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Purity: ≥98%
Idelalisib (CAL-101, GS-1101; trade name Zydelig), an approved anticancer drug, is a potent and selective p110δ inhibitor with IC50 of 2.5 nM in cell-free assays; it has 40- to 300-fold greater selectivity for p110δ than p110α/β/γ, and 400- to 4000-fold more selectivity to p110δ than C2β, hVPS34, DNA-PK and mTOR. Phosphatidylinositol-3-kinase p110δ acts as a focal point for signaling from cell surface receptors that are known to support malignant B-cell survival and proliferation. Idelalisib thus has the potential to have anti-tumor and immunomodulating effects. The use of idelalisib to treat various blood cancers, including leukemia, received FDA and EMA approval in July 2014.
| Targets |
p110δ (IC50 = 2.5 nM); p110γ (IC50 = 89 nM); p110β (IC50 = 565 nM); p110α (IC50 = 820 nM); hVps34 (IC50 = 978 nM); DNA-PK (IC50 = 6729 nM)
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| ln Vitro |
Idelalisib (CAL-101; GS-1101) is a highly selective and potent inhibitor of p110δ (EC50=8 nM). While no activity is seen against a panel of 402 different kinases at 10 μM, greater selectivity (400- to 4000-fold) is seen against related kinases C2, hVPS34, DNA-PK, and mTOR. At 10 μM, CAL-101 only reduces PDGF-induced pAkt by 25%. With an EC50 of 1.9 μM, idelalisib (CAL-101) inhibits LPA-induced pAkt. While formyl-methionyl-leucyl-leucyl-phenylalanine activation of p110γ is inhibited with an EC50 of 3 μM, idelalisib (CAL-101) blocks FcRI p110δ-mediated CD63 expression with an EC50 of 8 nM. As a result, CAL-101 has a 240–2500-fold selectivity for p110δ over the other class I PI3K isoforms in cell-based assays[1]. CAL-101 When compared to vehicle treatment alone, idelalisib (CAL-101) induces a significant increase in the apoptosis of chronic lymphocytic leukemia (CLL) cells (P<0.001). Without regard to interphase cytogenetics or IgVH mutation status, idelalisib (CAL-101) causes selective cytotoxicity in CLL cells[2].
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| ln Vivo |
In the brain homogenates of both p110D910A/D910A mice and Idelalisib (CAL-101) (40 mg/kg, i.v.) post-treated mice, a significant decrease in CD11b+Ly6G+ neutrophils has been noted[3].
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| Enzyme Assay |
PI3K assay is preformed on whole-cell lysates from CLL or normal B cells. There is an ELISA test for PI3K. In a nutshell, PI(4,5)P2 substrate and reaction buffer containing adenosine triphosphate (ATP) are combined with whole-cell extracts, and the mixture is then left to incubate at room temperature. The addition of PI(3,4,5)P3 detector combined with EDTA (ethylenediaminetetraacetic acid) and an hour of incubation at room temperature stop the reaction. The mixture is then transferred from each well to a PI3K ELISA plate and given an additional hour to incubate. After washing, plates are incubated for 30 minutes with a secondary detector. After a second wash, the plates are added to with 3,3′,5,5′-tetramethylbenzidine solution for 5 minutes, after which H2SO4 is added to halt all reactions. A 96-well plate reader from Labsystems reads plates at 450 nm.
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| Cell Assay |
MTT assays are performed to determine cytotoxicity. Briefly, 1×105 cells (CLL B cells or healthy volunteer T cells or NK cells) are incubated for 48 hours with different concentrations of Idelalisib (CAL-101) (0.1 μM, 1 μM, 5 μM, 10 μM), 25 μM LY294002, or vehicle control. MTT reagent is then added. In a Labsystems plate reader, absorbance is measured using spectrophotometry at 540 nm after the addition of DMSO. An annexin/PI flow cytometry method is also used to determine the viability of cells at different time intervals. The software program Expo-ADC32 is used to analyze the data. For each sample, at least 10,000 cells are counted. The percentage of all positive cells compared to the untreated control is how the results are expressed. It was used in experiments to study caspase-dependent apoptosis along with 100 μM Z-VAD. The addition of 1 μg/mL CD40L, 800 U/mL IL-4, 50 ng/mL BAFF, 20 ng/mL TNF-α, or coculturing on fibronectin- or stromal (HS-5 cell line)-coated plates are some of the experiments used to study survival signals. A 75 cm2 flask (80%–100% confluent) is plated per 6-well plate for stromal coculture 24 hours before CLL cells are added[2].
