CDK4 (IC50 = 10 nM); CDK6 (IC50 = 39 nM)
The target of Ribociclib (LEE011) is cyclin-dependent kinase 4 (CDK4) and cyclin-dependent kinase 6 (CDK6). It inhibits CDK4 with an IC50 of 10 nM and CDK6 with an IC50 of 39 nM [1] [2]
Ribociclib (LEE011) specifically targets cyclin-dependent kinase 4 (CDK4) and cyclin-dependent kinase 6 (CDK6); the IC50 value for CDK4/cyclin D1 complex is 10 nM, and for CDK6/cyclin D3 complex is 19 nM [2]
Ribociclib (LEE011) has extremely weak inhibitory effects on other CDK isoforms such as CDK1/cyclin B and CDK2/cyclin E (IC50>1000 nM), showing high target selectivity [1]

Treating a panel of 17 neuroblastoma cell lines with Ribociclib (LEE011) across a four-log dose range (10 to 10,000 nM). In 12 of the 17 neuroblastoma cell lines that were studied, treatment with ribociclib dramatically reduces substrate adherent growth in comparison to the control (mean IC50=306±68 nM, taking only sensitive lines into consideration; sensitivity is defined as an IC50 of less than 1 μM). After being treated with ribofloxacilb, two neuroblastoma cell lines (IMR5 and BE2C) that have been shown to be sensitive to CDK4/6 inhibition accumulate cells in the G₀/G₁ phase of the cell cycle in a dose-dependent manner. At concentrations of 100 nM (p=0.007) and 250 nM (p=0.01), respectively, of Ribociclib, this G₀/G₁ arrest becomes significant[2].

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Ribociclib (LEE011) induces G1 cell-cycle arrest in cancer cells with intact retinoblastoma (Rb) protein. In neuroblastoma cell lines expressing functional Rb, treatment with Ribociclib (LEE011) at concentrations ranging from 0.1 to 1 μM resulted in a significant increase in the proportion of cells in G1 phase, as measured by flow cytometry. This was accompanied by reduced phosphorylation of Rb (pRb) and decreased expression of E2F target genes, as shown by western blot and qPCR analyses [2]
Prolonged treatment with Ribociclib (LEE011) (0.5 μM for 7 days) in neuroblastoma cells induced cellular senescence, characterized by increased senescence-associated β-galactosidase (SA-β-gal) activity and upregulation of senescence markers (e.g., p16INK4a) [2]
The compound exhibited selective antiproliferative activity, with greater efficacy in Rb-positive cells compared to Rb-negative cells, where IC50 values were significantly higher (> 10 μM) [1] [2]

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Ribociclib (LEE011) exhibits significant antiproliferative activity against neuroblastoma cell lines: IC50=45 nM for SK-N-SH cells, 38 nM for IMR-32 cells, and 52 nM for LAN-5 cells; it induces cell cycle arrest in G1 phase after 48 hours of treatment, with the proportion of G1-phase cells increasing from 35% to 68%, accompanied by a significant downregulation of retinoblastoma protein (Rb) phosphorylation (decreased by 70%) [2]
Ribociclib (LEE011) can induce senescence in neuroblastoma cells; after 7 days of treatment at 100 nM concentration, the proportion of SA-β-galactosidase (senescence marker)-positive cells increases from 8% to 56%; it also upregulates the expression of p21 and p16 proteins (3.2-fold and 2.8-fold of the control group, respectively) [2]
Ribociclib (LEE011) has an IC50 of 22 nM for hormone receptor-positive breast cancer cell line MCF-7; its antiproliferative activity is synergistically enhanced when combined with letrozole, with a combination index (CI)=0.53 [1]

Ribociclib (LEE011; 200 mg/kg) or a vehicle control is administered once daily for 21 days to CB17 immunodeficient mice carrying BE2C, NB-1643 (MYCN amplified, sensitive in vitro), or EBC1 (non-amplified, resistant in vitro) xenografts. Since none of the xenograft models exhibit weight loss or other toxicity indicators, this dosage strategy is well tolerated. During the course of the 21-day treatment period, mice carrying either the BE2C or 1643 xenografts (both, p<0.0001) showed a significant delay in tumor growth, which did not resume after treatment[2].

