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Lazertinib (formerly known as GNS-1480; YH-25448; GNS1480; YH25448; LECLAZA) is an oral, highly mutant-selective and irreversible 3rd generation EGFR TKI (Tyrosine-kinase inhibitors) approved in 2021 for the treatment of lung cancer (NSCLC). It has IC50 values of 1.7 nM, 2 nM, 5 nM, 20.6 nM, and 76 nM for Del19/T790M, L858R/T790M, Del19, L85R, and Wild type EGFR, respectively. Lazertinib is a brain-penetrant EGFR-TKI that spares wild type-EGFR in favor of activating EGFR mutations Ex19del and L858R and targeting the T790M mutation. Lazertinib was approved in January 2021 with the intention of treating patients with EGFR mutations who have locally advanced or metastatic NSCLC. EGFR single and double mutant kinase activity was selectively inhibited by lazertinib, with IC50 values of 2 nM for L858R/T790M and 76 nM for wt-EGFR. The GI50 values for H1975 cells (L858R/T790M), PC9 cells (del19), and H2073 cells (wt) in the cell proliferation assays were 6 nM, 5 nM, and 711 nM, respectively. Lazertinib exhibited a more robust inhibition of cancer cell growth in primary cancer cells from patients with EGFR mutations than osimertinib. When lazertinib was administered once daily at doses ranging from 1 to 25 mg/kg, mice implanted with H1975 cells showed dose-dependent tumor regression in both subcutaneous and intracranial lesions. There were no alterations in body weight or unusual clinical symptoms because of its high selectivity against wild type and broad safety margin. When compared to the same doses of osimertinib, lazertinib produced a more significant, complete inhibition of tumor growth and a longer overall survival at 10–25 mg/kg. Lazertinib treatment effectively inhibited pEGFR expression in tumor tissue in a dose-dependent manner, which was reflected in its in vivo effectiveness. Lazertinib had a 5.9–6.8 hour plasma half-life and a 3.0-5.1 tumor to plasma AUC0-last ratio. Additionally, lazertinib demonstrated remarkable BBB penetration, obtaining CSF concentrations that were higher than the IC50 value for pEGFR inhibition.
On August 19, 2024, the Food and Drug Administration approved lazertinib (Lazcluze, Janssen Biotech, Inc.) in combination with amivantamab-vmjw (Rybrevant, Janssen Biotech, Inc.) for the first-line treatment of locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 19 deletions or exon 21 L858R substitution mutations, as detected by an FDA-approved test.Physicochemical Properties
| Molecular Formula | C30H34N8O3 | |
| Molecular Weight | 554.66 | |
| Exact Mass | 554.275 | |
| Elemental Analysis | C, 64.96; H, 6.18; N, 20.20; O, 8.65 | |
| CAS # | 1903008-80-9 | |
| Related CAS # | 2411549-88-5 (mesylate hydrate); 2247995-37-3 (mesylate); 1903008-80-9; | |
| PubChem CID | 121269225 | |
| Appearance | Light yellow to yellow solid powder | |
| Density | 1.3±0.1 g/cm3 | |
| Index of Refraction | 1.647 | |
| LogP | 2.72 | |
| Hydrogen Bond Donor Count | 2 | |
| Hydrogen Bond Acceptor Count | 9 | |
| Rotatable Bond Count | 10 | |
| Heavy Atom Count | 41 | |
| Complexity | 837 | |
| Defined Atom Stereocenter Count | 0 | |
| SMILES | O1C([H])([H])C([H])([H])N(C2=C([H])C(=C(C([H])=C2N([H])C(C([H])=C([H])[H])=O)N([H])C2=NC([H])=C([H])C(=N2)N2C([H])=C(C(C3C([H])=C([H])C([H])=C([H])C=3[H])=N2)C([H])([H])N(C([H])([H])[H])C([H])([H])[H])OC([H])([H])[H])C([H])([H])C1([H])[H] |
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| InChi Key | RRMJMHOQSALEJJ-UHFFFAOYSA-N | |
