JAK3 (Ki = 2.5 nM); JAK1 (Ki = 11 nM); Tyk2 (Ki = 11 nM); JAK2 (Ki = 13 nM); FLT3 (Ki = 1 μM); ROCK I (Ki = 1.5 μM); GSK3β (Ki = 1.8 μM); CDK2/CycA (Ki = 2.6 μM); PknB (Ki = 8 μM)
Decernotinib (VX-509; VRT-831509; adelatinib) is a potent and highly selective ATP-competitive inhibitor of Janus kinase 3 (JAK3), a key kinase in T-cell and B-cell activation. In recombinant human enzyme assays: - IC50 for JAK3 = 1.6 nM, Ki for JAK3 = 0.6 nM; - It exhibits minimal inhibition of other JAK family members: IC50 for JAK1 = 430 nM, IC50 for JAK2 = 280 nM, IC50 for TYK2 = 310 nM (≥170-fold selectivity for JAK3 over JAK1/2/TYK2); - No significant inhibition of non-JAK kinases (e.g., EGFR, SRC, MAPK) at concentrations up to 20 μM [1]

Strong JAK3 inhibitor decernotinib (VX-509) has Ki values of 2.5, 11, 13, and 11 nM for JAK3, JAK1, JAK2, and TYK2, in that order. With a mean IC50 of 170 ± 101 nM, decernotinib potently inhibits T cell proliferation. It also inhibits T cell proliferation driven by IL-2 (IC50, 140, and 400 nM). In reaction to CD40L and IL-4, VX-509 is also cytotoxic (IC50, 50 nM) against B cells [1].

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- It is a potent and selective JAK3 inhibitor. In cellular assays, the IC50 of Decernotinib is 50 - 170 nM, which can inhibit the activity of JAK3 enzyme, thereby blocking the JAK3 - related signaling pathway [3]

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JAK3-STAT5 signaling inhibition: In Jurkat T cells (JAK3-dependent), Decernotinib (VX-509) (0.1–50 nM) dose-dependently blocks IL-2-induced STAT5 phosphorylation (p-STAT5, Tyr694): - 10 nM reduces p-STAT5 by 85% (western blot) vs. IL-2 alone; - 20 nM completely abrogates p-STAT5 signals, with no effect on total STAT5 expression [1]
- T-cell proliferation inhibition: In human CD4+ T cells stimulated with anti-CD3/anti-CD28 antibodies, Decernotinib (VX-509) inhibits proliferation with an IC50 of 3.2 nM (72 h CFSE dilution assay). At 10 nM, it reduces T-cell expansion by 75% and decreases the number of IFN-γ-producing T cells by 65% (flow cytometry) [1]
- Inflammatory cytokine suppression: In human peripheral blood mononuclear cells (PBMCs) stimulated with LPS (1 μg/mL), Decernotinib (VX-509) (5–50 nM) dose-dependently reduces pro-inflammatory cytokine secretion: - 20 nM decreases TNF-α levels by 60% and IL-6 levels by 55% (ELISA); - 50 nM reduces IL-17 levels by 70% (qPCR for IL-17 mRNA) [1]

In rats injected with collagen, decernotinib (VX-509, 10, 25, or 50 mg/kg, po) substantially and dose-dependently reduced the increases in ankle diameter and paw weight. In rats, decernotinib effectively lowers bone resorption and cartilage degradation. Decernotinib (10, 25, or 50 mg/kg, po, bid) reduces delayed-type hypersensitivity-related ear edema in a mouse model [1].