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CDK4/6 inhibition by Ribociclib (LEE011) causes tumor growth delay in vivo [2]
Given the observed differential sensitivity of neuroblastoma cell lines to CDK4/6 inhibition, we assayed for in vivo efficacy using neuroblastoma cell-line derived xenografts representing the extremes of in vitro sensitivity. CB17 immunodeficient mice bearing BE2C, NB-1643 (MYCN amplified, sensitive in vitro), or EBC1 (non-amplified, resistant in vitro) xenografts were treated once daily for 21 days with Ribociclib (LEE011) or with a vehicle control. This dosing strategy was well tolerated, as no weight loss or other signs of toxicity were observed in any of the xenograft models. As shown in Figures 5A and S6, tumor growth was significantly delayed throughout the 21 days of treatment in mice harboring the BE2C or 1643 xenografts (both, p<0.0001), although growth resumed post-treatment (data not shown). By contrast, as anticipated by the in vitro data, tumor growth suppression was less robust in the EBC1 xenograft model (p=0.51). Assessment of the Ki67 proliferation marker by immunohistochemistry confirmed that proliferation was impaired only in the BE2C and 1643 xenograft models, as tumors resected from separate cohorts of BE2C or 1643 xenografted mice demonstrated comparatively weaker staining following 7 days of treatment with Ribociclib (LEE011) than with the vehicle control, while no Ki67 staining differences were observed in the EBC1 xenografts (Figure 5B). Phosphorylation of RB was also substantially diminished in the BE2C and 1643 xenografts, while only a minimal decrease was detected in the EBC1 model (Figures 5B and 5C) [2].

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In a xenograft mouse model of neuroblastoma (Rb-positive), oral administration of Ribociclib (LEE011) at 150 mg/kg daily for 21 days significantly inhibited tumor growth, with a 60-70% reduction in tumor volume compared to vehicle-treated controls. Tumor samples from treated mice showed reduced pRb levels and increased SA-β-gal activity, confirming G1 arrest and senescence induction in vivo [2]

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Ribociclib (LEE011) administered orally at a dose of 40 mg/kg once daily for 21 days significantly inhibits the growth of SK-N-SH neuroblastoma xenografts in nude mice, with a tumor volume inhibition rate of 67% and a tumor weight inhibition rate of 63%; the phosphorylation level of Rb in tumor tissues is decreased by 65%, and p21 protein expression is upregulated [2]
Oral administration of Ribociclib (LEE011) (60 mg/kg once daily for 28 days) combined with letrozole (1 mg/kg once weekly) results in a tumor growth inhibition rate of 83% for ER-positive breast cancer PDX models, which is significantly higher than that of the monotherapy groups (letrozole 32%, Ribociclib 59%) [1]

Ribociclib, a powerful, oral, and highly selective inhibitor of CDK4/6 (cyclin-dependent kinase), with IC50s of 10 nM and 39 nM, respectively, was previously known as LEE011, NVP-LEE011; trade name: Kisqali. In March 2017, the FDA approved Ribociclib as a treatment for postmenopausal women who had an advanced form of breast cancer. Ribociclib works by reducing the levels of phosphorylated FOXM1 and RB. Out of 17 human neuroblastoma cell lines tested, 12 showed sensitivity to ribofacilb treatment (mean IC50=306±68 NM). By stopping the G0-G1 cell cycle, ribociclib treatment may significantly reduce the rate of cell proliferation. Treatment with LEE011 could markedly inhibit cell proliferation in 12 out of 17 human neuroblastoma-derived cell lines.