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| Animal Protocol |
Mice: For Idelalisib (CAL-101) treatment, wild-type C57BL/6 mice are administered either 40 mg/kg Idelalisib (CAL-101) or vehicle DMSO, by 25 μL infusion into the femoral vein, 15 min before I/R (pre-treatment), or 3 and 6 h after initiation of reperfusion (post-treatment). The cerebral blood flow (CBF) of untreated animals and those given Idelalisib (CAL-101) was measured using a laser Doppler perfusion monitor. An 90-95% reduction in blood flow to the MCAO infarct region was observed in the CBF measurements taken right before and after MCAO, as well as again at 3 h after reperfusion. This reduction was consistent across groups.
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| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Following oral administration, the median Tmax was observed at 1.5 hours. Following a single dose of 150 mg of [14C] idelalisib, 78% and 14% of the radioactivity was excreted in feces and urine, respectively. GS-563117, idelalisib's major metabolite, accounted for 49% of the radioactivity in the urine and 44% in the feces. 23 L 14.9 L/hr Following oral administration of a single 150-mg dose of radiolabeled idelalisib, 78% of the dose was recovered in feces and 14% was recovered in urine; GS-563117 accounted for 44% of the dose recovered in feces and 49% of the dose recovered in urine. The administration of a single dose of Zydelig with a high-fat meal (900 calories: 525 calories fat, 250 calories carboydrates, and 125 calories protein) increased idelalisib AUC 1.4-fold relative to fasting conditions. Zydelig can be administered without regard to food. The median time to peak concentration (Tmax) was observed at 1.5 hours. Metabolism / Metabolites Idelalisib is metabolized by aldehyde oxidase and CYP3A to its major metabolite GS-563117, which is inactive against P110δ. Idelalisib is also metabolized to a minor extent by UGT1A4. Idelalisib, a potent phosphatidylinositol-3-kinase delta (PI3Kd) inhibitor, is metabolized primarily by aldehyde oxidase to form GS-563117 and to a lesser extent by cytochrome P450 (CYP) 3A and uridine 5'-diphospho-glucuronosyltransferase 1A4. In vitro, idelalisib inhibits P-glycoprotein (P-gp) and organic anion transporting polypeptides 1B1 and 1B3, and GS-563117 is a time-dependent CYP3A inhibitor. This study enrolled 24 healthy subjects and evaluated (1) the effect of idelalisib on the pharmacokinetics (PK) of digoxin, a P-gp probe substrate, rosuvastatin, a breast cancer resistance protein, and OATP1B1/OATP1B3 substrate, and midazolam, a CYP3A substrate; and (2) the effect of a strong inducer, rifampin, on idelalisib PK. On treatment, the most common clinical adverse events (AEs) were headache and pyrexia. Grade 3 transaminase increases were observed in 5 of 24 subjects and were reversible. Two subjects had serious AEs after treatment completion (grade 3 pyrexia and/or drug-induced liver injury). Idelalisib coadministration did not affect digoxin and rosuvastatin PK. Coadministration with idelalisib increased plasma exposures of midazolam (138% and 437% for maximum observed plasma concentration (Cmax) and area under the plasma concentration-time curve from time 0 extrapolated to infinity (AUCinf), respectively), consistent with the in vitro finding of CYP3A inhibition by GS-563117. Rifampin caused a substantial decrease in idelalisib (58% and 75%, Cmax and AUCinf , respectively) and GS-563117 exposures, indicating an enhanced contribution of CYP3A to idelalisib metabolism under a strongly induced state. Idelalisib is more than 84% bound to plasma proteins. Idelalisib is metabolized to its major metabolite, GS-563117, principally by cytochrome P-450 (CYP) isoenzyme 3A and aldehyde oxidase; the drug is metabolized only to a minor extent by uridine diphosphate-glucuronosyl transferase (UGT) 1A4.1 GS-563117 is inactive against PI3Kdelta in vitro. Idelalisib is metabolized via aldehyde oxidase and CYP3A with additional minor metabolism by UGT1A4. Biological Half-Life The terminal elimination half-life is 8.2 hours. The mean terminal half-life of idelalisib is 8.2 hours. |
| Toxicity/Toxicokinetics |
Toxicity Summary