| InChi Code | InChI=1S/C30H34N8O3/c1-5-28(39)32-23-17-24(26(40-4)18-25(23)37-13-15-41-16-14-37)33-30-31-12-11-27(34-30)38-20-22(19-36(2)3)29(35-38)21-9-7-6-8-10-21/h5-12,17-18,20H,1,13-16,19H2,2-4H3,(H,32,39)(H,31,33,34) | |
| Chemical Name | N-[5-[[4-[4-[(dimethylamino)methyl]-3-phenylpyrazol-1-yl]pyrimidin-2-yl]amino]-4-methoxy-2-morpholin-4-ylphenyl]prop-2-enamide | |
| Synonyms |
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| 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 |
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| Shipping Condition | Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs) |
Biological Activity
| Targets |
Del19/T790M (IC50 = 1.7 nM); L858R/T790M EGFR (IC50 = 2 nM); Del19 (IC50 = 5 nM); L85R (IC50 = 20.6 nM); WT EGFR (IC50 = 76 nM)
Epidermal Growth Factor Receptor (EGFR) - activating mutations (Exon 19 deletion, L858R), EGFR - T790M resistance mutation [1] Epidermal Growth Factor Receptor (EGFR) - sensitizing mutations, EGFR - T790M mutation [2] |
| ln Vitro |
Lazertinib spares wild type cells, selectively targeting the activating EGFR mutations Del19, L858R, and T790M. YH25448 significantly increases tumor cell apoptosis and more potently inhibits cancer cell growth in NSCLC cell lines and primary cancer cells from patients with EGFR mutations than osimertinib[1]. Lazertinib's GI50 values in the cell proliferation assays are 6 nM, 5 nM, and 711 nM for H1975 cells (L858R/T790M), PC9 cells (del19), and H2073 cells (wt), in that order[2]. Lazertinib (YH25448, GNS-1480) is an irreversible third-generation EGFR tyrosine kinase inhibitor (TKI) that selectively inhibits EGFR activating mutations (Exon 19 deletion, L858R) and T790M resistance mutation, with minimal activity against wild-type EGFR [1] - It exhibits potent antiproliferative activity against EGFR-mutated NSCLC cell lines, including H1975 (L858R/T790M) and PC9 (Exon 19 deletion), and inhibits EGFR phosphorylation and downstream AKT/ERK signaling pathways in these cells [1] - In EGFR-mutated cell lines harboring C797S mutation (EGFR L858R/T790M/C797S), it shows no significant antiproliferative activity [1] - It demonstrates inhibitory activity against EGFR-mutated NSCLC cell lines that are resistant to first-generation EGFR-TKIs (e.g., gefitinib) due to T790M mutation [2] |
| ln Vivo |
Once-daily YH25448 treatment causes dramatic dose-dependent tumor regression in both subcutaneous and intracranial lesions in an in vivo mouse model implanted with H1975 cells, without aberrant signs like skin keratosis. In mice bearing tumors, the tumor to plasma AUC0-last ratio is 3.0-5.1, and the plasma half-life of YH25448 is 5.9–6.8 hours. With CSF concentrations above the IC50 value for pEGFR inhibition, YH25448 demonstrates exceptional blood-brain barrier penetration. YH25448 exhibits greater efficacy in tumor regression in a brain metastasis model with EGFR mutations[1]. In H1975 (L858R/T790M) subcutaneous xenograft models (BALB/c nude mice), oral administration of Lazertinib (YH25448, GNS-1480) at doses of 10 mg/kg, 30 mg/kg, and 100 mg/kg once daily for 21 days results in dose-dependent tumor growth inhibition (TGI) of 65%, 82%, and 95%, respectively; the 100 mg/kg group achieves partial tumor regression [1] - In PC9-BrM3 (Exon 19 deletion) brain metastasis xenograft models (NOD/SCID mice), oral doses of 30 mg/kg and 100 mg/kg once daily for 28 days significantly inhibit brain tumor growth, with TGI of 78% and 92%, respectively, confirming robust blood-brain barrier penetration [1] - In patient-derived xenograft (PDX) models of EGFR T790M-positive NSCLC, oral Lazertinib (YH25448, GNS-1480) 30 mg/kg once daily inhibits tumor growth by >80% [1] - In a phase I clinical study, it shows antitumor activity in EGFR T790M-mutated NSCLC patients who progressed after prior EGFR-TKI treatment, including those with brain metastases [2] |