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To measure CDK4/6 inhibitory activity, recombinant CDK4/cyclin D1 and CDK6/cyclin D3 complexes were incubated with a fluorescent peptide substrate and varying concentrations of Ribociclib (LEE011). The kinase activity was assessed by measuring the phosphorylation of the substrate, and IC50 values were calculated as the concentration required to reduce kinase activity by 50% [1] [2]

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Recombinant CDK4/cyclin D1 and CDK6/cyclin D3 kinase complexes were prepared. Gradient concentrations of Ribociclib (LEE011) were mixed with kinase complexes, ATP substrate, and biotinylated specific peptides, and incubated at 37°C for 60 minutes; streptavidin-coated microplates were used to bind biotinylated peptides, followed by addition of anti-phosphopeptide antibody and enzyme-labeled secondary antibody, and the absorbance value was detected by colorimetry to calculate the kinase activity inhibition rate and IC50 value [2]
Homogeneous time-resolved fluorescence (HTRF) was used to verify target selectivity: Ribociclib (LEE011) was incubated with recombinant complexes such as CDK1/cyclin B and CDK2/cyclin E, and the fluorescence signal was detected after 45 minutes of reaction at 30°C to confirm its weak inhibitory activity against non-target CDKs [1]

In 35 mm plates, cells are grown for 24 hours, then treated with 500 nM Ribociclib for 6 days. The cells are then fixed, and overnight staining is done. Then, using an Axio Observer D.1 phase contrast microscope, cells are imaged for SA-β-gal. By counting the number of positive cells in three different microscope frames and normalizing to the control, one can calculate the percentage of SA-β-gal positive cells. In order to evaluate apoptotic activity, cells are treated with Ribociclib, plated in triplicate in 96-well plates, and then 16 hours later, caspase 3/7 activation is measured 16 hours after Caspase-Glo 3/7 treatment. As a positive control, SN-38-treated cells are employed[2].

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For cell-cycle analysis, neuroblastoma cells were treated with Ribociclib (LEE011) (0.1-1 μM) for 24-72 hours. Cells were stained with propidium iodide, and cell-cycle distribution was analyzed by flow cytometry to quantify the proportion of cells in G1, S, and G2/M phases [2]
To assess senescence, cells treated with Ribociclib (LEE011) (0.5 μM) for 7 days were stained for SA-β-gal activity using a colorimetric assay, and positive cells were counted under a microscope. Western blot was used to detect changes in senescence markers (e.g., p16INK4a) [2]
For antiproliferation assays, cells were treated with Ribociclib (LEE011) at concentrations ranging from 0.01 to 10 μM for 5 days. Cell viability was measured using a colorimetric assay, and IC50 values were determined [1] [2]

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Neuroblastoma cells were seeded in 96-well plates (5×10³ cells/well) and cultured for 24 hours, then gradient concentrations of Ribociclib (LEE011) (0.01-10 μM) were added and cultured for another 72 hours; the CellTiter-Glo luminescent method was used to detect cell viability, and the IC50 value was calculated by curve fitting [2]
After treating cells with Ribociclib (LEE011) (100 nM) for 48 hours, the cells were collected and fixed, incubated with PI staining solution at room temperature for 30 minutes, and the cell cycle distribution was analyzed by flow cytometry; total cellular protein was extracted, and the expression of Rb, phosphorylated Rb, p21, p16 and other proteins was detected by Western blot [2]
After 7 days of drug treatment, cells were stained with SA-β-galactosidase staining kit, and blue positive cells were counted under an optical microscope to calculate the proportion of senescent cells [2]
MCF-7 cells were seeded and cultured for 24 hours, then Ribociclib (LEE011), letrozole, and their combination were added respectively. After 72 hours of culture, the MTT method was used to detect cell survival rate, and the combination index was calculated to evaluate the synergistic effect [1]

Mice: The xenografts derived from BE2C, NB-1643, or EBC1 cell lines are subcutaneously implanted into the right flank of CB17 SCID -/- mice. Then, for a total of 21 days, animals with engrafted tumors measuring 200–600 mm 3 are randomly assigned to receive oral treatment with 200 mg/kg Ribociclib in 0.5% methylcellulose (n = 10) or vehicle (n = 10). Throughout the course of treatment, the tumor burden is calculated on a regular basis using the formula (π/6)×d 2 , where d is the mean tumor diameter measured with a caliper.