IDENTIFICATION AND USE: Idelalisib is a white to off-white powder. It is used as antineoplastic agent, and enzyme inhibitor. It is indicated for the treatment of patients with relapsed chronic lymphocytic leukemia, relapsed follicular B-cell non-Hodgkin lymphoma and relapsed small lymphocytic lymphoma. HUMAN STUDIES: Idelalisib is an inhibitor of PI3Kdelta kinase, which is expressed in normal and malignant B-cells. Idelalisib induced apoptosis and inhibited proliferation in cell lines derived from malignant B-cells and in primary tumor cells. Treatment of lymphoma cells with idelalisib resulted in inhibition of chemotaxis and adhesion, and reduced cell viability. Severe neutropenia has been reported in 31% of patients receiving idelalisib in clinical studies. Fatal cases of Stevens-Johnson syndrome and toxic epidermal necrolysis have occurred in patients treated with the drug. Fatal and/or serious hepatotoxicity occurred in 18% of patients treated with idelalisib monotherapy and 16% of patients treated with the drug in combinations. Fatal and serious intestinal perforation occurred in treated patients. Severe diarrhea or colitis occurred in 14% of patients treated with idelalisib monotherapy and 20% of patients treated with the drug in combinations. Fatal and serious pneumonitis occurred in patients treated with the drug. Fatal and/or serious infections occurred in 21% of patients treated with idelalisib monotherapy and 48% of patients treated with the drug in combinations. Idelalisib was not clastogenic in the in vitro chromosome aberration assay using human peripheral blood lymphocytes. ANIMAL STUDIES: Idelalisib was not carcinogenic in a 26-week study in transgenic mice when administered daily by oral gavage at doses up to 500 mg/kg/day in males and 1000 mg/kg/day in females. Idelalisib was not carcinogenic in a 2-year study in rats when administered daily by oral gavage. In an embryo-fetal development study in rats, pregnant animals receiving oral doses of idelalisib during the period of organogenesis (implantation to closure of the hard palate), embryo-fetal toxicities were observed at the mid- and high-doses that also resulted in maternal toxicity, based on reductions in maternal body weight gain. Adverse findings at idelalisib doses of 75 mg/kg/day included decreased fetal weights, external malformations (short tail), and skeletal variations (delayed ossification and/or unossification of the skull, vertebrae, and sternebrae). Additional findings were observed at 150 mg/kg/day dose of idelalisib and included urogenital blood loss, complete resorption, increased post-implantation loss, and malformations (vertebral agenesis with anury, hydrocephaly, and microphthalmia/anophthalmia). In a separate fertility study, treated female rats (25, 50, or 100 mg/kg/day of idelalisib) were mated with untreated males. There were no adverse effects on fertility parameters; however, there was a decrease in the number of live embryos at the high dose. Idelalisib did not induce mutations in the bacterial mutagenesis (Ames) assay. Idelalisib was genotoxic in males in the in vivo rat micronucleus study at a high dose of 2000 mg/kg. Hepatotoxicity In clinical trials of idelalisib combined with rituximab in patients with CLL and lymphoma, the rates of serum enzyme elevations during therapy ranged from 25% to 35% and were above 5 times the ULN in 5% to 8% (compared to 1% with placebo and rituximab). Severe instances of severe acute hepatocellular injury and acute liver failure were reported in patients receiving idelalisib alone and with rituximab, but the clinical features of the cases were not be described in detail. Serum enzyme elevations typically arose within 4 to 12 weeks of starting therapy and usually resolved rapidly with temporary discontinuation. In some instances, however, serum aminotransferases remained high despite stopping therapy, and in this situation corticosteroids appeared to have a beneficial effect. Most patients who developed significant serum enzyme elevations with idelalisib had a rapid recurrence upon rechallenge. In patients receiving corticosteroids, however, recurrence was less common and generally mild, allowing for restarting of therapy in many patients. Thus, idelalisib is a frequent cause of acute hepatocellular injury which may have an autoimmune component. Because of its many serious adverse events and limited efficacy in comparison to other agents, idelalisib has not been widely used and it potential for causing acute clinically apparent liver injury with jaundice has not been well defined. Because, idelalisib affects B cell function, it may also be capable of inducing reactivation of hepatitis B, although in published trials of the agent, reactivation was not reported. Likelihood score: D (possible cause of clinically apparent liver injury). Effects During Pregnancy and Lactation ◉ Summary of Use during Lactation No information is available on the clinical use of idelalisib during breastfeeding. Because idelalisib is more than 84% bound to plasma proteins, the amount in milk is likely to be low. It is sometimes given in combination with rituximab, which may increase the risk to the infant. The manufacturer recommends that breastfeeding be discontinued during idelalisib therapy and for at least 1 month after the last dose. ◉ Effects in Breastfed Infants Relevant published information was not found as of the revision date. ◉ Effects on