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DCZ3301 is an apoptosis inducer. DCZ3301 modulates JAK2/STAT3, ERK1/2, and PI3K/AKT pathways. DCZ3301 induces G2/M and M phase cell cycle arrest and inhibits cell proliferation and viability. DCZ3301 enhances DNA damage, inhibits DNA repair, and suppresses angiogenesis. DCZ3301 can be used for the research of diffuse large B-cell lymphoma, multiple myeloma and leukemia/lymphoma.
For research use only. We do not sell to patients.
DCZ3301 is an apoptosis inducer. DCZ3301 modulates JAK2/STAT3, ERK1/2, and PI3K/AKT pathways. DCZ3301 induces G2/M and M phase cell cycle arrest and inhibits cell proliferation and viability. DCZ3301 enhances DNA damage, inhibits DNA repair, and suppresses angiogenesis. DCZ3301 can be used for the research of diffuse large B-cell lymphoma, multiple myeloma and leukemia/lymphoma[1][2][3][4][5].
DCZ3301 (1-32 μM; 48 h) potently inhibits proliferation of OCI-LY8, NU-DUL-1, SUDHL-4, DB, and TMD8 DLBCL cell lines[1]. DCZ3301 (1-32 μM; 24-72 h) inhibits proliferation of OCI-LY8 and NU-DUL-1 DLBCL cell lines in a time-dependent manner[1]. DCZ3301 (2-20 μM; 48 h) inhibits proliferation of OCI-LY8 and NU-DUL-1 DLBCL cell lines in the presence of IL-6 or IGF-1, with its growth-inhibitory effect unaffected by these protumorigenic cytokines[1]. DCZ3301 (4-20 μM; 24-72 h) induces dose- and time-dependent apoptosis in OCI-LY8 and NU-DUL-1 DLBCL cell lines[1]. DCZ3301 (8-16 μM; 48 h) induces apoptosis in OCI-LY8 and NU-DUL-1 DLBCL cell lines via both extrinsic and intrinsic caspase-dependent pathways[1]. DCZ3301 (4 μM; 8-24 h) induces time-dependent G2/M phase cell cycle arrest in OCI-LY8 and NU-DUL-1 DLBCL cell lines when treated with 4 μM for 8, 12, or 24 h[1]. DCZ3301 (4-8 μM; 24 h) modulates cell cycle-related proteins (upregulating p-CHK2 and p21, downregulating cdc25A, cdc25C, and cyclinB1) in OCI-LY8 and NU-DUL-1 DLBCL cell lines[1]. DCZ3301 (8-16 μM; 48 h) regulates the Akt, ERK1/2, and JAK2/STAT3 signaling pathways[1]. DCZ3301 (4-8 μM; 48 h) has its antiproliferative effect enhanced in STAT3-knockdown OCI-LY8 and NU-DUL-1 DLBCL cell lines[1]. DCZ3301 (8-16 μM; 12-48 h) inhibits Lyn phosphorylation (Y507) in a dose- and time-dependent manner, with a corresponding decrease in STAT3 phosphorylation, in OCI-LY8 and NU-DUL-1 DLBCL cell lines[1]. DC50Z3301 (8-16 μM; 48 h) modulates DNA repair-related protein expression in NCI-H929R and RPMI-8226R5 BTZ-resistant multiple myeloma cells after 48 hours of treatment[2]. DCZ3301 (8 μM; 48 h) upregulates γ-H2A.X expression and induces γ-H2A.X foci formation in NCI-H929R and RPMI-8226R5 BTZ-resistant multiple myeloma cells, confirming enhanced DNA damage[2]. DCZ3301 (5 μM; 24 h) suppresses the migration of human umbilical vein endothelial cells (HUVECs) in a wound healing assay[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Induced apoptosis in OCI-LY8 and NU-DUL-1 cells in a dose- and time-dependent manner. Increased apoptosis rates with higher concentrations and longer incubation times, with statistically significant increases compared to controls.
