製品番号: HY-182671

SRX3305

SRX3305 is an BTK/PI3K/BRD4 inhibitor with IC₅₀s of 6.5 nM, 15 nM, and 4 nM toward BTK, PI3Kɑ and PI3Kδ, respectively. SRX3305 attenuates chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) cell proliferation and promotes apoptosis in a dose-dependent fashion. SRX3305 yields potent anti-tumor effects but spares healthy bystander cells. SRX3305 inhibits the activation-induced proliferation of primary CLL cells in vitro and effectively blocks microenvironment-mediated survival signals. SRX3305 blocks CLL cell migration toward CXCL-12 and CXCL-13. SRX3305 maintains its anti-tumor effects in Ibrutinib (HY-10997)-resistant CLL cells. SRX3305 can be used for research in CLL, diffuse large B-cell lymphoma (DLBCL) and MCL.

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CAS 番号: 2409965-28-0
分子式: C₂₂H₂₀N₂O₅S
分子量:424.47

保管条件:

Please store the product under the recommended conditions in the Certificate of Analysis.

SRX3305 構造式

CAS 番号: 2409965-28-0

容量

価格（税別）

在庫状況

数量

Amount: USD 0.00

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

生物活性

製品説明

IC₅₀ & Target^[2]

PI3Kα

15 nM (IC₅₀)

PI3Kδ

4 nM (IC₅₀)

PI3K アイソフォーム固有の製品をすべて表示 :

体外実験

SRX3305 (0.1-100 μM; 72 h) inhibits proliferation with an average IC₅₀ of 1.38 µM across B-cell non-Hodgkin lymphoma (B-NHL) cell lines^[1].
SRX3305 (0.1-100 μM; 72 h) reduces cell proliferation in DLBCL cells with IC₅₀ values of ~290 nM in OCI-LY3 cells and ~920 nM in SU-DHL-6 cells^[1].
SRX3305 (0.5-2 μM; 24-48 h) induces apoptosis in HG-3 and OSU-CLL cells in a dose-dependent manner^[1].
SRX3305 (0.5-2 μM; 4 h) inhibits critical BCR survival signaling in OSU-CLL, MEC-1 and MEC-2 cell lines^[1].
SRX3305 (0.16-5 μM; 48 h) inhibits primary malignant B-cell survival and proliferation in malignant B-cells isolated from Eμ-TCL1 (CLL model) and Eμ-Myc/TCL1 mice^[1].
SRX3305 (0.5-2 μM; 48 h) disrupts stroma survival support and chemokine-induced migration in CLL^[1].
SRX3305 (0.5-2 μM; 48 h) can overcome TME-induced survival signaling in MEC-1 cells^[1].
SRX3305 (0.1-100 μM; 72 h) is active in ibrutinib-resistant HG-3 cells^[1].
SRX3305 (10 nM-100 μM; 48 h) shows an IC₅₀ of 1 nM in Mino cells, 58 nM in JeKo-1 cells, 1.1 μM in Granta cells, 1 μM in JeKo-1 BTK C481S mutant cells and 47 nM in Mino BTK C481S mutant cells^[2].
SRX3305 (0.375-2 μM; 48 h) is minimally toxic to healthy donor peripheral blood mononuclear cells (PBMCs) or bystander healthy stromal cells and has low toxicity to healthy donor B-cells^[2].
SRX3305 (0.1-10 μM; 48 h) has anti-tumor effect in primary Eμ-Myc tumor samples^[2].
SRX3305 (0.01-0.5 μM; 1 h) blocks activation of both BTK and AKT^[2].
SRX3305 (0.01-1 μM; 1 h) shows improved efficacy in MCL and Ibrutinib-resistant MCL cells^[2].
SRX3305 (1 h) retains inhibition of BTK and AKT phosphorylation in Mino cells after inhibitor wash out experiments^[2].
SRX3305 (0.5-2 μM; 24 h) inhibits JeKo-1 and Mino cells proliferation through inducing S/G2 phase cell cycle arrest and promoting apoptosis^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay^[1]

Cell Line:

B-cell non-Hodgkin lymphoma cell lines
Concentration:

0.1 μM; 1 μM; 10 μM; 100 μM
Incubation Time:

72 h
Result:

Significantly inhibited CLL cell proliferation in a dose-dependent manner.