Lactation and Breastmilk Relevant published information was not found as of the revision date. Protein Binding Idelalisib is greater than 84% bound to human plasma proteins with no concentration dependence. Interactions Fatal and/or serious hepatotoxicity occurred in 18% of patients treated with Zydelig monotherapy and 16% of patients treated with Zydelig in combination with rituximab or with unapproved combination therapies. Idelalisib, a potent phosphatidylinositol-3-kinase delta (PI3Kd) inhibitor, is metabolized primarily by aldehyde oxidase to form GS-563117 and to a lesser extent by cytochrome P450 (CYP) 3A and uridine 5'-diphospho-glucuronosyltransferase 1A4. In vitro, idelalisib inhibits P-glycoprotein (P-gp) and organic anion transporting polypeptides 1B1 and 1B3, and GS-563117 is a time-dependent CYP3A inhibitor. This study enrolled 24 healthy subjects and evaluated (1) the effect of idelalisib on the pharmacokinetics (PK) of digoxin, a P-gp probe substrate, rosuvastatin, a breast cancer resistance protein, and OATP1B1/OATP1B3 substrate, and midazolam, a CYP3A substrate; and (2) the effect of a strong inducer, rifampin, on idelalisib PK. On treatment, the most common clinical adverse events (AEs) were headache and pyrexia. Grade 3 transaminase increases were observed in 5 of 24 subjects and were reversible. Two subjects had serious AEs after treatment completion (grade 3 pyrexia and/or drug-induced liver injury). Idelalisib coadministration did not affect digoxin and rosuvastatin PK. Coadministration with idelalisib increased plasma exposures of midazolam (138% and 437% for maximum observed plasma concentration (Cmax) and area under the plasma concentration-time curve from time 0 extrapolated to infinity (AUCinf), respectively), consistent with the in vitro finding of CYP3A inhibition by GS-563117. Rifampin caused a substantial decrease in idelalisib (58% and 75%, Cmax and AUCinf , respectively) and GS-563117 exposures, indicating an enhanced contribution of CYP3A to idelalisib metabolism under a strongly induced state. Idelalisib is approved for the treatment of relapsed chronic lymphocytic leukemia together with Rituximab and for monotherapy of follicular B-cell non-Hodgkin's lymphoma and small lymphocytic lymphoma. It is a potent and selective phosphatidylinositol 3-kinase-d (PI3K-d) inhibitor. PI3K-d primarily is expressed in B-cells and prevents effectively proliferation in malignant B-cells. We provide a detailed report on treatment history and photo documentation of acute adverse effects of radiation therapy with simultaneous Idelalisib medication in one case of B-CLL. Radiosensitivity tests were performed for the index patient under Idelalisib and after the addition of Idelalisib to healthy individuals' blood. Radiosensitivity in human lymphocytes was analyzed with a three color in situ hybridization assay. Primary skin fibroblasts were studied after a treatment with Idelalisib for apoptosis, necrosis and cell cycle using flow cytometry. DNA double-strand break repair was analyzed by gammaH2AX immunostaining. The index patient presented a strong grade 2 radiodermatitis and grade 3 mucositis after irradiation with 20 Gy and a simultaneous intake of Idelalisib. Irradiations without Idelalisib medication were well tolerated and resulted in not more than grade 1 radiodermatitis. The index patient under Idelalisib had a radiosensitivity of 0.62 B/M which is in the range of clearly radiosensitive patients. A combined treatment of lymphocytes with 2 Gy and 10 nmol/L Idelalisib showed a tendency to an increased radiosensitivity. We found a clear increase of apoptosis as a result of the combined treatment in the Idelalisib dose range of 1 to 100 nmol/L compared to solely irradiated cells or solely Idelalisib treated cells (p=0.05). A combined Idelalisib radiotherapy treatment has an increased risk of side effects. However, combined therapy seems to be feasible when patients are monitored closely. Concomitant use of idelalisib with an inducer of P-gp may result in decreased systemic exposure to idelalisib. When the potent CYP3A and P-gp inducer rifampin was administered concomitantly with idelalisib, systemic exposure to idelalisib was decreased. For more Interactions (Complete) data for Idelalisib (8 total), please visit the HSDB record page. |
| References |
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| Additional Infomation |
Therapeutic Uses