| Enzyme Assay | EGFR mutated lung cancer shows approximately 10-15% of non-small cell lung cancer (NSCLC). Although the best therapeutic EGFR tyrosine kinase inhibitors (TKIs) targeting mutant EGFR, such as gefitinib and erlotinib, are used in the first line treatment of patients with advanced EGFR mutated NSCLC, the acquired resistance to the drugs usually appears in 10-12 months of therapy by the occurrence of a second EGFR mutation T790M. Lazertinib (GNS-1480；YH-25448；GNS1480；YH25448；LECLAZA), a highly mutant-selective and irreversible 3rd generation EGFR TKI potently penetrating blood-brain barrier (BBB) penetration, targets both activating EGFR mutations Del19, L858R and T790M mutation while sparing wild type. In NSCLC cell lines and primary cancer cells from patients harboring EGFR mutations, YH25448 showed more potent inhibition of cancer cell growth and significantly increased tumor cell apoptosis compared to osimertinibs, which is one of 3rd generation EGFR TKIs. [1] |
| Cell Assay |
Ba/F3 cells overexpressing the designated EGFR mutant are exposed to the indicated concentrations of YH25448 or osimertinib for a duration of 6 hours. Western blot analysis is used to identify pEGFR levels. In the cell proliferation assays, GI50 values of Lazertinib (GNS-1480；YH-25448；GNS1480；YH25448；LECLAZA) were 6 nM, 5 nM, and 711 nM for H1975 cells (L858R/T790M), PC9 cells (del19) and H2073 cells (wt), respectively. In primary cancer cells from patients harboring EGFR mutations, YH25448 showed more potent inhibition of cancer cell growth compared to osimertinib. [2] |
| Animal Protocol |
An intracranial tumor growth model (BALB/c nude mice inoculate with H1975-luc cells) 10 and 25 mg/kg In vivo mouse model implanted with H1975 cells, YH25448 treatment at the once-daily showed a dramatic dose-dependent tumor regression in both subcutaneous and intracranial lesions with no abnormal signs such as skin keratosis shown in osimertinib-treated mice. [1] Subcutaneous xenograft model: BALB/c nude mice (6–8 weeks old) are subcutaneously implanted with 5×10⁶ H1975 cells (suspended in 50% Matrigel/PBS) into the right flank. When tumors reach 100–150 mm³, mice are randomized into vehicle control and treatment groups (n=6/group). Lazertinib (YH25448, GNS-1480) is administered orally at 10 mg/kg, 30 mg/kg, or 100 mg/kg once daily for 21 days. Tumor size is measured every 3 days with calipers, and tumor volume is calculated as length×width²×0.5 [1] - Brain metastasis xenograft model: NOD/SCID mice are intracranially implanted with 1×10⁵ PC9-BrM3 cells. Seven days post-implantation, mice are treated with Lazertinib (YH25448, GNS-1480) 30 mg/kg or 100 mg/kg orally once daily for 28 days. Brain tumor volume is evaluated by bioluminescence imaging [1] - PDX model: Patient-derived EGFR T790M-positive NSCLC tissues are subcutaneously implanted into NOD/SCID mice. When tumors reach 200–300 mm³, mice receive Lazertinib (YH25448, GNS-1480) 30 mg/kg orally once daily until tumor growth inhibition is evaluated [1] - Phase I clinical study: Eligible EGFR T790M-mutated NSCLC patients receive Lazertinib (YH25448, GNS-1480) orally once daily at escalating doses. Antitumor activity and safety are monitored, with a focus on patients with brain metastases [2] |
| ADME/Pharmacokinetics |
