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Purity: ≥98%
Bortezomib (formerly also known as PS-341; trade name Velcade among others), a dipeptide boronic acid derivative, is cell-permeable, reversible, potent and highly selective inhibitor of the 20S proteasome that may have antitumor effects. In a test without cells, it inhibits the 20S proteasome with a Ki of 0.6 nM. The controlled breakdown of proteins involved in cell cycle regulation and tumor growth is facilitated by the ubiquitin-proteasome pathway. Tumor growth should be significantly impacted and cell death should result from dysregulating the degradation of these proteins. Bortezomib was licensed in 2003 in the United States and Europe for the treatment of relapsed multiple myeloma and mantle cell lymphoma. It is a potent 20S proteasome inhibitor with potential antineoplastic activity. A big protease complex called the 26S proteasome breaks down ubiquinated proteins; benetezomib reversibly inhibits this complex. Bortezomib amplifies the cytotoxic effects of chemotherapy and radiation while delaying the growth of tumors in vivo.
| Targets |
NF-κB; 20S proteasome (Ki = 0.6 nM)
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| ln Vitro |
is a highly selective, reversible inhibitor of the 26S proteasome, which is mainly involved in the breakdown of misfolded proteins and is crucial for controlling the cell cycle. It is a boronic acid dipeptide. It has been demonstrated that exposure to boratezomib stabilizes p21, p27, and p53 in addition to the proapoptotic Bax and Bid proteins, caveolin-1, and inhibitor κB-α, which stops nuclear factor κB-induced cell survival pathways from activating. Additionally, boratezomib stimulates the endoplasmic reticulum stress response and proapoptotic c-Jun-NH2 terminal kinase. Changes in these cellular protein levels cause cancer cells to proliferate less, migrate less, and undergo apoptosis more frequently.[2] It has been demonstrated that boratezomib can enter cells and block the intracellular proteolysis of long-lived proteins by proteasomes at a concentration that can stop 50% of the proteolysis at about 0.1 μM. Throughout the panel of 60 cancer cell lines obtained from various human tumors from the US National Cancer Institute (NCI), the average growth inhibition of 50% value for Bortezomib is 7 nM. Bortezomib (100 nM) treatment of PC-3 cells for 8 hours causes a decrease in G1 cell count and an increase in G2-M cell accumulation. PC-3 cells are killed by benetezomib at 24 and 48 hours, with IC50 values of 100 and 20 nM, respectively. Nuclear condensation is brought on by benezomib 16–24 hours after treatment. In a time-dependent manner, benezomib treatment causes PARP cleavage; at 24 hours, concentrations as low as 100 nM are effective.[1]
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| ln Vivo |
In xenograft models of multiple myeloma, adult T-cell leukemia, lung, breast, prostate, pancreatic, head and neck, and colon cancer, as well as melanoma, the anticancer effects of bortezomib as a single agent have been shown.[2] In the Lewis lung cancer model, oral bortezomib 1.0 mg/kg daily for 18 days results in tumor growth delays and a reduction in the number of metastases. A single dose of up to 5 mg/kg of borectezomib markedly reduced the percentage of breast tumor cells that survived. Takedaskomib When given weekly for four weeks, 1.0 mg/kg of prostate cancer reduces tumor growth in murine xenograft models by 60%. When administered at a dose of 1.0 mg/kg for four weeks, pancreatic cancer murine xenografts grow 72% or 84% less, and tumor cell apoptosis rises. Treatment with 1.0 mg/kg Bortezomib causes a notable reduction in the growth of human plasmacytoma xenografts, an increase in the apoptosis and overall survival of tumor cells, and a decrease in tumor angiogenesis. [3]
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| Enzyme Assay |
Suc-Leu-Leu-Val-Tyr-AMC in DMSO and 2.00 mL of assay buffer (20 mM HEPES, 0.5 mM EDTA, 0.035% SDS, pH 7.8) are added to a 3 mL fluorescence cuvette in a typical kinetic run. The cuvette is then placed in the jacketed cell holder of a fluorescence spectrophotometer. A water bath that circulates keeps the reaction temperature at 37°C. One microliter to ten microliters of the stock enzyme solution are added to the cuvette once the reaction solution has reached thermal equilibrium, which takes five minutes. The degree of fluorescence emission that increases at 440 nm (λex= 380 nm) when AMC is cleaved from peptide-AMC substrates indicates the progress of the reaction.
