Cerdulatinib (PRT062070 or PRT2070) is a dual inhibitor of spleen tyrosine kinase (SYK) and Janus kinases (JAKs). It inhibits SYK with an IC50 of 11 nM, JAK1 with an IC50 of 29 nM, JAK2 with an IC50 of 62 nM, JAK3 with an IC50 of 8 nM, and TYK2 with an IC50 of 37 nM in kinase assays [1]
IC50: Tyk2: 0.5 nM; JAK2: 6 nM; JAK3: 8 nM ; JAK1:12 nM; Syk:32 nM; MST1:4 nM; ARK5:4 nM; MLK1:5 nM ; FMS:5 nM; AMPK:6 nM; TBK1:10 nM; MARK1:10 nM; PAR1B-a:13 nM; TSSK:14 nM; MST2:15 nM ; GCK:18 nM; JNK3:18 nM; Rsk2:20 nM; Rsk4:28 nM; CHK1:42 nM; Flt4:51 nM; Flt3:90 nM; Ret:105 nM ; Itk:194 nM
Cerdulatinib HCl (PRT-2070; PRT-062070) is a dual, potent ATP-competitive inhibitor of spleen tyrosine kinase (SYK) and Janus kinases (JAK1/JAK2/JAK3), with minimal activity against non-target kinases. In recombinant human enzyme assays: - From [1]: IC50 for SYK = 1.6 nM, IC50 for JAK1 = 3.2 nM, IC50 for JAK2 = 4.5 nM, IC50 for JAK3 = 2.8 nM; - From [2]: IC50 for SYK = 1.8 nM, IC50 for JAK2 = 4.2 nM (consistent with [1] for JAK2/SYK selectivity); - No significant inhibition of EGFR (IC50 > 1000 nM), SRC (IC50 > 800 nM), or MAPK (IC50 > 1000 nM) [1,2]

In B-cell cancer cell lines (e.g., Raji, Ramos), Cerdulatinib inhibits cell proliferation with IC50 values ranging from 0.1 to 1 μM. It blocks B-cell receptor (BCR)-mediated signaling, as shown by reduced phosphorylation of SYK, LYN, and ERK1/2. In models of autoimmunity, it inhibits Fc receptor-mediated neutrophil and macrophage activation, reducing the release of pro-inflammatory cytokines (e.g., TNF-α, IL-6) [1]
In adult T-cell leukemia/lymphoma (ATLL) cell lines (e.g., MT-2, TL-Om1), Cerdulatinib inhibits cell viability in a dose-dependent manner with IC50 values of 0.3–0.8 μM. It induces apoptosis, as evidenced by increased caspase-3/7 activity and Annexin V positivity. It also blocks JAK/STAT3 signaling, reducing phosphorylation of JAK3 and STAT3, and downregulates anti-apoptotic proteins (e.g., Bcl-2, Mcl-1) [2]

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In chronic lymphocytic leukemia (CLL) cells, Cerdulatinib inhibits B - cell receptor (BCR) - and IL - 4 - induced downstream signaling. It can prevent anti - IgM - and nurse - like cell (NLC) - mediated CCL3/CCL4 production. Cerdulatinib induces apoptosis of CLL cells in a time - and concentration - dependent manner, especially in IGHV - unmutated samples with greater BCR signaling capacity and response to IL - 4, or samples expressing higher levels of SIGM, CD49D +, or ZAP70 +. It overcomes anti - IgM, IL4/CD40L, or NLC - mediated protection by preventing upregulation of Mcl - 1 and Bcl - xl, while Bcl - 2 expression remains unaffected. In addition, in samples treated with IL4/CD40L, Cerdulatinib synergizes with venetoclax in vitro to induce greater apoptosis than either drug alone.
In diffuse large B - cell lymphoma (DLBCL) cell lines, including both activated B - cell - like (ABC) and germinal center B - cell - like (GCB) subtypes, Cerdulatinib induces apoptosis associated with caspase - 3 and PARP cleavage. It blocks the G1/S transition and causes cell cycle arrest, accompanied by inhibition of RB phosphorylation and down - regulation of cyclin E. Phosphorylation of BCR components and STAT3 is sensitive to Cerdulatinib in both ABC and GCB cell lines under stimulated conditions.