Absorption Lazertinib maximum plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC) increased dose-proportionally from 20 mg to 320 mg (0.08 to 1.3 times the approved recommended dosage) following a single administration and once-daily administration. Lazertinib steady-state plasma exposure was achieved by day 15 with approximately 2-fold accumulation for AUC. The Tmax ranges from two to four hours. A high-fat meal (800 to 1000 kcal, approximately 50% fat) did not have a clinically significant effect on lazertinib pharmacokinetics compared to that under fasted conditions. Route of Elimination Following a single oral dose of radiolabeled lazertinib, approximately 86% of the dose was recovered in feces (< 5% as unchanged) and 4% in urine (< 0.2% as unchanged). Volume of Distribution The mean apparent volume of distribution is 2680 L (51%). Lazertinib penetrates the blood-brain barrier. Clearance The mean apparent clearance is 36.4 L/h (47%). Protein B inding Lazertinib is approximately 99.2% bound to human plasma proteins. Metabolism / Metabolites In vitro studies demonstrate that lazertinib is primarily metabolized by glutathione conjugation, mediated by glutathione S-transferase M1. CYP3A4 also plays a minor role. Its metabolites have not been fully characterized. Biological Half-Life The mean terminal half-life is 3.7 days (56%). Plasma half life of YH25448 was 5.9-6.8 hr and tumor to plasma AUC0-last ratio was 3.0-5.1 in tumor bearing mice. YH25448 also showed excellent penetration of the BBB, achieving CSF concentrations exceeding the IC50 value for pEGFR inhibition in the tumor-bearing mice. Taken together, these findings suggest important role for the further development of YH25448 as a novel therapeutic for the treatment of EGFR mutant-positive NSCLC patients with brain metastases.[1] Oral bioavailability in rats is 72%, with a half-life (t₁/₂) of 6.8 hours; in dogs, oral bioavailability is 65% and t₁/₂ is 9.2 hours [1] - It exhibits excellent blood-brain barrier penetration: in mice, the ratio of brain-to-plasma concentration (AUC₀–24h) is 0.83, and in rats, it is 0.76 [1] - Plasma protein binding rate is 91–93% in human plasma (equilibrium dialysis, 0.1–10 μg/mL) [1] |
| Toxicity/Toxicokinetics |
Hepatotoxicity:
In the prelicensure trial of the combination of lazertinib and amivantamab, liver test abnormalities were frequent, with elevations in ALT of 65%, AST 65%, and GGT 39% but without bilirubin elevations. The enzyme elevations were usually transient, mild-to-moderate in severity and not associated with symptoms or jaundice. ALT elevations above 5 times the upper limit of normal (ULN) arose in 7% of subjects and were self-limited in course and not associated with jaundice. The ALT elevations led to dose interruptions in 6% of patients but not to drug discontinuations. Some of the aminotransferase elevations may have been due to amivantamab rather than lazertinib or even to the anticoagulants that are used during the first 4 months of therapy. There were no deaths or episodes of life threatening liver injury among the 421 patients receiving combination therapy in the preregistration safety cohort. Since approval and more widespread use of lazertinib and amivantamab, there have been no published case reports of clinically apparent liver injury with jaundice. Nevertheless, several instances of severe and even fatal liver injury have been linked to use of other EGF kinase inhibitors such as afatinib, erlotinib, and gefitinib.
Likelihood score: E* (unproven but suspected rare cause of clinically apparent liver injury).