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| Cell Assay |
The MTT dye absorbance of the cells is used to measure the inhibitory effect of boratezamib on cell growth. For the final four hours of the 48-hour cultures, cells are pulsed with 10 μL of 5 mg/mL MTT in each well. This is followed by 100 μL of isopropanol containing 0.04 N HCl. The absorbance is determined with a spectrophotometer at 570 nm.
Pretreatment with bortezomib sensitized multiple myeloma, myeloid leukemia, and renal cancer cells but not normal B lymphocytes to TRAIL/Apo2L-induced apoptosis. In an in vivo experiment, bone marrow and renal cancer cell mixtures, with or without bortezomib and/or TRAIL/Apo2L, were transplanted into the bone marrow of mice. Whereas all the mice receiving cells treated with TRAIL/Apo2L died of leukemia within 35 days, 50% of those receiving cells treated with bortezomib and 90% of those receiving cells treated with both TRAIL/Apo2L and bortezomib survived more than 100 days.[2] Through inhibition of NF-κB, bortezomib not only promotes apoptosis of cancer cells but also sensitizes these cells to chemotherapy, radiation or immunotherapy. However, because specific NF-κB inhibition alone via PS-1145 only partially inhibits proliferation of tumor cells, the cytotoxic activity of bortezomib must also depend on altered regulation of other signal transduction pathway targets.[2] Interestingly, sensitivity to proteasome inhibition was partially dependent on the p53 status of breast and lung cancer in vitro, but bortezomib-induced apoptosis and/or chemosensitization were p53 independent in prostate, multiple myeloma, and colon cancer cells. Therefore, the degree of variability in the sensitivity to bortezomib with respect to p53 status appears cell-type dependent.[2] A recently published study found that bortezomib prevented activation of caveolin-1 in multiple myeloma cells.[2] |
| Animal Protocol |
Human plasmacytoma xenografts RPMI 8226
1 mg/kg i.v. twice weekly for 4 weeks, then once weekly Following weekly i.v. treatment of PS-341 to mice bearing the PC-3 tumor, a significant decrease (60%) in tumor burden was observed in vivo. Direct injection of PS-341 into the tumor also caused a substantial (70%) decrease in tumor volume with 40% of the drug-treated mice having no detectable tumors at the end of the study. Studies also revealed that i.v. administration of PS-341 resulted in a rapid and widespread distribution of PS-341, with highest levels identified in the liver and gastrointestinal tract and lowest levels in the skin and muscle. Modest levels were found in the prostate, whereas there was no apparent penetration of the central nervous system. An assay to follow the biological activity of the PS-341 was established and used to determine temporal drug activity as well as its ability to penetrate tissues. As such, PS-341 was shown to penetrate PC-3 tumors and inhibit intracellular proteasome activity 1.0 h after i.v. dosing. These data illustrate that PS-341 not only reaches its biological target but has a direct effect on its biochemical target, the proteasome. Importantly, the data show that inhibition of this target site by PS-341 results in reduced tumor growth in murine tumor models. Together, the results highlight that the proteasome is a novel biochemical target and that inhibitors such as PS-341 represent a unique class of antitumor agents. PS-341 is currently under clinical evaluation for advanced cancers.[1] |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Following intravenous administration of 1 mg/m2 and 1.3 mg/m2 doses, the mean Cmax of bortezomib were 57 and 112 ng/mL, respectively. In a twice-weekly dosing regimen, the Cmax ranged from 67 to 106 ng/mL at the dose of 1 mg/m2 and 89 to 120 ng/mL for the 1.3 mg/m2 dose. In patients with multiple myeloma, the Cmax of bortezomib followig subcutaneous administration was lower than that of intravenously-administered dose; however, the total systemic exposure of the drug was equivalent for both routes of administration. There is a wide interpatient variability in drug plasma concentrations. Bortezomib is eliminated by both renal and hepatic routes. The mean distribution volume of bortezomib ranged from approximately 498 to 1884 L/m2 in patients with multiple myeloma receiving a single- or repeat-dose of 1 mg/m2 or 1.3 mg/m2. Bortezomib distributes into nearly all tissues, except for the adipose and brain tissue. Following the administration of a first dose of 1 mg/m2 and 1.3 mg/m2, the mean mean total body clearances were 102 and 112 L/h, respectively. The clearances were 15 and 32 L/h after the subsequent dose of 1 and 1.3 mg/m2, respectively. Following intravenous administration of 1 mg/sq m and 1.3 mg/sq m doses to 24 patients with multiple myeloma (n=12, per