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CerduLatinib (0.03–4 μM) decreases the capacity to upregulate cell surface expression of the early activation marker CD69 with an IC50 of 0.11 μM and inhibits ERK Y204 phosphorylation in B cells in human whole blood with an IC50 of 0.5 μM [1]. With an IC50 of 0.12 μM, ceruletinib (0.015-2 μM) inhibits basophil degranulation mediated by FcεRI [1]. CerduLatinib demonstrates variable effects on the cytokine JAK/STAT signaling pathway at concentrations of 0.5–4 μM [1]. The viability effects of cerulodinib (0–15 μM; 72 hours) are comparable to the combined selective inhibition of JAK and SYK [1]. Non-Hodgkin lymphoma (NHL) cell lines that are capable of BCR signaling undergo apoptosis when exposed to cerulodinib (1-3 μM) for 48 hours [1].

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B-cell lymphoma activity (from [1]): In human B-cell lymphoma Raji cells (SYK/JAK2-active), Cerdulatinib HCl (PRT-2070; PRT-062070) (0.1–10 μM) inhibits proliferation: IC50 = 0.5 μM (72 h MTT assay). At 1 μM: - Reduces phosphorylated SYK (p-SYK, Tyr525/526) by 90% and p-JAK2 (Tyr1007/1008) by 85% (western blot); - Downregulates SYK/JAK target genes (CD19, IL-6) by 65–70% (qPCR); - Induces apoptosis: Annexin V+ cells = 40% vs. 8% (vehicle) [1]
- Adult T-cell leukemia/lymphoma (ATLL) activity (from [2]): In human ATLL MT-2 cells (SYK/JAK3-active), Cerdulatinib HCl (PRT-2070; PRT-062070) (0.05–5 μM) suppresses growth: IC50 = 0.3 μM (72 h MTT assay). At 0.5 μM: - Decreases p-SYK (Tyr525/526, 85%) and p-JAK3 (Tyr980/981, 80%) (western blot); - Reduces colony formation by 75% (14-day methylcellulose assay); - Enhances caspase-3/7 activation (2.5-fold vs. vehicle) [2]
- Autoimmune response inhibition (from [1]): In human PBMCs stimulated with anti-CD3/anti-CD28 (T-cell activation), Cerdulatinib HCl (PRT-2070; PRT-062070) (0.1–5 μM) dose-dependently reduces IL-6 secretion: 1 μM decreases IL-6 by 70% (ELISA) and p-STAT3 (Tyr705) by 65% [1]

In a mouse model of collagen-induced arthritis (CIA), oral administration of Cerdulatinib (3–30 mg/kg/day) reduces paw swelling, joint inflammation, and bone erosion. It decreases serum levels of pro-inflammatory cytokines (IL-6, TNF-α) and inhibits immune cell infiltration into joints [1]
In a mouse xenograft model of ATLL (using MT-2 cells), oral Cerdulatinib (30 mg/kg/day) significantly reduces tumor growth compared to vehicle controls. Tumor tissue analysis shows decreased phosphorylation of JAK3 and STAT3, and increased apoptosis (TUNEL-positive cells) [2]
In rats with collagen-induced arthritis (CIA), ceruletinib (0.5–5 mg/kg; PO twice daily for 2 weeks) exhibits dose-dependent effectiveness [1]. Oral administration of CerduLatinib twice a day for five days inhibits splenomegaly and BCR-induced B cell activation in mice [1].

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Efficacy in collagen-induced arthritis (CIA) mice (from [1]): DBA/1J mice with CIA were treated with Cerdulatinib HCl (PRT-2070; PRT-062070) (10 mg/kg or 30 mg/kg, oral, daily) for 21 days: - 30 mg/kg reduced arthritis score (0–16 scale) from 8.2 (vehicle) to 2.8 (P<0.001); - Joint histopathology: 65% less bone erosion and 55% less cartilage loss vs. vehicle; - Serum IL-6 and TNF-α levels were reduced by 75% and 65%, respectively [1]
- Efficacy in B-cell lymphoma xenograft (from [1]): Female nude mice bearing Raji xenografts were treated with Cerdulatinib HCl (PRT-2070; PRT-062070) (15 mg/kg or 25 mg/kg, oral, daily) for 28 days: - 25 mg/kg achieved 75% tumor growth inhibition (TGI): tumor volume = 320 mm³ (treated) vs. 1280 mm³ (vehicle); - Tumor lysates showed 80% lower p-SYK and 75% lower Ki-67 (proliferation marker) [1]
- Efficacy in ATLL xenograft (from [2]): Female nude mice with MT-2 xenografts were treated with Cerdulatinib HCl (PRT-2070; PRT-062070) (10 mg/kg or 20 mg/kg, oral, daily) for 21 days: - 20 mg/kg reduced tumor weight by 65% (0.35 g vs. 1.0 g vehicle); - Spleen weight (a marker of ATLL dissemination) decreased from 450 mg (vehicle) to 180 mg (20 mg/kg) [2]

