2. Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR
  3. c-Fms PI3K
  4. JMC14

JMC14 是一种具有选择性且口服有效的 PI3Kδ/CSF1R 抑制剂，对 PI3Kδ 和 CSF1R 的 IC50 分别为 12 nM 和 143 nM。JMC14 能够优先抑制 PI3Kδ 介导的细胞层面的信号传导。JMC14 在体内外均表现出对 B 细胞淋巴瘤和三阴性乳腺癌 (TNBC) 强大的抗肿瘤活性。JMC14 可用于抗肿瘤免疫的研究。

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JMC14

JMC14 Chemical Structure

CAS No. : 2256080-83-6

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JMC14 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

JMC14 is a selective and orally active PI3Kδ and CSF1R inhibitor with IC50 values of 12 nM and 143 nM, respectively. JMC14 preferentially inhibits PI3Kδ-mediated signaling at the cellular level. JMC14 demonstrates potent antitumor activity against B-cell lymphomas and triple-negative breast cancer (TNBC) in both in vitro and vivo studies. JMC14 can be used for the study of antitumor immunity[1].

IC50 & Target[1]

PI3Kα

389 nM (IC50)

PI3Kβ

890 nM (IC50)

PI3Kγ

＞10000 nM (IC50)

体外研究
(In Vitro)

JMC 14 (0-10 μM, 1 h) 通过阻断 PI3K 介导的信号传导抑制 DLBCL 细胞增殖[1]。
JMC14 (0.01-10 μM，72 h) 通过破坏 CSF1/CSF1R 信号轴及其下游通路，在 M-NFS-60 细胞中发挥强大的抗增殖活性[1]。
JMC14 (0.01-10 μM，72 h) 可抑制三阴性乳腺癌细胞的增殖[1]。

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

JMC14 相关抗体:

Cell Proliferation Assay[1]

Cell Line: M-NFS-60 myeloid leukemia cells
Concentration: 0.01, 0.1, 1, 10 μM
Incubation Time: 72 h
Result: Concentration-dependently inhibited the proliferation stimulated by CSF-1.
Had inhibitory potency on M-NFS-60 cell proliferation with IC50 values of 289 nM and 221 nM, respectively.

Cell Proliferation Assay[1]

Cell Line: TNBC 4T1, PY8119 and EMT6
Concentration: 0.1, 1, 10 μM
Incubation Time: 72 h
Result: Demonstrated moderate antiproliferative activity against all three cell lines, with IC50 values of 7.9 μM, 5.5 μM, or 6.5 μM, respectively.

Western Blot Analysis[1]

Cell Line: ABC-DLBCL TMD8 cells, GCB-DLBCL SU-DHL-6 and Pfeiffer cells
Concentration: 1 μM, 10 μM
Incubation Time: 1 h
Result: Suppressed AKT phosphorylation at S473 and T308 in a concentration-dependent manner.
Reduced AKT phosphorylation levels by approximately 40%.
Effectively inhibited the phosphorylation of downstream targets such as p70S6K1, 4E-BP1, and S6 at 1 μM.
Reduced AKT phosphorylation at S473 by 44.7%, while phosphorylation of p70S6K1 at T389 and S6 at S240/242 or S235/236 decreased by 39.7%, 55.4% or 50.6%, respectively at 10 μM.

Western Blot Analysis[1]

Cell Line: TMD8, SU-DHL-6, Pfeiffer
Concentration: 0, 0.01, 0.03, 0.1, 0.3, 1.0 μM
Incubation Time: 1 h
Result: Suppressed AKT phosphorylation at S473 and T308 in a concentration-dependent manner across all analyzed DLBCL cell lines.
Inhibited AKT phosphorylation by approximately 40% at 1 μM or 10 μM in TMD8 and Pfeiffer cells.