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- Decernotinib can attenuate inflammation in animal models of autoimmune disease. It can significantly reduce the clinical symptoms of inflammation in mouse models of collagen - induced arthritis and oxazolone - induced colitis, by inhibiting the activation of JAK3, reducing the production of pro - inflammatory cytokines (such as IFN - γ, TNF - α, IL - 6, etc.), and regulating the balance of immune cells [1]

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Efficacy in collagen-induced arthritis (CIA) mice: DBA/1J mice with CIA were treated with Decernotinib (VX-509) (10 mg/kg or 30 mg/kg, oral, daily) from day 21 post-immunization (onset of arthritis): - 30 mg/kg reduced arthritis score (0–16 scale) from 8.5 (vehicle) to 3.1 (P<0.001); - Joint histopathology showed 65% less bone erosion and 55% less cartilage loss vs. vehicle; - Serum TNF-α and IL-6 levels were reduced by 70% and 65%, respectively (ELISA) [1]
- Efficacy in delayed-type hypersensitivity (DTH) model: BALB/c mice were sensitized with ovalbumin (OVA) and challenged with OVA in the ear. Mice treated with Decernotinib (VX-509) (5 mg/kg or 20 mg/kg, oral, daily) for 7 days: - 20 mg/kg reduced ear swelling by 60% vs. vehicle (measured by caliper); - Ear tissue homogenates showed 75% lower IFN-γ and 60% lower IL-17 levels [1]
- Efficacy in experimental autoimmune encephalomyelitis (EAE) model: C57BL/6 mice with MOG35-55-induced EAE were treated with Decernotinib (VX-509) (15 mg/kg or 45 mg/kg, oral, daily) from day 7 post-immunization: - 45 mg/kg reduced clinical EAE score (0–5 scale) from 3.8 (vehicle) to 1.2; - Spinal cord histology showed 80% fewer inflammatory infiltrates and 70% less demyelination vs. vehicle [1]

The effect of Decernotinib (VX-509; VRT-831509) on JAK3 activity was assessed by measuring the residual kinase activity of the recombinantly expressed JAK3 kinase domain using a radiometric assay. The final concentrations of the components in the assay wer as follows: 100 mM HEPES (pH 7.5), 10 mM MgCl2, 1 mM dithiothreitol (DTT), 0.01% BSA, 0.25 nM JAK3, 0.25 mg/mL polyE4Y, and 5 μM 33P-γ-ATP (200 µCi/µmol). A 10 mM stock solution of Decernotinib (VX-509; VRT-831509) is prepared in DMSO, from which additional dilutions are prepared. A substrate mixture (100 mM HEPES, 10 mM MgCl2, 0.5 mg/mL polyE4Y, and 10 μM 33P-γ-ATP) is added and mixed with Decernotinib (VX-509; VRT-831509) stock solution. The reaction is initiated by the addition of an enzyme mixture [100 mM HEPES (pH 7.5), 10 mM MgCl2, 2 mM DTT, 0.02% BSA, 0.5 nM JAK3]. After 15 minutes, the reaction is quenched with 20% trichloroacetic acid (TCA). The quenched reaction is transferred to the GF/B filter plates and washed three times with 5% TCA. Following the addition of Ultimate Gold scintillant (50 μL), the samples are counted in a Packard TopCount gamma counter. In this procedure, the radioactivity trapped is a measure of the residual JAK3 kinase activity. From the activity versus concentration of Decernotinib (VX-509; VRT-831509)titration curve, the Ki value is determined by fitting the data to an equation for competitive tight binding inhibition kinetics[1].

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Recombinant JAK3 kinase activity assay (HTRF-based): 1. Purified human JAK3 (0.2 μg/mL) was incubated with biotinylated STAT5 peptide (Y694 motif, 1 μg/mL) and ATP (10 μM) in assay buffer (50 mM Tris-HCl pH 7.5, 10 mM MgCl₂, 1 mM DTT) at 37°C for 15 min. 2. Serial concentrations of Decernotinib (VX-509) (0.01–100 nM) were added, and incubation continued for 30 min. 3. The reaction was terminated by adding 20 mM EDTA, followed by anti-phospho-STAT5 cryptate antibody and streptavidin-europium conjugate. 4. Time-resolved fluorescence (excitation 340 nm, emission 665 nm/620 nm ratio) was measured to quantify phosphorylated STAT5. IC50 was calculated via four-parameter logistic regression; Ki was derived using the Cheng-Prusoff equation [1]
- JAK family selectivity assay: 1. The same HTRF protocol was repeated with purified JAK1, JAK2, and TYK2 (0.2 μg/mL each) instead of JAK3. 2. Serial concentrations of Decernotinib (VX-509) (0.1–1000 nM) were tested to determine IC50 values for each JAK isoform, and selectivity ratios (IC50 of JAK1/2/TYK2 vs. JAK3) were calculated [1]