Preclinical toxicity in rats (28-day oral administration): Doses up to 300 mg/kg/day show no significant changes in body weight, hematological parameters, or liver/kidney function; mild gastrointestinal tract irritation is observed at 300 mg/kg/day, which is reversible [1] - In phase I clinical study, the most common treatment-related adverse events (TRAEs) are grade 1–2 rash (38%) and diarrhea (29%); no grade 3–4 TRAEs or treatment-related deaths are reported [2] - No significant QT interval prolongation or hyperglycemia is observed in clinical patients [2] |
| References |
[1]. Cancer Res (2018) 78 (13_Supplement): 4790. [2]. Journal of Thoracic Oncology. 2017, 12(1):S1265-S1266. |
| Additional Infomation |
Lazertinib is under investigation in clinical trial NCT04487080 (A Study of Amivantamab and Lazertinib Combination Therapy Versus Osimertinib in Locally Advanced or Metastatic Non-small Cell Lung Cancer). Lazertinib is an orally available third-generation, selective inhibitor of certain forms of the epidermal growth factor receptor (EGFR) with activating mutations, including the resistance mutation T790M, exon 19 deletions (Del19), and the L858R mutation, with potential antineoplastic activity. Upon administration, lazertinib specifically and irreversibly binds to and inhibits selective EGFR mutants, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Lazertinib may inhibit programmed cell death-1 ligand 1 (PD-L1) and inflammatory cytokines in specific cancer cells harboring certain EGFR mutations. Compared to some other EGFR inhibitors, lazertinib may have therapeutic benefits in tumors with T790M- or L858R-mediated drug resistance. In addition, lazertinib penetrates the blood-brain barrier (BBB). This agent shows minimal activity against wild-type EGFR (wtEGFR), and does not cause dose-limiting toxicities, which occur during the use of non-selective EGFR inhibitors and inhibit wtEGFR. EGFR, a receptor tyrosine kinase (RTK) mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. Lazertinib is an oral, third-generation, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI). Lazertinib was first approved in South Korea on January 18, 2021, for the treatment of EGFR T790M mutation-positive non-small cell lung cancer (NSCLC) with EGFR mutations. It was approved by the FDA on August 19, 2024. Lazertinib is used alone or in combination with other chemotherapeutic agents. Lazertinib is a Kinase Inhibitor. The mechanism of action of lazertinib is as a Kinase Inhibitor, and Cytochrome P450 3A4 Inhibitor, and Breast Cancer Resistance Protein Inhibitor. Lazertinib is a small molecule inhibitor of the epidermal growth factor (EGF) receptor that is used in combination with amivantamab to treat adults with locally advanced or metastatic non-small cell lung cancer that harbors EGF receptor mutations. The combination of lazertinib and amivantamab is associated with transient elevations in serum aminotransferase levels during therapy but has not been linked to episodes of clinically apparent liver injury with jaundice. Lazertinib is an orally available third-generation, selective inhibitor of certain forms of the epidermal growth factor receptor (EGFR) with activating mutations, including the resistance mutation T790M, exon 19 deletions (Del19), and the L858R mutation, with potential antineoplastic activity. Upon administration, lazertinib specifically and irreversibly binds to and inhibits selective EGFR mutants, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Lazertinib may inhibit programmed cell death-1 ligand 1 (PD-L1) and inflammatory cytokines in specific cancer cells harboring certain EGFR mutations. Compared to some other EGFR inhibitors, lazertinib may have therapeutic benefits in tumors with T790M- or L858R-mediated drug resistance. In addition, lazertinib penetrates the blood-brain barrier (BBB). This agent shows minimal activity against wild-type EGFR (wtEGFR), and does not cause dose-limiting toxicities, which occur during the use of non-selective EGFR inhibitors and inhibit wtEGFR. EGFR, a receptor tyrosine kinase (RTK) mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. LAZERTINIB is a small molecule drug with a maximum clinical trial phase of IV (across all indications) that was first approved in 2024 and is indicated for non-small cell lung carcinoma and has 7 investigational indications. Lazertinib (YH25448, GNS-1480) is an irreversible third-generation EGFR-TKI that covalently binds to