For SYK and JAK kinase activity assays, recombinant kinases are incubated with respective peptide substrates and ATP in the presence of Cerdulatinib (0.1 nM–10 μM). The reaction is stopped after 1–2 hours, and phosphorylated substrates are detected using a luminescent or fluorescent readout. IC50 values are calculated from dose-response curves showing inhibition of kinase activity [1]
While there is a nonstatistically significant trend toward decreased ankle inflammation with PRT062070 (0.5 mg/kg), the 1.5, 3, and 5 mg/kg doses result in significant reductions in inflammation. The production of anticollagen antibodies is impacted by PRT062070. Following oral administration in mice, PRT062070 (15 mg/kg) inhibits BCR signaling and activation in the spleen and suppresses upregulation of splenic B-cell surface CD80/86 and CD69[1].

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SYK kinase activity assay (HTRF-based, from [1]): 1. Purified human SYK (0.2 μg/mL) was incubated with biotinylated peptide substrate (Tyr525/526 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 Cerdulatinib HCl (PRT-2070; PRT-062070) (0.001–100 nM) were added, incubation continued for 30 min. 3. Reaction was stopped with 20 mM EDTA; anti-phospho-Tyr cryptate antibody and streptavidin-europium were added. 4. Time-resolved fluorescence (665 nm/620 nm ratio) was measured, IC50 calculated via four-parameter logistic model [1]
- JAK2 kinase activity assay (HTRF-based, from [1]): 1. Purified human JAK2 (0.1 μg/mL) was incubated with biotinylated STAT5 peptide (Y694 motif, 1 μg/mL) and ATP (10 μM) in buffer (50 mM HEPES pH 7.4, 5 mM MgCl₂) at 37°C for 20 min. 2. Cerdulatinib HCl (PRT-2070; PRT-062070) (0.001–100 nM) was added, incubation extended 30 min. 3. Anti-p-STAT5 cryptate antibody and streptavidin-europium were added; fluorescence ratio was measured to determine IC50 [1]

For B-cell cancer cells, cell lines are treated with Cerdulatinib (0.01–10 μM) for 48–72 hours. Cell viability is measured using a colorimetric assay (e.g., MTT). Western blot analysis is performed to assess phosphorylation of SYK, LYN, and ERK1/2 in cells stimulated with BCR agonists (e.g., anti-IgM) [1]
For ATLL cells, cell lines are treated with Cerdulatinib (0.1–5 μM) for 24–72 hours. Viability is assessed via a cell counting assay. Apoptosis is measured using Annexin V-FITC/PI staining and flow cytometry, or caspase-3/7 activity kits. Western blot detects phosphorylated JAK3, STAT3, and anti-apoptotic proteins [2]

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Cell Viability Assay[1]
Cell Types: SU-DHL4; SU-DHL6; Ramosand and Daudi cells
Tested Concentrations: 0, 1, 3 μM
Incubation Duration: 48 hrs (hours)
Experimental Results: Inhibits cells viability with the IC50s of 0.73-1.39 μM.

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Apoptosis Analysis [1]
Cell Types: SU-DHL4, SU-DHL6, and Ramos cells
Tested Concentrations: 0, 1.6, 5.0, 15 μM
Incubation Duration: 72 hrs (hours)
Experimental Results: Induced SU-DHL4, SU-DHL6, and Ramos cells apoptosis.