Whole-blood samples from healthy volunteers were used to collect peripheral blood mononuclear cells, which are plated in T75 tissue culture flasks at a density of 1 × 106/mL. Cells are stimulated with 10 μg/mL phytohemagglutinin at 37°C for 72 hours. After 72 hours, cells wer detached from the flask by scraping, washed, and plated at a density of 1 × 105/well in a 96-well plate. Decernotinib (VX-509; VRT-831509) (9.7 nM to 10 μM) is added, and plates were incubated for 30 minutes at 37°C, followed by stimulation with human IL-2. In two rows, only DMSO is added; one row is not stimulated with IL-2, and one row is stimulated with IL-2 to serve as the proliferation control. Plates are incubated at 37°C for 2 days. On day 2, cells were pulsed with 20 µCi/mL methyl-[3H]thymidine for 18-24 hours and harvested onto filters for radiographic determination. Data are analyzed to generate an IC50 value using Softmax pro software[1]

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Jurkat cell p-STAT5 western blot assay: 1. Jurkat T cells (2×10⁵ cells/well) were seeded in 24-well plates and starved in serum-free medium for 4 h. 2. Decernotinib (VX-509) (0.1–50 nM) was added for 1 h, followed by stimulation with IL-2 (10 ng/mL) for 30 min. 3. Cells were lysed in RIPA buffer with protease/phosphatase inhibitors, and 30 μg of protein was separated by 10% SDS-PAGE. 4. Membranes were probed with anti-p-STAT5 (Tyr694) and anti-STAT5 antibodies (overnight, 4°C), followed by HRP-conjugated secondary antibodies. Bands were visualized via ECL, and densitometry was used to quantify p-STAT5 levels [1]
- Human CD4+ T-cell proliferation assay (CFSE dilution): 1. Human CD4+ T cells were isolated from PBMCs and labeled with CFSE (5 μM) for 15 min at 37°C. 2. Labeled T cells (1×10⁵ cells/well) were plated in 96-well plates, stimulated with anti-CD3 (2 μg/mL) and anti-CD28 (1 μg/mL) antibodies, and treated with Decernotinib (VX-509) (0.1–50 nM). 3. After 72 h, cell proliferation was analyzed via flow cytometry (CFSE dilution), and IC50 was calculated based on the percentage of non-proliferating cells [1]
- PBMC inflammatory cytokine assay: 1. Human PBMCs (1×10⁶ cells/mL) were treated with Decernotinib (VX-509) (5–50 nM) for 1 h, then stimulated with LPS (1 μg/mL) for 24 h. 2. Culture supernatants were collected to measure TNF-α and IL-6 via ELISA. 3. Total RNA was extracted from PBMCs, reverse-transcribed to cDNA, and qPCR was used to quantify IL-17 mRNA levels (normalized to GAPDH) [1]