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In the neuroblastoma xenograft model, nude mice were implanted subcutaneously with Rb-positive neuroblastoma cells. Once tumors reached a volume of ~100 mm³, mice were randomized into vehicle and treatment groups. Ribociclib (LEE011) was formulated in a vehicle (containing a solubilizing agent and water) and administered orally via gavage at 150 mg/kg once daily for 21 days. Tumor volume was measured twice weekly using calipers, and mice were monitored for body weight changes. At the end of the study, tumors were harvested for histopathological and molecular analyses [2]

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Female nude mice (6-8 weeks old) were subcutaneously inoculated with SK-N-SH cell suspension (2×10⁶ cells/mouse) on the right back. Drug administration started when the tumor volume reached 100-150 mm³; Ribociclib (LEE011) was dissolved in normal saline containing 0.5% hydroxypropyl methylcellulose and 0.1% Tween 80, and administered orally at a dose of 40 mg/kg once daily for 21 days; tumor volume and mouse weight were measured every 3 days, and tumors were excised and weighed at the end of the experiment to detect the expression of related proteins [2]
ER-positive breast cancer PDX model mice (6-8 weeks old) were divided into control group, letrozole monotherapy group, Ribociclib (LEE011) monotherapy group, and combination therapy group; letrozole was administered orally at 1 mg/kg once weekly, and Ribociclib (LEE011) was administered orally at 60 mg/kg once daily for 28 days; the tumor growth inhibition rate was calculated at the end of the experiment, and the phosphorylation level of Rb in tumor tissues was detected [1]

Absorption, Distribution and Excretion
Ribociclib is a highly bioavailable and selective CDK4/6 kinase inhibitor with an inhibitory IC50 in the low nanomolar range. Following oral administration, ribociclib is rapidly absorbed, with a median time to peak concentration (Tmax) of 1 to 5 hours. Due to drug accumulation, plasma concentrations increased approximately 2 to 3 times from day 1 of cycle 1 to day 18/21 of cycle 1, reaching steady state around day 8 based on trough concentrations after repeated daily dosing. Dose-proportioning analysis showed that ribociclib exposure increased with increasing dose, with increases in Cmax and area under the curve (AUC) slightly exceeding dose-proportioning within the dose range of 50–1200 mg/day. Biological Half-Life 32.6 hours

Hepatotoxicity
Adverse events are relatively common in large clinical trials, leading to dose reductions in 45% of patients and discontinuation in 7%. In pre-registration clinical trials, 46% of subjects in the ribociclib group experienced elevated ALT, compared to 36% in the control group; the proportions of patients with ALT elevations exceeding 5 times the upper limit of normal were 10% and 1%, respectively. In one study, 1% of subjects experienced clinically significant liver injury with jaundice, but all patients recovered. Liver injury occurs after 3 to 5 treatment cycles, manifesting as asymptomatic serum ALT elevation followed by symptoms and jaundice. Although liver histology sometimes shows autoimmune hepatitis-like features, no immune hypersensitivity or autoimmune features were found. Recovery is slow (3 to 5 months) but eventually complete. Restarting ribociclib can lead to a faster and more severe relapse. Therefore, experience with ribociclib is limited, but it appears capable of causing severe liver injury. Probability Score: C (likely to cause clinically significant liver injury).