OCI-LY8, NU-DUL-1 (diffuse large B-cell lymphoma cell lines)
Concentration:
8 μM; 16 μM
Incubation Time:
48 h
Result:
Caused a dose-dependent increase in cleaved caspase-3, caspase-8, caspase-9, and PARP, while downregulating Bcl-2 and Bcl-xL and upregulating Bax. Suppressed apoptosis in NU-DUL-1 cells when pre-incubated with pan-caspase inhibitor Z-VAD-FMK.
OCI-LY8, NU-DUL-1 (diffuse large B-cell lymphoma cell lines)
Concentration:
4 μM
Incubation Time:
8 h; 12 h; 24 h
Result:
Caused a time-dependent accumulation of cells in the G2/M phase in both OCI-LY8 and NU-DUL-1 cell lines, with statistically significant increases (P < 0.05, P < 0.001) compared to controls at 12 and 24 h.
OCI-LY8, NU-DUL-1 (diffuse large B-cell lymphoma cell lines)
Concentration:
8 μM; 16 μM
Incubation Time:
48 h
Result:
Upregulated phosphorylated ERK1/2, downregulated phosphorylated Akt, phosphorylated JAK2, and phosphorylated STAT3, and reduced c-Myc expression in a dose-dependent manner in both OCI-LY8 and NU-DUL-1 cells.
OCI-LY8, NU-DUL-1 (diffuse large B-cell lymphoma cell lines, STAT3 knockdown)
Concentration:
4, 8 μM
Incubation Time:
48 h
Result:
Enhanced antiproliferative efficacy in STAT3-knockdown OCI-LY8 and NU-DUL-1 cells compared to negative control siRNA-transfected cells, with statistically significant differences (P < 0.05) observed at both concentrations.
OCI-LY8, NU-DUL-1 (diffuse large B-cell lymphoma cell lines)
Concentration:
8 μM; 16 μM
Incubation Time:
12 h; 24 h; 36 h; 48 h
Result:
Downregulated phosphorylated Lyn (Y507) in a dose- and time-dependent manner, while having no effect on phosphorylated Syk. Decreased phosphorylated Lyn correlated with a synchronous decrease in phosphorylated STAT3.
OCI-LY8, NU-DUL-1 (diffuse large B-cell lymphoma cell lines, Lyn-overexpressing)
Concentration:
16 μM
Incubation Time:
24 h
Result:
Caused a greater suppression of phosphorylated STAT3 in Lyn-overexpressing cells compared to control cells after 24 h, despite Lyn-overexpressing cells exhibiting higher levels of phosphorylated STAT3 than control cells without treatment.
BTZ-resistant multiple myeloma cell lines NCI-H929R and RPMI-8226R5
Concentration:
8 μM
Incubation Time:
48 h
Result:
Increased γ-H2A.X expression and formation of γ-H2A.X foci, indicating increased DNA double-strand breaks.\nInduced the formation of multipolar mitotic spindles, a hallmark of mitotic catastrophe.
