituting the kinase domain of EGFR that lead to increased receptor activation and where efficacy is predicted by 1) clinically meaningful tumor shrinkage with the recommended dose of afatinib and/or 2) inhibition of cellular proliferation or EGFR tyrosine kinase phosphorylation at concentrations of afatinib sustainable at the recommended dosage according to validated methods. The most commonly found of these mutations are exon 21 L858R substitutions and exon 19 deletions. Moreover, afatinib demonstrated inhibition of autophosphorylation and/or in vitro proliferation of cell lines expressing wild-type EGFR and in those expressing selected EGFR exon 19 deletion mutations, exon 21 L858R mutations, or other less common non-resistant mutations, at afatinib concentrations achieved in patients. In addition, afatinib inhibited in vitro proliferation of cell lines overexpressing HER2. Genetic alterations in the kinase domain of the epidermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC) patients are associated with sensitivity to treatment with small molecule tyrosine kinase inhibitors. Although first-generation reversible, ATP-competitive inhibitors showed encouraging clinical responses in lung adenocarcinoma tumors harboring such EGFR mutations, almost all patients developed resistance to these inhibitors over time. Such resistance to first-generation EGFR inhibitors was frequently linked to an acquired T790M point mutation in the kinase domain of EGFR, or upregulation of signaling pathways downstream of HER3. Overcoming these mechanisms of resistance, as well as primary resistance to reversible EGFR inhibitors driven by a subset of EGFR mutations, will be necessary for development of an effective targeted therapy regimen. Here, we show that BIBW2992, an anilino-quinazoline designed to irreversibly bind EGFR and HER2, potently suppresses the kinase activity of wild-type and activated EGFR and HER2 mutants, including erlotinib-resistant isoforms. Consistent with this activity, BIBW2992 suppresses transformation in isogenic cell-based assays, inhibits survival of cancer cell lines and induces tumor regression in xenograft and transgenic lung cancer models, with superior activity over erlotinib. These findings encourage further testing of BIBW2992 in lung cancer patients harboring EGFR or HER2 oncogenes.[1] Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cause of cancer death in the United States. Treatment of locally advanced disease is associated with significant acute side effects and can lead to chronic disabilities, while the prognosis of recurrent or metastatic disease is very poor. This highlights the need for better therapeutic options. Epidermal growth factor receptor is overexpressed in 90% of HNSCC patients and is an attractive therapeutic target in this patient population. Afatinib is a potent, irreversible pan-ErbB inhibitor. Preliminary studies in HNSCC show promising activity. Areas covered: This article reviews the current data evaluating small molecules inhibitors of the ErbB family in the treatment of HNSCC with a specific emphasis on afatinib, a second-generation, irreversible, pan-ErbB inhibitor. It also provides a description of afatinib's drug characteristics, pharmacokinetics and toxicity profile as well as details of the published and ongoing clinical trials evaluating its efficacy in HNSCC patients. Expert opinion: Phase II trials in HNSCC show that daily oral treatment with afatinib is tolerable. Most common toxicities are skin rash and diarrhea. Afatinib has clinical activity as a single agent in a subset of refractory and/or metastatic HNSCC patients. It is thought that ongoing Phase III trials should better clarify the role of this compound in the treatment of HNSCC.[2] Hepatotoxicityepatotoxicity Elevations in serum aminotransferase levels are common during afatinib therapy occurring in 20% to 50% of patients, but rising above 5 times the upper limit of the normal range in only 1% to 2%. Hepatic failure is said to have occurred in 0.2% of patients and to have resulted in several fatalities. Hepatotoxicity appears to be a class effect among protein kinase inhibitors of EGFR2, although liver injury appears to be more frequent and more severe with gefitinib than with afatinib and erlotinib. Specific details of the liver injury associated with afatinib such as latency, serum enzyme pattern, clinical features and course, have not been published. Other EGFR inhibitors, such as erlotinib and gefitinib typically cause liver injury arising within days or weeks of starting therapy and presenting abruptly with hepatocellular enzyme elevations and a moderate-to-severe course. Immunoallergic and autoimmune features are not common. The rate of clinically significant liver injury and hepatic failure is increased in patients with preexisting cirrhosis or hepatic impairment due to liver tumor burden. Likelihood score: D (possible cause of clinically apparent liver injury). Elevations in serum aminotransferase levels are common during afatinib therapy occurring in 20% to 50% of patients, but rising above 5 times the upper limit of the normal range in only 1% to 2%. Hepatic failure is said to have occurred in 0.2% of patients and to have resulted in several fatalities. Hepatotoxicity appears to be a class effect among protein kinase inhibitors of EGFR2, although liver injury appears to be more frequent and more severe with gefitinib than with afatinib and erlotinib. Specific details of the liver injury associated with afatinib such as latency, serum enzyme pattern, clinical features and course, have not been published. Other EGFR inhibitors, such as erlotinib and gefitinib typically cause liver injury arising within days or weeks of starting therapy and presenting abruptly with hepatocellular enzyme elevations and a moderate-to-severe course. Immunoallergic and autoimmune features are not common. The rate of clinically significant liver injury and hepatic failure is increased in patients with preexisting cirrhosis or hepatic impairment due to liver tumor burden. Likelihood score: D (possible cause of clinically apparent liver injury). |
| Molecular Formula |
C26H27CLFN5O7
|
|---|---|
| Molecular Weight |
575.97328877449
|
| Exact Mass |
665.153
|
| CAS # |
1398312-64-5
|
| Related CAS # |
Afatinib;850140-72-6;Afatinib dimaleate;850140-73-7;(E/Z)-Afatinib;439081-18-2;Afatinib-d6;1313874-96-2
|
| PubChem CID |
66547001
|
| Appearance |
Typically exists as solid at room temperature
|
| Hydrogen Bond Donor Count |
6
|
| Hydrogen Bond Acceptor Count |
16
|
| Rotatable Bond Count |
10
|
| Heavy Atom Count |
46
|
| Complexity |
773
|
| Defined Atom Stereocenter Count |
1
|
| SMILES |
CN(C)C/C=C/C(=O)NC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=C(C=C3)F)Cl)O[C@H]4CCOC4.C(=O)(C(=O)O)O.C(=O)(C(=O)O)O
|
| InChi Key |
NHTYOYNDYHAMAE-IACUOYJGSA-N
|
| InChi Code |
InChI=1S/C24H25ClFN5O3.2C2H2O4/c1-31(2)8-3-4-23(32)30-21-11-17-20(12-22(21)34-16-7-9-33-13-16)27-14-28-24(17)29-15-5-6-19(26)18(25)10-15;2*3-1(4)2(5)6/h3-6,10-12,14,16H,7-9,13H2,1-2H3,(H,30,32)(H,27,28,29);2*(H,3,4)(H,5,6)/b4-3+;;/t16-;;/m0../s1
|
| Chemical Name |
(E)-N-[4-(3-chloro-4-fluoroanilino)-7-[(3S)-oxolan-3-yl]oxyquinazolin-6-yl]-4-(dimethylamino)but-2-enamide;oxalic acid
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
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
|
|---|---|
| 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 | 1.7362 mL | 8.6810 mL | 17.3620 mL | |
| 5 mM | 0.3472 mL | 1.7362 mL | 3.4724 mL | |
| 10 mM | 0.1736 mL | 0.8681 mL | 1.7362 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.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