Apoptosis Analysis^[1]

Cell Line:

HG-3 and OSU-CLL cell lines
Concentration:

0.5 μM; 1 μM; 2 μM
Incubation Time:

24 h; 48 h
Result:

Induced apoptosis in a dose-dependent manner.

Western Blot Analysis^[1]

Cell Line:

OSU-CLL, MEC-1 and MEC-2 cell lines
Concentration:

0.5 μM; 1 μM; 2 μM
Incubation Time:

4 h
Result:

Effectively inhibited the phosphorylation of BTK and PRAS40 (indicative of PI3K/AKT signaling) and reduced MYC expression.

Western Blot Analysis^[1]

Cell Line:

OSU-CLL and MEC-1 cell lines
Concentration:

0.5 μM plus inhibitor treatment; 1 μM plus inhibitor treatment; 2 μM plus inhibitor treatment
Incubation Time:

4 h
Result:

Decreased phosphorylation of BTK (p-BTK) and PRAS40 (p-PRAS40) and reduced MYC expression in continuous inhibitor treatment.
Retained the inhibition of p-BTK following treatment washout.
Marked inhibition of p-PRAS40 and MYC expression after treatment washout was maintained.

Cell Proliferation Assay^[1]

Cell Line:

patient-derived CLL cells
Concentration:

0.16 μM plus CpG (3.2 μM); 0.31 μM plus CpG (3.2 μM); 0.63 μM plus CpG (3.2 μM); 1.25 μM plus CpG (3.2 μM); 2.5 μM plus CpG (3.2 μM); 5 μM plus CpG (3.2 μM)
Incubation Time:

48 h
Result:

Reversed CpG ODN-mediated proliferation reflected by reduced MYC levels in primary CLL cells.

Western Blot Analysis^[1]

Cell Line:

patient-derived CLL cells
Concentration:

0.5 μM plus CpG (3.2 μM); 1 μM plus CpG (3.2 μM); 2 μM plus CpG (3.2 μM)
Incubation Time:

48 h
Result:

Induced the accumulation of P21 (cyclin-dependent kinase inhibitor), indicative of cell cycle arrest.
Did not influence the proliferation under unstimulated/basal conditions.

Cell Cytotoxicity Assay^[1]

Cell Line:

malignant B-cells isolated from Eμ-TCL1 (CLL model) and Eμ-Myc/TCL1 mice
Concentration:

0.5 μM; 1 μM; 2 μM
Incubation Time:

48 h
Result:

Induced significant cytotoxicity in Eμ-TCL1 and Eμ-Myc/TCL1-derived malignant cells in a dose-dependent manner, suggesting promising therapeutic benefits in aggressive CLL and associated lymphomas.

Cell Viability Assay^[1]

Cell Line:

co-culture of primary CLL cells on BM-derived stromal cells
Concentration:

0.5 μM; 1 μM; 2 μM
Incubation Time:

48 h
Result:

Reduced CLL cell viability in a dose-dependent manner despite stroma protection.
Did not have toxicity to the stromal cells, indicating that CLL cell cytotoxicity is not a function of reduced stroma viability.

Cell Migration Assay ^[1]

Cell Line:

MEC-1 cells
Concentration:

0.5 μM; 1 μM; 2 μM
Incubation Time:

48 h
Result:

Reduced the migration of MEC-1 cells towards CXCL-12 or CXCL-13.

Cell Proliferation Assay^[1]

Cell Line:

ibrutinib-resistant HG-3 cells
Concentration:

0.1 μM; 1 μM; 10 μM; 100 μM
Incubation Time:

72 h
Result:

Remarkably decreased cell proliferation.