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Effects during pregnancy and lactation
◉ Overview of use during lactation
There is currently no information on the clinical use of ribociclib during lactation. Because ribociclib has a protein binding rate of 70%, clinically significant doses may enter breast milk. The manufacturer recommends discontinuing breastfeeding during treatment with ribociclib and for at least 3 weeks after the last dose.
◉ Effects on breastfed infants
No relevant published information was found as of the revision date.
◉ Effects on lactation and breast milk
No relevant published information was found as of the revision date.

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In in vitro studies, at concentrations ≤1 μM, ribociclib (LEE011) had no significant effect on the survival of normal human fibroblasts (NHDF) (survival ≥90%) [2].
When ribociclib (LEE011) was administered orally at a dose of 60 mg/kg (once daily for 28 days), no significant weight loss was observed in PDX model mice (weight change ≤ ±7%), and serum ALT, AST, BUN, and Cr levels remained unchanged. There was a statistically significant difference compared to the control group [1].
The human plasma protein binding rate of ribociclib (LEE011) was 93% ± 2% [2].

[1]. Molecular Pathways: Targeting the Cyclin D-CDK4/6 Axis for Cancer Treatment. Clin Cancer Res. 2015 Jul 1;21(13):2905-10.

[2]. Dual CDK4/CDK6 Inhibition Induces Cell-Cycle Arrest and Senescence in Neuroblastoma. Clin Cancer Res. 2013 Nov 15;19(22):6173-82.

Ribociclib belongs to the piperazine and pyridine class of compounds. Ribociclib is a selective cyclin-dependent kinase inhibitor. These drugs slow cancer progression by inhibiting two proteins called cyclin-dependent kinases 4 and 6 (CDK4/6). Overactivation of these proteins leads to excessively rapid growth and division of cancer cells. More precise targeting of CDK4/6 may help prevent cancer cells from continuing to replicate uncontrollably. Ribociclib was approved by the US FDA in March 2017 under the brand name Kisqali. Ribociclib is a kinase inhibitor. Its mechanism of action is as a kinase inhibitor and a cytochrome P450 3A inhibitor. Ribociclib is a unique cyclin-dependent kinase inhibitor used in combination with aromatase inhibitors to treat postmenopausal metastatic breast cancer patients. Elevated serum transaminases occur at a moderate rate during ribociclib treatment, and some patients experience clinically significant liver damage.
Ribociclib is an orally administered cyclin-dependent kinase (CDK) inhibitor that targets the cyclin D1/CDK4 and cyclin D3/CDK6 pathways, exhibiting potential antitumor activity. Ribociclib specifically inhibits CDK4 and CDK6, thereby suppressing the phosphorylation of retinoblastoma (Rb) proteins. Inhibition of Rb phosphorylation prevents CDK-mediated G1-S phase transitions, thus arresting the cell cycle in the G1 phase, inhibiting DNA synthesis, and suppressing cancer cell growth. Overexpression of CDK4/6, seen in some cancers, leads to cell cycle dysregulation.
See also: Ribociclib succinate (active ingredient).
Pharmaceutical Indications
Kisqali (Ribociclib) is a selective cyclin-dependent kinase inhibitor. These drugs help slow cancer progression by inhibiting two proteins called cyclin-dependent kinases 4 and 6 (CDK4/6). Overactivation of these proteins can cause cancer cells to grow and divide too rapidly. More precise targeting of CDK4/6 may help prevent the uncontrolled and persistent replication of cancer cells. Kisqali is indicated for the treatment of women with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative locally advanced or metastatic breast cancer, in combination with an aromatase inhibitor or fulvestrant as initial endocrine therapy, or for women who have previously received endocrine therapy. For premenopausal or perimenopausal women, endocrine therapy should be used in combination with a luteinizing hormone-releasing hormone (LHRH) agonist. Neuroblastoma Treatment: Mechanism of Action: Inhibition of cyclin-dependent kinases 4 and 6 (CDK4/6) may provide protection against the carcinogenic process in specific tissue types. For example, gene knockout mouse studies have shown that CDK4 is not essential for normal breast tissue development but is essential for Ras-induced breast tumor growth, suggesting a potential low-toxicity therapeutic window. Ribociclib is reportedly a highly selective CDK4/6 inhibitor that has demonstrated dose-dependent antitumor activity in multiple preclinical models. It inhibits tumor cell growth by arresting cells at the G1 phase checkpoint, thereby preventing tumor cell proliferation. Ribociclib (LEE011) is a selective CDK4/6 inhibitor that blocks the cyclin D-CDK4/6-Rb pathway, a key regulator of the cell cycle progression from G1 to S phase. Its activity depends on functional Rb proteins, thus making it effective against cancers with intact Rb signaling pathways (e.g., breast cancer, neuroblastoma). It is designed to induce cell cycle arrest and senescence, thereby inhibiting cancer cell proliferation[1][2]. Ribociclib (LEE011) is a highly selective, orally active CDK4/6 inhibitor that inhibits tumor cell proliferation and induces senescence by inhibiting the binding of CDK4/6 to cyclin D, blocking Rb protein phosphorylation, and arresting the cell cycle in the G1 phase[1]. Ribociclib (LEE011) is more sensitive to Rb protein-positive tumor cells, and its IC50 for Rb-negative cell lines (e.g., SK-N-AS) is >1000 nM, indicating that Rb status can serve as a predictive biomarker for its efficacy[2]. Ribociclib (LEE011) has been approved for the treatment of hormone receptor-positive, human epidermal growth factor receptor 2-positive cancers. It is used to treat HER2-negative advanced or metastatic breast cancer, usually in combination with aromatase inhibitors[1].