each dose level), the mean maximum plasma concentrations of bortezomib (Cmax) after the first dose (Day 1) were 57 and 112 ng/mL, respectively. In subsequent doses, when administered twice weekly, the mean maximum observed plasma concentrations ranged from 67 to 106 ng/mL for the 1 mg/sq m dose and 89 to 120 ng/mL for the 1.3 mg/sq m dose. The mean elimination half-life of bortezomib upon multiple dosing ranged from 40 to 193 hours after the 1 mg/sq m dose and 76 to 108 hours after the 1.3 mg/sq m dose. The mean total body clearances was 102 and 112 L/hr following the first dose for doses of 1 mg/sq m and 1.3 mg/sq m, respectively, and ranged from 15 to 32 L/hr following subsequent doses for doses of 1 and 1.3 mg/sq m, respectively. The mean distribution volume of bortezomib ranged from approximately 498 to 1884 L/sq m following single- or repeat-dose administration of 1 mg/sq m or 1.3mg/sq m to patients with multiple myeloma. This suggests bortezomib distributes widely to peripheral tissues. The binding of bortezomib to human plasma proteins averaged 83% over the concentration range of 100 to 1000 ng/mL. It is not known whether bortezomib is excreted in human milk. For more Absorption, Distribution and Excretion (Complete) data for BORTEZOMIB (6 total), please visit the HSDB record page. Metabolism / Metabolites Bortezomib is primarily metabolized by CYP3A4, CYP2C19, and CYP1A2. CYP2D6 and CYP2C9 are also involved in drug metabolism, but to a smaller extent. Oxidative deboronation, which involves the removal of boronic acid from the parent compound, is the main metabolic pathway. Metabolites of bortezomib are pharmacologically inactive and more than 30 metabolites have been identified in human and animal studies. In vitro studies with human liver microsomes and human cDNA-expressed cytochrome P450 isozymes indicate that bortezomib is primarily oxidatively metabolized via cytochrome P450 enzymes 3A4, 2C19, and 1A2. Bortezomib metabolism by CYP 2D6 and 2C9 enzymes is minor. The major metabolic pathway is deboronation to form 2 deboronated metabolites that subsequently undergo hydroxylation to several metabolites. Deboronated bortezomib metabolites are inactive as 26S proteasome inhibitors. Pooled plasma data from 8 patients at 10 min and 30 min after dosing indicate that the plasma levels of metabolites are low compared to the parent drug. ... The P450 inhibition potential of bortezomib and its major deboronated metabolites M1 and M2 and their dealkylated metabolites M3 and M4 was evaluated in human liver microsomes for the major P450 isoforms 1A2, 2C9, 2C19, 2D6, and 3A4/5. Bortezomib, M1, and M2 were found to be mild inhibitors of CYP2C19 (IC(50) approximately 18.0, 10.0, and 13.2 microM, respectively), and M1 was also a mild inhibitor of CYP2C9 (IC(50) approximately 11.5 microM). However, bortezomib, M1, M2, M3, and M4 did not inhibit other P450s (IC(50) values > 30 microM). There also was no time-dependent inhibition of CYP3A4/5 by bortezomib or its major metabolites. ... ... Bortezomib binds the proteasome via the boronic acid moiety, and therefore, the presence of this moiety is necessary to achieve proteasome inhibition. Metabolites in plasma obtained from patients receiving a single intravenous dose of bortezomib were identified and characterized by liquid chromatography/mass spectrometry (LC/MS) and liquid chromatography/tandem mass spectrometry (LC/MS/MS). Metabolite standards that were synthesized and characterized by LC/MS/MS and high field nuclear magnetic resonance spectroscopy (NMR) were used to confirm metabolite structures. The principal biotransformation pathway observed was oxidative deboronation, most notably to a pair of diastereomeric carbinolamide metabolites. Further metabolism of the leucine and phenylalanine moieties produced tertiary hydroxylated metabolites and a metabolite hydroxylated at the benzylic position, respectively. Conversion of the carbinolamides to the corresponding amide and carboxylic acid was also observed. Human liver microsomes adequately modeled the in vivo metabolism of bortezomib, as the principal circulating metabolites were observed in vitro. Using cDNA-expressed cytochrome P450 isoenzymes, it was determined that several isoforms contributed to the metabolism of bortezomib, including CYP3A4, CYP2C19, CYP1A2, CYP2D6, and CYP2C9. ... Biological Half-Life The mean elimination half-life of bortezomib ranged from 40 to 193 hours following a multiple dosing regimen at a 1 mg/m2 dose. The half-life ranged from 76 to 108 hours after multiple dosing of 1.3 mg/m2 bortezomib. The mean elimination half-life of bortezomib upon multiple dosing ranged from 40 to 193 hours after the 1 mg/sq m dose and 76 to 108 hours after the 1.3 mg/sq m dose. |
| Toxicity/Toxicokinetics |
Hepatotoxicity