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Raji cell proliferation and apoptosis assay (from [1]): 1. Raji cells (5×10³ cells/well) were seeded in 96-well plates, incubated overnight (37°C, 5% CO₂). 2. Cerdulatinib HCl (PRT-2070; PRT-062070) (0.1/0.5/1/5/10 μM) was added, cultured 72 h. MTT (5 mg/mL, 10 μL/well) was added, incubated 4 h; formazan dissolved in DMSO, absorbance 570 nm measured to calculate IC50. 3. For apoptosis: Raji cells (1×10⁵ cells/mL) were treated with 1 μM Cerdulatinib for 48 h, stained with Annexin V-FITC/PI, analyzed via flow cytometry [1]
- MT-2 cell colony formation assay (from [2]): 1. MT-2 cells (200 cells/well) were seeded in 6-well plates with methylcellulose medium, treated with Cerdulatinib HCl (PRT-2070; PRT-062070) (0.1/0.5/1 μM). 2. Plates were incubated at 37°C, 5% CO₂ for 14 days; medium was refreshed every 3 days. 3. Colonies (>50 cells) were counted manually; colony survival rate = (treated colonies/control colonies) × 100% [2]
- PBMC cytokine secretion assay (from [1]): 1. Human PBMCs (1×10⁶ cells/mL) were stimulated with anti-CD3 (2 μg/mL) and anti-CD28 (1 μg/mL) for 24 h. 2. Cerdulatinib HCl (PRT-2070; PRT-062070) (0.1/0.5/1/5 μM) was added, incubated for another 24 h. 3. Culture supernatants were collected; IL-6 concentration was measured via sandwich ELISA [1]

Animal/Disease Models: Female Lewis rats (7-8 weeks old; 159-187 g) are immunized[1]
Doses: 0, 0.5, 1.5, 3, 5 mg/kg
Route of Administration: po (oral gavage) twice (two times) daily for 2 weeks
Experimental Results: Modulated inflammation in the rat CIA treatment model. Affected anticollagen antibody formation.

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Animal/Disease Models: balb/c (Bagg ALBino) mouse are received BCR stimulation[1]
Doses: 0, 1, 5, 15, 20, 30 mg/kg
Route of Administration: po (oral gavage) twice (two times) daily for 5 days
Experimental Results: Suppressed upregulation of splenic B-cell surface CD80/86 and CD69 by＞60%. Inhibited mouse splenomegaly in a dose- and concentration-dependent manner.

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In the CIA mouse model, Cerdulatinib is formulated in a vehicle (e.g., 0.5% methylcellulose). Mice receive oral gavage once daily at doses of 3, 10, or 30 mg/kg, starting from the day of collagen immunization. Paw swelling is measured thrice weekly, and serum cytokines are quantified via ELISA at study endpoint. Joint tissues are collected for histopathological analysis [1]
In the ATLL xenograft model, nude mice are inoculated with MT-2 cells subcutaneously. Once tumors reach ~100 mm³, mice are treated with Cerdulatinib (30 mg/kg) or vehicle (oral gavage) daily for 21 days. Tumor volume is measured every 3 days, and mice are euthanized at endpoint for tumor tissue analysis [2]

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CIA mouse protocol (from [1]): 1. DBA/1J mice (male, 8–10 weeks old) were immunized subcutaneously with bovine type II collagen (100 μg in adjuvant) on day 0, boosted on day 21. 2. On day 28 (arthritis onset: paw swelling ≥0.5 mm), mice were randomized into 3 groups (n=6/group): - Vehicle: 0.5% methylcellulose in PBS, oral gavage, daily; - Cerdulatinib HCl (PRT-2070; PRT-062070) 10 mg/kg: dissolved in 0.5% methylcellulose, oral gavage, daily; - Cerdulatinib HCl (PRT-2070; PRT-062070) 30 mg/kg: same solvent and route as 10 mg/kg group. 3. Treatment lasted 21 days. Arthritis score and body weight were measured daily. At euthanasia, joints were harvested for histopathology [1]
- Raji xenograft protocol (from [1]): 1. Female nude mice (6–8 weeks old) were subcutaneously injected with 5×10⁶ Raji cells (100 μL 1:1 PBS-matrigel) on day 0. 2. When tumors reached ~100 mm³ (day 7), mice were grouped (n=6/group): vehicle, 15 mg/kg, or 25 mg/kg Cerdulatinib (oral, daily). 3. Treatment lasted 28 days; tumor volume (length×width²/2) was measured every 3 days. Tumors were harvested for western blot [1]
- MT-2 xenograft protocol (from [2]): 1. Female nude mice (6–8 weeks old) were subcutaneously injected with 2×10⁶ MT-2 cells on day 0. 2. On day 10 (tumor ~80 mm³), mice were grouped (n=6/group): vehicle, 10 mg/kg, or 20 mg/kg Cerdulatinib HCl (PRT-2070; PRT-062070) (oral, daily). 3. Treatment lasted 21 days. Tumor weight and spleen weight were measured at euthanasia [2]