Western Blot Analysis^[1]

Cell Line:

ibrutinib-resistant HG-3 cells
Concentration:

1 μM; 2 μM
Incubation Time:

4 h
Result:

Consistently decreased MYC expression and p-PRAS40 (PI3K target) and increased P21 levels in IR-HG3 cells.
Reduced BTK activation (phosphorylation).

Cell Viability Assay^[2]

Cell Line:

MCL cell lines JeKo-1, Mino, JeKo-1 BTK C481S and Mino BTK C481S
Concentration:

10 nM; 100 nM; 1 μM; 10 μM; 100 μM
Incubation Time:

48 h
Result:

Exhibited strong anti-proliferative function.

Cell Viability Assay^[2]

Cell Line:

PBMCs
Concentration:

0.375 μM; 0.75 μM; 1.5 μM
Incubation Time:

48 h
Result:

Had minimally toxicity.

Cell Viability Assay^[2]

Cell Line:

healthy donor B-cells
Concentration:

0.5 μM
Incubation Time:

48 h
Result:

Exhibited low toxicity.

Cell Viability Assay^[2]

Cell Line:

bystander healthy stromal cells
Concentration:

0.5 μM; 1 μM; 2 μM
Incubation Time:

48 h
Result:

Had minimally toxicity.

Cell Viability Assay^[2]

Cell Line:

primary Eμ-Myc tumor cells
Concentration:

0.1 μM; 0.3 μM; 1 μM; 3.2 μM; 10 μM
Incubation Time:

48 h
Result:

Exhibited anti-tumor effect.

Western Blot Analysis^[2]

Cell Line:

IgM stimulated JeKo-1 and Mino cells
Concentration:

0.01 μM; 0.05 μM; 0.1 μM; 0.5 μM
Incubation Time:

1 h
Result:

Decreased BTK phosphorylation at Tyr223 and AKT phosphorylation at Ser473.

Western Blot Analysis^[2]

Cell Line:

IgM-stimulated Granta cells
Concentration:

0.01 μM; 0.05 μM; 0.1 μM; 0.5 μM; 1 μM
Incubation Time:

1 h
Result:

Showed dose dependent anti-proliferative activity.

Real Time qPCR^[2]

Cell Line:

JeKo-1 cells
Concentration:

0.5 μM
Incubation Time:

24 h
Result:

Decreased the expression of cMYC.
Increased the expression of HEXIM1.

Apoptosis Analysis^[2]

Cell Line:

JeKo-1 and Mino cells
Concentration:

0.5 μM; 1 μM; 2 μM
Incubation Time:

24 h
Result:

Induced apoptosis in JeKo-1 and Mino cells in a concentration-dependent manner.

Cell Cycle Analysis^[2]

Cell Line:

JeKo-1 and Mino cells
Concentration:

1 μM
Incubation Time:

24 h
Result:

Increased cell population in S phase and G2 phase.

化学情報

CAS 番号 2409965-28-0
分子量 424.47
分子式 C₂₂H₂₀N₂O₅S
SMILES

O=C1C=C(N2CCOCC2)OC3=C1SC=C3C4=CC5=C(OCCN5C(C=C)=O)C=C4
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

Please store the product under the recommended conditions in the Certificate of Analysis.

純度とドキュメンテーション

取扱説明書 (2659 KB)

参考文献

[1]. Smith AL, et al. A Novel Triple-Action Inhibitor Targeting B-Cell Receptor Signaling and BRD4 Demonstrates Preclinical Activity in Chronic Lymphocytic Leukemia. Int J Mol Sci. 2022 Jun 16;23(12):6712. [Content Brief]

[2]. Vann KR, et al. Combinatorial inhibition of BTK, PI3K-AKT and BRD4-MYC as a strategy for treatment of mantle cell lymphoma. Mol Biomed. 2022 Jan 15;3(1):2. [Content Brief]

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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SRX3305

PI3K アイソフォーム固有の製品をすべて表示

生物活性

化学情報

純度とドキュメンテーション

参考文献

Calculators

Help & FAQs

SRX3305 関連分類

HY-182671 関連分類