In large clinical trials of bortezomib, elevations in serum aminotransferase levels were common, occurring in ~10% of patients. However, values greater than 5 times the upper limit of normal (ULN) were rare, occurring in Bortezomib is typically given with other chemotherapeutic agents including cyclophosphamide and dexamethasone which can cause reactivation of hepatitis B. However, there have been no reports of reactivation of hepatitis B specifically attributable to bortezomib alone. Likelihood score: C (probable cause of clinically apparent drug induced liver injury). Protein Binding Over the concentration range of 100 to 1000 ng/mL, bortezomib is about 83% bound to human plasma proteins. Interactions Hypoglycemia and hyperglycemia have been reported in patients with diabetes mellitus who received bortezomib concomitantly with oral antidiabetic agents. If bortezomib is used concomitantly with oral antidiabetic agents, blood glucose concentrations should be monitored carefully and dosage of the antidiabetic agent adjusted as necessary. Potential interaction (increased risk of peripheral neuropathy) when bortezomib is used concomitantly with other drugs associated with peripheral neuropathy (eg, amiodarone, antiviral agents, isoniazid, nitrofurantoin, hydroxymethylglutaryl-coenzyme A [HMG-CoA] reductase inhibitors [statins]). Potential interaction (increased risk of hypotension) when bortezomib is used with drugs that can cause hypotension. Dosage adjustment of hypotensive agents may be necessary. ... In a preclinical toxicology study, bortezomib-treated rats resulted in liver enlargement (35%). Ex vivo analyses of the liver samples showed an 18% decrease in cytochrome P450 (P450) content, a 60% increase in palmitoyl coenzyme A beta-oxidation activity, and a 41 and 23% decrease in CYP3A protein expression and activity, respectively. Furthermore, liver samples of bortezomib-treated rats had little change in CYP2B and CYP4A protein levels and activities. To address the likelihood of clinical drug-drug interactions, the P450 inhibition potential of bortezomib and its major deboronated metabolites M1 and M2 and their dealkylated metabolites M3 and M4 was evaluated in human liver microsomes for the major P450 isoforms 1A2, 2C9, 2C19, 2D6, and 3A4/5. Bortezomib, M1, and M2 were found to be mild inhibitors of CYP2C19 (IC(50) approximately 18.0, 10.0, and 13.2 microM, respectively), and M1 was also a mild inhibitor of CYP2C9 (IC(50) approximately 11.5 microM). However, bortezomib, M1, M2, M3, and M4 did not inhibit other P450s (IC(50) values > 30 microM). There also was no time-dependent inhibition of CYP3A4/5 by bortezomib or its major metabolites. Based on these results, no major P450-mediated clinical drug-drug interactions are anticipated for bortezomib or its major metabolites. ... |
| References | |
| Additional Infomation |
Therapeutic Uses
Antineoplastic Agents; Protease Inhibitors Bortezomib injection is indicated for the treatment of patients with multiple myeloma who have received at least 1 prior therapy. /Included in US product label/ Bortezomib injection is indicated for the treatment of patients with mantle cell lymphoma who have received at least 1 prior therapy. /Included in US product label/ Drug Warnings Known hypersensitivity to bortezomib, boron, or mannitol. Bortezomib mainly causes sensory peripheral neuropathy, but severe motor peripheral neuropathy also has been reported. In the phase III trial, peripheral neuropathy occurred in 36% of patients receiving bortezomib and 9% of patients receiving dexamethasone. Grade 3 or 4 peripheral neuropathy occurred in 7 or less than 1%, respectively, of patients receiving bortezomib. Following dosage adjustments, amelioration or resolution of peripheral neuropathy was reported in 51% of patients with grade 2 or higher peripheral neuropathy within a median of 3.5 months from onset. About 8% of patients discontinued bortezomib therapy because of peripheral neuropathy. Patients receiving bortezomib should be monitored for manifestations of neuropathy (eg, burning sensation, hyperesthesia, hypoesthesia, paresthesia, discomfort, neuropathic pain). Dose and/or frequency of administration of bortezomib should be adjusted in patients who experience new-onset or exacerbation of peripheral neuropathy. In the phase III trial, asthenia (ie, fatigue, malaise, weakness) was reported in 61% of patients receiving bortezomib and 45% of patients receiving dexamethasone. Grade 3 asthenia occurred in 12 versus 6%, respectively, of patients receiving bortezomib or dexamethasone. About 3% of patients receiving bortezomib and 2% of patients receiving dexamethasone discontinued therapy because of asthenia. For more Drug Warnings (Complete) data for BORTEZOMIB (26 total), please visit the HSDB