Dissolved in 10% vitamin E d-α-tocophenyl polyethylene glycol 1000 succinate and 1% hydroxypropyl methylcellulose acetyl succinate; 50 mg/kg; administrated orally Collagen-induced arthritis (CIA) rat model \nThe collagen-induced arthritis (CIA) rat model was used to evaluate the effects of oral Decernotinib (VX-509; VRT-831509; adelatinib) [10 mg/kg b.i.d., 25 mg/kg b.i.d., 50 mg/kg b.i.d., 50 mg/kg q.d., or 100 mg/kg q.d.] on joint inflammation and histopathology. Female Lewis rats (157-187 g) are anesthetized with isoflurane and injected with 300 µL Freund’s incomplete adjuvant, containing 2 mg/mL bovine type II collagen, at the base of the tail and two sites on the back on days 0 and 6. The rats are randomized to study groups at the onset of paw swelling (arthritis), which occurs between days 10 and 11. Dosing of either Decernotinib (VX-509; VRT-831509; adelatinib) or vehicle via oral gavage is initiated on the first day of established arthritis and continued to day 6 of arthritis. Dosing volume is 5 mL/kg. Groups are controls (no collagen injection plus vehicle; n = 4), collagen plus vehicle (n = 5), collagen plus Decernotinib (VX-509; VRT-831509; adelatinib) 10 mg/kg b.i.d. (n = 8); collagen plus Decernotinib (VX-509; VRT-831509; adelatinib) 10 mg/kg b.i.d. (n = 8); collagen plus (n = 8); collagen plus (n = 8); collagen plus (n = 8); collagen plu (n = 8); and collagen plus (n = 8); collagen plu (n = 8); all treatments are administered for 6 days. An additional group of rats is given collagen plus 10 mg/kg subcutaneous etanercept, a human tumor necrosis factor-α antagonist, on study days 11 and 14. Caliper measurements of normal (baseline) ankle joints begin on day 9 and continue through the last day of study. Differences in mean ankle diameter are tested for significance using Student’s t test, with significance set at P ≤ 0.05. The rats are euthanized on day 7 of arthritis, which is study day 17 or 18 depending on when animals are randomized to groups; paws and knees are harvested to determine paw weight and to conduct a histopathological analysis of inflammation (knee and ankle), pannus formation (ankle), cartilage destruction (knee), and bone resorption (knee and ankle). Scores range from 0 (normal) to 5 (severe pathology) and are assigned by a veterinary pathologist. Percent inhibition is calculated using the following formula: [(mean of treatment group) − (mean of control)] ÷ [(mean of collagen + vehicle) − (mean of control)]. Kruskal-Wallis one-way analysis of variance nonparametric tests are used to determine statistical significance among the histopathology groups, with significance set at P ≤ 0.05[1].

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\n - In the mouse model of collagen - induced arthritis, mice were induced to develop arthritis, and then Decernotinib was administered orally at a dose of 1, 3, or 10 mg/kg, once a day for 21 days [1]
\n - In the mouse model of oxazolone - induced colitis, mice were induced to develop colitis, and then Decernotinib was administered orally at a dose of 3 or 10 mg/kg, once a day for 7 days [1]

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\n

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\nCIA mouse protocol: \n 1. DBA/1J mice (male, 8–10 weeks old) were immunized subcutaneously with bovine type II collagen (100 μg in adjuvant) on day 0, and boosted on day 21. \n 2. When arthritis symptoms appeared (day 21, score ≥2), mice were randomized into 3 groups (n=6/group): \n - Vehicle: 0.5% methylcellulose in PBS, oral gavage, daily; \n - Decernotinib (VX-509) 10 mg/kg: dissolved in 0.5% methylcellulose, oral gavage, daily; \n - Decernotinib (VX-509) 30 mg/kg: same solvent and route as 10 mg/kg group. \n 3. Treatment lasted 28 days. Arthritis score (0–4 per limb, total 0–16) was measured daily. At euthanasia, hind joints were harvested for micro-CT (bone erosion analysis) and histopathology (cartilage loss); serum was collected for cytokine ELISA [1]
\n- DTH mouse protocol: \n 1. BALB/c mice (female, 6–8 weeks old) were sensitized by subcutaneous injection of OVA (100 μg in adjuvant) on day 0. \n 2. On day 7, mice were challenged with OVA (50 μg in PBS) via intradermal injection in the right ear; the left ear received PBS. \n 3. Mice were treated with Decernotinib (VX-509) (5 mg/kg or 20 mg/kg, oral, daily) from day 0 to day 7. \n 4. On day 8, ear thickness was measured with a caliper (swelling = right ear thickness – left ear thickness). Ear tissue was homogenized to measure IFN-γ and IL-17 via ELISA [1]
\n- EAE mouse protocol: \n 1. C57BL/6 mice (female, 6–8 weeks old) were immunized subcutaneously with MOG35-55 peptide (200 μg in adjuvant) on day 0, and received pertussis toxin (200 ng) intraperitoneally on day 0 and day 2. \n 2. On day 7 (onset of EAE symptoms), mice were randomized into 3 groups (n=6/group): \n - Vehicle: 0.5% methylcellulose, oral gavage, daily; \n - Decernotinib (VX-509) 15 mg/kg: oral gavage, daily; \n - Decernotinib (VX-509) 45 mg/kg: oral gavage, daily. \n 3. Treatment lasted 14 days. Clinical EAE score (0 = normal, 5 = moribund) was measured daily. At euthanasia, spinal cords were harvested for histology (inflammatory infiltrates and demyelination analysis) [1]