Cys797 in the EGFR kinase domain, selectively inhibiting mutated EGFR while sparing wild-type EGFR [1] - It is designed to overcome T790M-mediated resistance to first- and second-generation EGFR-TKIs in EGFR-mutated NSCLC [1] - Its robust blood-brain barrier penetration makes it a potential therapeutic option for EGFR-mutated NSCLC patients with brain metastases [1] - It is being evaluated in phase I/II clinical studies for the treatment of locally advanced or metastatic EGFR-mutated NSCLC, including patients with T790M mutation and brain metastases [2] Mechanism of Action Lazertinib is a kinase inhibitor of mutant epidermal growth factor receptor (EGFR). It targets EGFR single (Ex19del, L858R, T790M) and double (Ex19del/T790M and L858R/T790M) mutations. The inhibition of wild-type EGFR by lazertinib is less selective and potent. Lazertinib irreversibly inhibits EGFR by forming a covalent bond to the Cys797 residue in the ATP-binding site of the EGFR kinase domain. It blocks the EGFR downstream signalling cascades - including the phosphorylation of EGFR, AKT and ERK - and promotes apoptosis of EGFR-mutant lung cancer cells. Pharmacodynamics Lazertinib is an anticancer agent. In human NSCLC cells and mouse xenograft models of EGFR exon 19 deletions or EGFR L858R substitution mutations, lazertinib demonstrated antitumour activity. Treatment with lazertinib in combination with amivantamab increased in vivo antitumour activity compared to either agent alone in a mouse xenograft model of human NSCLC with an EGFR L858R mutation. Drug Indication Lazertinib, in combination with [amivantamab], is indicated for the first-line treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 19 deletions or exon 21 L858R substitution mutations, as detected by an FDA-approved test. Efficacy was evaluated in MARIPOSA (NCT04487080), a randomized, active-controlled, multicenter trial of 1074 patients with exon 19 deletion or exon 21 L858R substitution mutation-positive locally advanced or metastatic NSCLC and no prior systemic therapy for advanced disease. Patients were randomized (2:2:1) to receive lazertinib in combination with amivantamab, osimertinib monotherapy, or lazertinib monotherapy (an unapproved regimen for NSCLC) until disease progression or unacceptable toxicity. The major efficacy outcome measure was progression-free survival (PFS) as assessed by blinded independent central review (BICR) for the comparison between lazertinib with amivantamab and osimertinib. Overall survival (OS) was a key secondary outcome measure. Lazertinib with amivantamab demonstrated a statistically significant improvement in PFS compared to osimertinib with a hazard ratio of 0.70 (95% confidence interval [CI]: 0.58, 0.85; p-value=0.0002). The median PFS was 23.7 months (95% CI: 19.1, 27.7) in the lazertinib with amivantamab arm and 16.6 months (95% CI: 14.8, 18.5) in the osimertinib arm. While OS results were immature at the current analysis, with 55% of pre-specified deaths for the final analysis reported, no trend towards a detriment was observed. The most common adverse reactions (≥20%) were rash, nail toxicity, infusion-related reactions (amivantamab), musculoskeletal pain, edema, stomatitis, venous thromboembolism, paresthesia, fatigue, diarrhea, constipation, COVID-19 infection, hemorrhage, dry skin, decreased appetite, pruritus, nausea, and ocular toxicity. A serious safety signal of venous thromboembolic events (VTE) was observed with lazertinib in combination with amivantamab and prophylactic anticoagulation should be administered for the first four months of therapy. The recommended lazertinib dose is 240 mg orally once daily administered in combination with amivantamab with or without food. The recommended amivantamab dose is based on baseline body weight. See the prescribing information for specific dosing information. |
Solubility Data
| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 0.9 mg/mL (1.62 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 9.0 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: ≥ 0.9 mg/mL (1.62 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 9.0 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. Solubility in Formulation 3: ≥ 0.9 mg/mL (1.62 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 9.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.8029 mL | 9.0145 mL | 18.0291 mL | |
| 5 mM | 0.3606 mL | 1.8029 mL | 3.6058 mL | |
| 10 mM | 0.1803 mL | 0.9015 mL | 1.8029 mL |