Antineoplastic Agents; Enzyme Inhibitors /CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Idelalisib is included in the database. Zydelig is indicated, in combination with rituximab, for the treatment of patients with relapsed chronic lymphocytic leukemia (CLL) for whom rituximab alone would be considered appropriate therapy due to other co-morbidities. /Included in US product label/ Zydelig is indicated for the treatment of patients with relapsed follicular B-cell non-Hodgkin lymphoma (FL) who have received at least two prior systemic therapies. Accelerated approval was granted for this indication based on Overall Response Rat. An improvement in patient survival or disease related symptoms has not been established. Continued approval for this indication may be contingent upon verification of clinical benefit in confirmatory trials. /Included in US product label/ Zydelig is indicated for the treatment of patients with relapsed small lymphocytic lymphoma (SLL) who have received at least two prior systemic therapies. /Included in US product label/ Drug Warnings /BOXED WARNING/ WARNING: FATAL AND SERIOUS TOXICITIES: HEPATIC. Fatal and/or serious hepatotoxicity occurred in 16% to 18% of Zydelig-treated patients. Monitor hepatic function prior to and during treatment. Interrupt and then reduce or discontinue Zydelig as recommended. /BOXED WARNING/ WARNING: FATAL AND SERIOUS TOXICITIES: SEVERE DIARRHEA, COLITIS. Fatal and/or serious and severe diarrhea or colitis occurred in 14% to 20% of Zydelig-treated patients. Monitor for the development of severe diarrhea or colitis. Interrupt and then reduce or discontinue Zydelig as recommended. /BOXED WARNING/ WARNING: FATAL AND SERIOUS TOXICITIES: PNEUMONITIS. Fatal and/or serious pneumonitis occurred in 4% of Zydelig-treated patients. Monitor for pulmonary symptoms and bilateral interstitial infiltrates. Interrupt or discontinue Zydelig as recommended. /BOXED WARNING/ WARNING: FATAL AND SERIOUS TOXICITIES: INFECTIONS. Fatal and/or serious infections occurred in 21% to 48% of Zydelig-treated patients. Monitor for signs and symptoms of infection. Interrupt Zydelig if infection is suspected. For more Drug Warnings (Complete) data for Idelalisib (20 total), please visit the HSDB record page. |
| Molecular Formula |
C22H18FN7O
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|---|---|
| Molecular Weight |
415.42
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| Exact Mass |
415.155
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| Elemental Analysis |
C, 63.61; H, 4.37; F, 4.57; N, 23.60; O, 3.85
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| CAS # |
870281-82-6
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| Related CAS # |
Idelalisib-d5;1830330-31-8
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| PubChem CID |
11625818
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| Appearance |
white solid powder
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| Density |
1.5±0.1 g/cm3
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| Index of Refraction |
1.741
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| LogP |
2.96
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
31
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| Complexity |
685
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| Defined Atom Stereocenter Count |
1
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| SMILES |
[C@@H](C1=NC2C=CC=C(C=2C(=O)N1C1C=CC=CC=1)F)(CC)NC1=NC=NC2N=CNC1=2
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| InChi Key |
IFSDAJWBUCMOAH-HNNXBMFYSA-N
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| InChi Code |
InChI=1S/C22H18FN7O/c1-2-15(28-20-18-19(25-11-24-18)26-12-27-20)21-29-16-10-6-9-14(23)17(16)22(31)30(21)13-7-4-3-5-8-13/h3-12,15H,2H2,1H3,(H2,24,25,26,27,28)/t15-/m0/s1
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| Chemical Name |
(S)-2-(1-(9H-purin-6-ylamino)propyl)-5-fluoro-3-phenylquinazolin-4(3H)-one
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| Synonyms |
GS1101; CAL-101; GS 1101; CAL101; GS-1101; CAL 101; Idelalisib; trade name Zydelig
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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 |
| 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: ≥ 2.5 mg/mL (6.02 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 25.0 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: ≥ 2.5 mg/mL (6.02 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 25.0 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (6.02 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 30%PEG 400 (dissolve first)+0.5% Tween 80 +5% Propylene glycol : 30mg/mL |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4072 mL | 12.0360 mL | 24.0720 mL | |
| 5 mM | 0.4814 mL | 2.4072 mL | 4.8144 mL | |
| 10 mM | 0.2407 mL | 1.2036 mL | 2.4072 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.
1630GCC: Zydelig Maintenance in B-Cell Non-Hodgkin's Lymphoma After Autologous Stem Cell Transplantation
CTID: NCT03133221
Phase: Phase 2 Status: Active, not recruiting
Date: 2024-09-19
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
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