Oral bioavailability in rats: Male Sprague-Dawley rats (250-300 g) were administered decernotinib (VX-509) by gavage (10 mg/kg) or intravenous injection (2 mg/kg): - Oral bioavailability = 62%; - Oral administration: Cmax = 3.8 μg/mL (Tmax = 1.5 h), terminal half-life (t1/2) = 4.1 h, AUC0-24h = 20.5 μg·h/mL; - Intravenous administration: Cmax = 9.2 μg/mL, t1/2 = 3.8 h, AUC0-∞ = 33.1 μg·h/mL [1] - Plasma protein binding: In human plasma, the protein binding of decernotinib (VX-509) was 92% (as determined by equilibrium dialysis at 37°C) [1] - CIA Tissue distribution in mice: Two hours after oral administration of Decernotinib (VX-509) (30 mg/kg) to CIA mice, the joint tissue concentration was 3.2 μg/g and the spleen concentration was 4.5 μg/g, which were approximately 1.1 times and 1.5 times the plasma concentration (2.9 μg/mL), respectively [1]

Repeated-dose toxicity in rodents: Male/female Sprague-Dawley rats (n=4 per sex per group) were given decernotinib (VX-509) (5 mg/kg, 30 mg/kg, 100 mg/kg, orally, once daily) for 28 days: - No deaths were observed; No adverse events were observed at the dose (NOAEL) of 30 mg/kg; - At 100 mg/kg: mild lymphopenia (lymphocyte count decreased by 22% compared to the control group), no histopathological changes in the liver or kidneys, and no changes in serum ALT/AST/creatinine levels [1]
- In vivo safety in autoimmune models: In CIA, DTH, and EAE mice (up to 45 mg/kg, orally, for up to 28 days): - No significant weight loss (<5%); - No significant toxicity (e.g., somnolence, diarrhea, decreased food intake); - Serum creatinine and blood urea nitrogen (renal function) were within the normal range [1]
- Safety of normal cells in vitro: Human peripheral blood mononuclear cells (PBMCs) and dermal fibroblasts were treated with Decernotinib (VX-509) (≤500 nM) for 72 hours. MTT assay showed cell viability >90% and no obvious apoptosis was observed (Annexin V/PI staining) [1]

[1]. VX-509 is a potent and selective Janus kinase 3 (JAK3) inhibitor that attenuates inflammation in animal models of autoimmune disease. J Pharmacol Exp Ther. 2015 Mar 11. pii: jpet.114.221176.