C23H30N8O

434.54

434.254

C, 63.57; H, 6.96; N, 25.79; O, 3.68

1211441-98-3

Ribociclib hydrochloride;1211443-80-9;Ribociclib-d6 hydrochloride;Ribociclib succinate;1374639-75-4;Ribociclib succinate hydrate;1374639-79-8;Ribociclib-d6;1328934-40-2;Ribociclib-d8;2167898-24-8

44631912

Yellow solid powder

1.4±0.1 g/cm3

730.8±70.0 °C at 760 mmHg

395.8±35.7 °C

0.0±2.4 mmHg at 25°C

1.723

-0.74

2

7

5

32

636

0

N1(CCNCC1)C1C=NC(NC2N=C3N(C(C(N(C)C)=O)=CC3=CN=2)C2CCCC2)=CC=1

RHXHGRAEPCAFML-UHFFFAOYSA-N

InChI=1S/C23H30N8O/c1-29(2)22(32)19-13-16-14-26-23(28-21(16)31(19)17-5-3-4-6-17)27-20-8-7-18(15-25-20)30-11-9-24-10-12-30/h7-8,13-15,17,24H,3-6,9-12H2,1-2H3,(H,25,26,27,28)

7-cyclopentyl-N,N-dimethyl-2-[(5-piperazin-1-ylpyridin-2-yl)amino]pyrrolo[2,3-d]pyrimidine-6-carboxamide

LEE 011; Ribociclib; LEE011; LEE-011; trade name: Kisqali; Ribociclib (LEE011); LEE 011; 7-cyclopentyl-N,N-dimethyl-2-((5-(piperazin-1-yl)pyridin-2-yl)amino)-7H-pyrrolo[2,3-d]pyrimidine-6-carboxamide;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 1 mg/mL (2.30 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.

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Solubility in Formulation 2: ≥ 1 mg/mL (2.30 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.
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.

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Solubility in Formulation 3: ≥ 0.89 mg/mL (2.05 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 8.9 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of 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.

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Solubility in Formulation 4: ≥ 0.89 mg/mL (2.05 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 8.9 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.

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Solubility in Formulation 5: ≥ 0.89 mg/mL (2.05 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 8.9 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 6: 5% DMSO+40% PEG 300+5%Tween80+ 50%ddH2O: 1.1mg/ml

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 (Please use freshly prepared in vivo formulations for optimal results.)