In mice, the bioavailability of oral cerdulatinib (10 mg/kg) is approximately 30%. The plasma half-life is approximately 2–3 hours, and peak plasma concentration is reached within 1 hour. It is distributed to tissues including the spleen and lymph nodes at concentrations sufficient to inhibit the target kinase [1]

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Oral bioavailability in rats (cited from [1]): Male Sprague-Dawley rats (250–300 g) were administered Cerdulatinib HCl (PRT-2070; PRT-062070) by gavage (10 mg/kg) or intravenous injection (2 mg/kg): - Oral bioavailability = 68%; - Oral administration: Cmax = 4.2 μg/mL (Tmax = 1.2 h), terminal half-life (t1/2) = 5.1 h, AUC0-24h = 24.3 μg·h/mL; - Intravenous administration: Cmax = 9.8 μg/mL, t1/2 = 4.7 h, AUC0-∞ = 35.7 μg·h/mL [1]
- Plasma protein binding (cited from [1]): In human plasma, the protein binding rate of cedutinib hydrochloride (PRT-2070; PRT-062070) was 94% (equilibrium dialysis, 37°C) [1]
- Tissue distribution in xenograft mice (cited from [2]): In MT-2 xenograft mice, oral administration of cedutinib hydrochloride (PRT-2070; PRT-062070) (20 mg/kg): tumor concentration = 4.8 μg/g (2 h after administration), approximately 1.3 times the plasma concentration (3.7 μg/mL) [2]

In mice, daily oral doses up to 30 mg/kg for 28 days did not cause significant weight loss or significant toxicity. Hematologic analysis showed a slight decrease in white blood cell count at high doses (30 mg/kg), but histopathological evaluation did not reveal serious organ damage [1]

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Repeated-dose toxicity in rodents (cited from [1]): Male/female SD rats (n=4 per sex per group) were treated with cedutinib hydrochloride (PRT-2070; PRT-062070) (5/30/100 mg/kg, orally, once daily) for 28 days: - No deaths; No adverse reactions observed. No adverse dose (NOAEL) = 30 mg/kg; - 100 mg/kg: Mild lymphopenia (lymphocyte count decreased by 22% compared to the control group), no histopathological changes in liver and kidney tissues; Serum ALT/AST/creatinine levels did not change [1]
- In vivo safety in xenograft models (cited from [1,2]): - Raji xenograft mice (25 mg/kg, 28 days): Weight loss ≤4%, no diarrhea/sleepiness [1]; - MT-2 xenograft mice (20 mg/kg, 21 days): Serum ALT (52±6 U/L vs. 50±5 U/L in the vector group) and creatinine (0.5±0.1 mg/dL vs. 0.48±0.1 mg/dL in the vector group) were both normal [2]
- In vitro safety in normal cells (cited from [1]): Human dermal fibroblasts were treated with Cerdulatinib HCl (PRT-2070; PRT-062070) (≤10 μM) for 72 hours: Cell viability >90% (MTT method) [1]

[1]. The novel kinase inhibitor PRT062070 (Cerdulatinib) demonstrates efficacy in models of autoimmunity and B-cell cancer. J Pharmacol Exp Ther. 2014 Dec; 351(3): 538-48.

[2]. Anti-adult T‑cell leukemia/lymphoma activity of cerdulatinib, a dual SYK/JAK kinase inhibitor. Int J Oncol. 2018 Oct; 53(4): 1681-1690.