record page. Pharmacodynamics Bortezomib works to target the ubiquitin-proteasome pathway, an essential molecular pathway that regulates intracellular concentrations of proteins and promotes protein degradation. The ubiquitin-proteasome pathway is often dysregulated in pathological conditions, leading to aberrant pathway signalling and the formation of malignant cells. In one study, patient-derived chronic lymphocytic leukemia (CLL) cells contained 3-fold higher levels of chymotrypsin-like proteasome activity than normal lymphocytes. By reversibly inhibiting proteasome, bortezomib prevents proteasome-mediated proteolysis. Bortezomib exerts a cytotoxic effect on various cancer cell types _in vitro_ and delays tumour growth _in vivo_ in nonclinical tumour models. Bortezomib inhibits the proteasome activity in a dose-dependent manner. In one pharmacodynamic study, more than 75% of proteasome inhibition was observed in whole blood samples within one hour after dosing of bortezomib. |
| Molecular Formula |
C19H25BN4O4
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|---|---|
| Molecular Weight |
384.24
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| Exact Mass |
384.196
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| Elemental Analysis |
C, 59.39; H, 6.56; B, 2.81; N, 14.58; O, 16.66
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| CAS # |
179324-69-7
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| Related CAS # |
Bortezomib-d8
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| PubChem CID |
387447
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| Appearance |
White solid powder
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| Density |
1.2±0.1 g/cm3
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| Melting Point |
122-124°C
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| Index of Refraction |
1.564
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| LogP |
2.45
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
9
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| Heavy Atom Count |
28
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| Complexity |
500
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| Defined Atom Stereocenter Count |
2
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| SMILES |
CC(C[C@H](NC([C@@H](NC(C1=CN=CC=N1)=O)CC1=CC=CC=C1)=O)B(O)O)C
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| InChi Key |
GXJABQQUPOEUTA-RDJZCZTQSA-N
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| InChi Code |
InChI=1S/C19H25BN4O4/c1-13(2)10-17(20(27)28)24-18(25)15(11-14-6-4-3-5-7-14)23-19(26)16-12-21-8-9-22-16/h3-9,12-13,15,17,27-28H,10-11H2,1-2H3,(H,23,26)(H,24,25)/t15-,17-/m0/s1
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| Chemical Name |
[(1R)-3-methyl-1-[[(2S)-3-phenyl-2-(pyrazine-2-carbonylamino)propanoyl]amino]butyl]boronic acid
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| Synonyms |
NSC 681239; PS-341; PS341; MLN-341; PS 341; LDP-341; LDP 341; LDP341; MLN341; PS-341; Bortezomib (PS-341); Ps 341; Bortezomib accord; MLN 341. Brand name: VELCADE
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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: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 4 mg/mL (10.41 mM) (saturation unknown) in 10% EtOH + 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 40.0 mg/mL clear EtOH 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: ≥ 4 mg/mL (10.41 mM) (saturation unknown) in 10% EtOH + 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 40.0 mg/mL clear EtOH 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: ≥ 4 mg/mL (10.41 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: ≥ 2.5 mg/mL (6.51 mM) (saturation unknown) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 5: ≥ 2.5 mg/mL (6.51 mM) (saturation unknown) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 6: ≥ 2.08 mg/mL (5.41 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 7: ≥ 2.08 mg/mL (5.41 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. Solubility in Formulation 8: ≥ 2.08 mg/mL (5.41 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 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. Solubility in Formulation 9: ≥ 0.5 mg/mL (1.30 mM) (saturation unknown) in 1% DMSO 99% Saline (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 | 2.6025 mL | 13.0127 mL | 26.0254 mL | |
| 5 mM | 0.5205 mL | 2.6025 mL | 5.2051 mL | |
| 10 mM | 0.2603 mL | 1.3013 mL | 2.6025 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.
Virotherapy and Natural History Study of KHSV-Associated Multricentric Castleman s Disease With Correlates of Disease Activity
CTID: NCT00092222
Phase: Phase 2 Status: Active, not recruiting
Date: 2024-11-25
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