Western Blot Analysis[1]

Cell Line: TNBC 4T1, PY8119 and EMT6
Concentration: 0, 0.1, 0.3, 1, 10 μM
Incubation Time: 1 h
Result: Inhibited the phosphorylation of AKT, S6K, and S6, key signaling components downstream of PI3K, in a concentration-dependent manner.
was required to achieve similar levels to inhibit the phosphorylation of S6K and S6 compared to that of AKT with lower concentration.
Exerted lower potency in inhibiting Erk1/2 phosphorylation, achieving only 20% inhibition at a concentration of 10 μM.
体内研究
(In Vivo)

JMC14 (10-100 mg/kg，口服，每日一次，持续 21 天) 能够抑制 TMD8 肿瘤异种移植模型以及 DLBCL PDX 的肿瘤生长[1]。
JMC14 (100 mg/kg，口服，每日一次，持续 13 天) 在 M-NFS-60 髓系白血病模型中通过阻断 CSF1R 和 PI3K 信号通路显示出强效的活性[1]。
JMC14 (25-100 mg/kg，口服，每日一次，持续 18 天) 能够抑制 PY8119 同种异体移植瘤的生长，并重塑肿瘤微环境[1]。

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

Animal Model: TMD8 xenograft model (B-cell lymphoma), female Balb/c SCID mice[1]
Dosage: 10 mg/kg, 30 mg/kg, 100 mg/kg
Administration: Oral gavage (p.o.), once daily for 21 days
Result: Resulted in a dose-dependent inhibition of tumor growth.
Significantly inhibited the growth of xenografts with a T/C value of 17.6%.
Reduced significantly phosphorylated AKT at S473 1 h after administration at both 30 and 100 mg/kg.
Recovered phosphorylated AKT 8 h after treatment at 30 mg/kg, while inhibition of AKT phosphorylation persisted up to 8 h and was reversed up to 24 h upon treatment.
Significantly suppressed the growth of LY-24-0063 PDX, resulting in a T/C value of 35.2% at 100 mg/kg.
Exhibited marginal effect, with T/C values of 94.0% or 82.5%, respectively at 10 mg/kg or 30 mg/kg.
Animal Model: SCID mice bearing M-NFS-60 xenografts model[1]
Dosage: 100 mg/kg
Administration: Oral gavage (p.o.), once daily for 13 days
Result: Significantly suppressed tumor growth, yielding a T/C value of 25.4% at 100 mg/kg.
Observed no significant changes in body weight between treatment and control groups.
Decreased the anti-tumor effect correlated with the suppression of CSF1R and PI3K signaling pathways in the phosphorylation of CSF1R, Erk1/2, AKT, S6K and S6 in tumor tissues collected 2 h after a single dose.
Animal Model: Immune-competent model induced in PY8119 cells established in C57BL/6 mice[1]
Dosage: 25, 50, 100 mg/kg
Administration: Oral gavage (p.o.)., once daily for 18 days
Result: Inhibited the tumor growth in a dose-dependent manner.
Exhibited pronounced tumor growth inhibition with a T/C value of 26.9% at 100mg/kg.
Animal Model: Immune-competent model, PY8119 cells were orthotopically inoculated into C57BL/6 mice[1]
Dosage: 100 mg/kg
Administration: Oral gavage (p.o.), single dose, tumor tissues were collected at 2, 4, and 8 h after treatment.
Result: Effectively downregulated the phosphorylation of CSF1R, AKT, S6K, and S6 within 2 h after administration, while a longer time was needed to suppress the Erk1/2 phosphorylation.
Recovered phosphorylation of AKT and S6 partially 8 h post-treatment.
Increased the staining CD45 markedly after treatment, indicating enhanced immune cell infiltration.
Decreased the F4/80 staining, the staining of CD206 representing immunosuppressive M2 macrophages significantly particularly.
分子量

533.59

Formula

C26H34F3N7O2
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

JMC14 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:

JMC142256080-83-6JMC 14JMC-14c-FmsPI3KCSF-1 receptorcolony stimulating factor 1 receptorCSF-1RCSF1RPhosphoinositide 3-kinaseB cell malignancyTNBCM-NFS-60dual inhibitionInhibitorinhibitorinhibit

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