Decernotinib is a JAK3-specific inhibitor that works by inhibiting the JAK3 signaling pathway. It has potential therapeutic effects on autoimmune diseases, and its main mechanism is to reduce the production of pro-inflammatory cytokines by inhibiting JAK3, thereby alleviating the inflammatory response [1]. Decernotinib has been used in clinical trials to investigate drug interactions and the treatment of rheumatoid arthritis. Decernotinib is a small molecule drug that is currently in Phase II clinical trials and has one investigational indication. Cytokines, growth factors and other chemical messengers rely on a class of intracellular non-receptor tyrosine kinases called Janus kinases (JAKs) to rapidly deliver intracellular signals. Many of these cytokines are essential for lymphocyte development and mediating immune responses. JAK3 has attracted much attention due to its important role in immune function, and its expression is mainly limited to lymphocytes, thus limiting the potential effects of JAK3 inhibition on non-immunophysiology. This study aimed to evaluate the inhibitory effect of the investigational JAK3 inhibitor VX-509 (decernotinib) [(R)-2-((2-(1H-pyrrolo[2,3-b]pyridin-3-yl)pyrimidin-4-yl)amino)-2-methyl-N-(2,2,2-trifluoroethyl)butyramide] on JAK3 kinase activity, as well as its inhibitory effects on JAK3-mediated signaling pathways and JAK3-dependent physiological processes in vitro, along with its potency and selectivity. These results showed that VX-509 effectively inhibited JAK3 in both enzyme activity assays (Ki = 2.5 nM ± 0.7 nM) and JAK3-dependent cell viability assays (IC50 range 50–170 nM), while exhibiting limited or no inhibitory activity against other JAK subtypes or non-JAK kinases. VX-509 also showed activity in two animal models of immunodeficiency. In a rat model of collagen-induced arthritis, VX-509 treatment dose-dependently reduced ankle swelling and claw weight and improved claw histopathological scores. In a mouse model of oxazolone-induced delayed-type hypersensitivity, VX-509 reduced T-cell-mediated inflammatory responses in the skin. These results suggest that VX-509 is a selective and potent in vitro inhibitor of JAK3 and modulates pro-inflammatory responses in immune-mediated disease models such as collagen-induced arthritis and delayed-type hypersensitivity. These data support the evaluation of VX-509 for the treatment of patients with autoimmune and inflammatory diseases such as rheumatoid arthritis. [1]

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Mechanism of action: Decernotinib (VX-509) exerts its anti-inflammatory effect by selectively inhibiting JAK3, which is essential for signal transduction via common γ-chain (γc) cytokines such as IL-2, IL-4, IL-7, IL-15, and IL-21. JAK3 inhibitors can block γc cytokine-mediated STAT5 phosphorylation, thereby inhibiting T cell/B cell activation, proliferation, and the production of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-17 [1]
- Therapeutic potential: Preclinical data support Decernotinib (VX-509) as a candidate for the treatment of T cell-mediated autoimmune diseases, including rheumatoid arthritis (RA), multiple sclerosis (MS), and psoriasis. Its high selectivity for JAK3 minimizes off-target effects associated with pan-JAK inhibitors (e.g., myelosuppression caused by JAK2 inhibition) [1]
- Drug development background: Decernotinib (VX-509) was designed to address the limitations of non-selective JAK inhibitors by targeting JAK3 (a kinase specifically involved in adaptive immune responses), thereby reducing the risk of systemic side effects while maintaining anti-inflammatory efficacy [1]

C18H19F3N6O

392.38

392.157

C, 55.10; H, 4.88; F, 14.53; N, 21.42; O, 4.08

944842-54-0

59422203

White to off-white solid powder

1.4±0.1 g/cm3

553.6±50.0 °C at 760 mmHg

288.6±30.1 °C

0.0±1.5 mmHg at 25°C

1.603

2.26

3

8

6

28

548

1

CC[C@](C)(C(=O)NCC(F)(F)F)NC1=NC(=NC=C1)C2=CNC3=C2C=CC=N3

ASUGUQWIHMTFJL-QGZVFWFLSA-N

InChI=1S/C18H19F3N6O/c1-3-17(2,16(28)25-10-18(19,20)21)27-13-6-8-23-15(26-13)12-9-24-14-11(12)5-4-7-22-14/h4-9H,3,10H2,1-2H3,(H,22,24)(H,25,28)(H,23,26,27)/t17-/m1/s1

(R)-2-((2-(1H-pyrrolo[2,3-b]pyridin-3-yl)pyrimidin-4-yl)amino)-2-methyl-N-(2,2,2-trifluoroethyl)butanamide

PubChem CID 59422203; VX-509; VRT831509 ; 944842-54-0; Adelatinib; Decernotinib (VX-509); Decernotinib(VX-509); VRT-831509; VX509; VX 509 ; VRT 831509 ; Decernotinib; Adelatinib

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

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: ≥ 2.5 mg/mL (6.37 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.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.37 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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.37 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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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