2. PI3K/Akt/mTOR Protein Tyrosine Kinase/RTK
  3. PI3K Btk
  4. SRX3305

SRX3305 是一种 BTK/PI3K/BRD4 抑制剂，对 BTK、PI3Kα 和 PI3Kδ 的 IC50 值分别为 6.5 nM、15 nM 和 4 nM。SRX3305 以剂量依赖的方式抑制慢性淋巴细胞白血病 (CLL) 和套细胞淋巴瘤 (MCL) 细胞的增殖并促进细胞凋亡 (apoptosis)。SRX3305 具有强效的抗肿瘤作用，但不损害健康细胞。SRX3305 在体外抑制原代 CLL 细胞的活化诱导增殖，并有效阻断微环境介导的生存信号。SRX3305 还可抑制 CLL 细胞向 CXCL-12 和 CXCL-13 的迁移。SRX3305 在对 Ibrutinib (HY-10997) 耐药的 CLL 细胞中仍保持其抗肿瘤活性。SRX3305 可用于 CLL、弥漫性大 B 细胞淋巴瘤 (DLBCL) 和 MCL 的研究。

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SRX3305

SRX3305 Chemical Structure

CAS No. : 2409965-28-0

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SRX3305 相关抗体

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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[1][2].

IC50 & Target[2]

PI3Kα

15 nM (IC50)

PI3Kδ

4 nM (IC50)

体外研究
(In Vitro)

SRX3305 (0.1-100 μM；72 小时) 可抑制 B-NHL 细胞系的增殖，平均 IC50 值为 1.38 µM[1]。
SRX3305 (0.1-100 μM；72 小时) 可降低 DLBCL 细胞的增殖，在 OCI-LY3 细胞中的 IC50 值约为 290 nM，在 SU-DHL-6 细胞中的 IC50 值约为 920 nM[1]。
SRX3305 (0.5-2 μM；24-48 小时) 可剂量依赖性地诱导 HG-3 和 OSU-CLL 细胞凋亡[1]。
SRX3305 (0.5-2 μM；4 小时) 可抑制 OSU-CLL、MEC-1 和 MEC-2 细胞系中的关键 BCR 存活信号通路[1]。
SRX3305 (0.16-5 μM；48 小时) 可抑制从 Eμ-TCL1 (CLL 模型) 和 Eμ-Myc/TCL1 小鼠中分离的恶性 B 细胞的存活和增殖[1]。
SRX3305 (0.5-2 μM；48 小时) 可破坏 CLL 中基质对细胞存活的支持作用以及趋化因子诱导的细胞迁移[1]。
SRX3305 (0.5-2 μM；48 小时) 可克服 MEC-1 细胞中 TME 诱导的存活信号通路。[1]。
SRX3305 (0.1-100 μM；72 小时) 对伊布替尼耐药的 HG-3 细胞具有活性[1]。
SRX3305 (10 nM-100 μM；48 小时) 在 Mino 细胞中的 IC50 为 1 nM，在 JeKo-1 细胞中为 58 nM，在 Granta 细胞中为 1.1 μM，在 JeKo-1 BTK C481S 突变细胞中为 1 μM，在 Mino BTK C481S 突变细胞中为 47 nM[2]。
SRX3305 (0.375-2 μM；48 小时) 对健康供体外周血单核细胞 (PBMC) 或周围健康基质细胞的毒性极低，对健康供体 B 细胞的毒性也很低[2]。
SRX3305 (0.1-10 μM；48 小时) 对原发性 Eμ-Myc 肿瘤样本具有抗肿瘤作用[2]。
SRX3305 (0.01-0.5 μM；1 小时) 可阻断 BTK 和 AKT 的激活[2]。
SRX3305 (0.01-1 μM；1 小时) 在 MCL 细胞和伊布替尼耐药的 MCL 细胞中显示出更高的疗效[2]。
在抑制剂洗脱实验后，SRX3305 (1 小时) 仍能抑制 Mino 细胞中的 BTK 和 AKT 磷酸化[2]。
SRX3305 (0.5-2 μM; 24 小时) 通过诱导 S/G2 期细胞周期停滞和促进细胞凋亡来抑制 JeKo-1 和 Mino 细胞增殖[2]。

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

SRX3305 相关抗体:

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.
分子量

424.47

Formula

C22H20N2O5S
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

SRX3305 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    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.

Keywords:

SRX33052409965-28-0SRX 3305SRX-3305PI3KBtkPhosphoinositide 3-kinaseBruton tyrosine kinaseBTK/PI3K/BRD4 inhibitorapoptosismicroenvironment-mediated survival signalsCXCL-12CXCL-13CLLDLBCLMCLInhibitorinhibitorinhibit

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