In Vivo
DCZ3301 (40 mg/kg; i.p.; daily; 12 days) significantly inhibits diffuse large B-cell lymphoma xenograft tumor growth in BALB/c nude mice[1]. DCZ3301 (50 mg/kg; i.p.; 2 consecutive days followed by 1 day of vehicle; for 20 days) significantly inhibits tumor growth in a BTZ-resistant multiple myeloma xenograft model, reduces tumor cell proliferation[2]. DCZ3301 (50 mg/kg; i.p.; daily; 14 days) does not induce significant acute liver or kidney toxicity in healthy BALB/C nude mice[2]. DCZ3301 (30 mg/kg; i.p.; daily; 14 days) significantly inhibits T-cell leukemia/lymphoma xenograft tumor growth in BALB/c nude mice[3]. Treatment with DCZ3301 (30 mg/kg; i.p.; daily; 14 days) significantly inhibits tumor growth and reduces tumor weight in a Jurkat cell xenograft model of T-cell leukemia[4]. DCZ3301 (50-200 μM; topical eye drops; three times daily; 7 days) significantly reduces corneal neovascularization area and attenuates corneal stroma edema in alkali-burned mice, with 200 μM producing a larger reduction in CNV area compared to vehicle control[5]. DCZ3301 (200 μM; topical eye drops; three times daily; 7 days) does not significantly affect corneal epithelial thickness or endothelial cell density in healthy BALB/c mice[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Reduced tumor volume significantly compared to controls by day 12 (P < 0.05). Showed no significant difference in mouse body weight compared to controls. Increased cell necrosis in tumor tissues via H&E staining. Increased apoptotic cells in tumor tissues via TUNEL staining. Downregulated phosphorylated STAT3 expression in tumor tissues via immunohistochemistry. Showed no evidence of organ dysfunction or growth disorder in functional organs.
Animal Model:
BALB/C nude mice (weight monitored during study)[2]
Dosage:
50 mg/kg
Administration:
i.p.; 2 consecutive days followed by 1 day of vehicle; for 20 days
Result:
Significantly reduced tumor volume compared to control group on day 20. Did not cause changes in mouse body weight or significant differences in serum levels of ALT, AST, Cr, or BUN. Increased tumor cell shrinkage and fragmentation relative to controls. Reduced Ki-67 expression in tumor tissue. Increased cleaved-caspase 3 expression in tumor tissue. Upregulated γ-H2A.X, phospho-ATM, and phospho-CHK1 expression in tumor tissue. Increased percentage of TUNEL-positive cells in tumors.
Animal Model:
BALB/C nude mice (weight monitored during study)[2]
Dosage:
50 mg/kg
Administration:
i.p.; daily; 14 days
Result:
Showed no significant differences in serum levels of ALT, AST, Cr, or BUN compared to vehicle-treated controls.
Animal Model:
BALB/c nude (5-week-old male, subcutaneous xenograft with Jurkat cells)[3]
Dosage:
30 mg/kg
Administration:
i.p.; daily; 14 days
Result:
Reduced final tumor volumes to statistically significant levels (P < 0.01). Reduced final tumor weights to statistically significant levels (P < 0.001). Caused no significant change in mouse body weight compared to vehicle controls.
Reduced tumor volume by a statistically significant margin on days 12 and 14 of treatment (P < 0.01). Lowered final tumor weight significantly compared to controls (P < 0.001). Caused no significant change in mouse body weight compared to vehicle-treated groups.
Animal Model:
BALB/c (6-8 week old male, alkali-burn induced corneal neovascularization)[5]
Dosage:
50 μM; 200 μM
Administration:
topical eye drops; three times daily; 7 days
Result:
Significantly reduced the ratio of corneal neovascularization (CNV) area compared to vehicle control (P < 0.01). Significantly reduced the ratio of CNV area compared to vehicle control (P < 0.0001). Greatly reduced corneal stroma thickness compared to vehicle control (P < 0.001). Greatly reduced corneal stroma thickness compared to vehicle control (P < 0.0001).
Did not cause a significant difference in central corneal epithelial thickness compared to saline-treated controls (P > 0.05). Did not cause a significant difference in corneal endothelial cell density compared to saline-treated controls (P > 0.05). Maintained regular shape of corneal endothelial cells.
Room temperature in continental US; may vary elsewhere.
Storage
Powder
-20°C
3 years
In solvent
-80°C
6 months
-20°C
1 month
Solvent & Solubility
In Vitro:
DMSO : 50 mg/mL (107.57 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
2.1513 mL
10.7566 mL
21.5132 mL
5 mM
0.4303 mL
2.1513 mL
4.3026 mL
10 mM
0.2151 mL
1.0757 mL
2.1513 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Protocol 1
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (5.38 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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