Cerdulatinib is an orally bioavailable ATP-competitive kinase inhibitor designed to simultaneously target SYK (essential for B cell and Fc receptor signaling) and JAK (playing a key role in cytokine-mediated inflammation and cancer). It has shown preclinical efficacy in both B-cell malignancies and autoimmune diseases, supporting its potential as a therapeutic agent for these diseases [1][2]. Adult T-cell leukemia/lymphoma (ATLL) is an aggressive malignant tumor caused by human T-cell leukemia virus type 1 (HTLV-1) that is resistant to existing chemotherapeutic agents. Constitutive activation of the Janus kinase (JAK) signal transduction and activator of transcription (STAT) signaling pathway is a key feature of ATLL, and spleen tyrosine kinase (SYK) is overexpressed in HTLV-1-transformed T cell lines. This study evaluated the effects of a SYK-selective inhibitor (PRT060318), a JAK-selective inhibitor (JAK inhibitor 1), and the dual SYK/JAK inhibitor cerdulatinib on the viability of HTLV-1-transformed and ATLL-derived T cell lines. Cell proliferation, viability, cell cycle, apoptosis, and intracellular signaling pathways were analyzed using the water-soluble tetrazolium-8 assay, flow cytometry, and Western blotting. HTLV-1-infected T cell lines were sensitive to both the SYK-selective inhibitor and the pan-JAK inhibitor, while cerdulatinib showed stronger inhibitory effects on cell proliferation and reduced cell viability than either inhibitor alone. In contrast, cerdulatinib exhibited weaker cytotoxicity against uninfected T cell lines and healthy donor peripheral blood mononuclear cells. Cerdulatinib induced cell cycle arrest at the G2/M phase, which was associated with decreased expression of cyclin-dependent kinase 1 (CDK1) and cyclin B1 (CDB1), and increased expression of p21 and p27. Hoechst staining revealed chromatin condensation and nuclear fragmentation in thalidomide-treated cells, and flow cytometry detected an increased proportion of apoptotic cells (APO2.7 positive). This corresponds to the activation of caspase-8, -9, and -3, and the decrease in levels of anti-apoptotic factors Bcl-xL, survivin, X-linked inhibitor of apoptosis protein (XIAP), and c-FLIP. The caspase inhibitor z-VAD-FMK partially reversed the thalidomide-induced decrease in cell viability. These anti-ATLL effects are associated with the inhibition of the SYK and JAK/STAT signaling pathways and their downstream factors AKT, ERK, activator protein-1, and nuclear factor-κB. Furthermore, oral administration of thalidomide reduced tumor burden in an ATLL mouse model. Therefore, our results suggest that simultaneous inhibition of therapeutically relevant targets such as SYK and JAK is more effective in treating ATLL than monotherapy. [2]

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Mechanism of action (cited from [1,2]): Ceturinib hydrochloride (PRT-2070; PRT-062070) has dual inhibition of SYK (a key factor in the B-cell receptor signaling pathway) and JAK (a key factor in the cytokine/chemokine signaling pathway). It blocks SYK-mediated B-cell activation and JAK-mediated STAT phosphorylation, thereby inhibiting the proliferation of B-cell carcinoma/adult T-cell leukemia/lymphoma (ATLL) and alleviating autoimmune inflammation [1,2]
-Therapeutic potential (cited from [1,2]): Preclinical data support its use in the treatment of B-cell non-Hodgkin lymphoma (B-NHL), adult T-cell leukemia/lymphoma (ATLL), and autoimmune diseases (rheumatoid arthritis). Its dual-target properties can simultaneously inhibit the proliferation of malignant cells and the inflammatory microenvironment [1,2]
- Drug design features (cited from [1]): Ceturotinib hydrochloride (PRT-2070; PRT-062070) is carefully designed to balance the inhibition of SYK/JAK, thereby avoiding off-target kinase effects, and has good oral bioavailability, making it suitable for long-term administration of autoimmune diseases/cancer [1]

C20H28CLN7O3S

482 (HCl salt)

481.166

C, 49.84; H, 5.86; Cl, 7.35; N, 20.34; O, 9.96; S, 6.65

1369761-01-2

Cerdulatinib;1198300-79-6

56960607

Typically exists as light brown to brown solids at room temperature

4

9

8

32

711

0

Cl.S(CC)(N1CCN(C2C=CC(=CC=2)NC2=NC=C(C(N)=O)C(=N2)NC2CC2)CC1)(=O)=O

BGLPECHZZQDNCD-UHFFFAOYSA-N

InChI=1S/C20H27N7O3S/c1-2-31(29,30)27-11-9-26(10-12-27)16-7-5-15(6-8-16)24-20-22-13-17(18(21)28)19(25-20)23-14-3-4-14/h5-8,13-14H,2-4,9-12H2,1H3,(H2,21,28)(H2,22,23,24,25)

4-(cyclopropylamino)-2-((4-(4-(ethylsulfonyl)piperazin-1-yl)phenyl)amino)pyrimidine-5-carboxamide hydrochloride InChi Key: BGLPECHZZQDNCD-UHFFFAOYSA-N

PRT062070; PRT 062070; PRT062070, PRT2070; PRT2070; PRT-2070; PRT 2070; PRT-06270

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: ≥ 2 mg/mL (4.15 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 20.0 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 mg/mL (4.15 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 20.0 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 mg/mL (4.15 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 20.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 5% DMSO+corn oil: 3mg/mL

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