2. Metabolic Enzyme/Protease Stem Cell/Wnt Neuronal Signaling Apoptosis
  3. PAI-1 Ser/Thr Protease Furin MMP Notch Apoptosis
  4. TM5614 sodium

TM5614 sodium 是一种具有口服活性的特异性 PAI-1 抑制剂，其 IC50 <6.95 μM。TM5614 sodium 可阻断 PAI-1 与丝氨酸蛋白酶 (serine proteases) 或 LRP-1 之间的相互作用，增强纤溶酶生成。TM5614 sodium 恢复巨噬细胞胞葬作用，促进巨噬细胞极化。TM5614 sodium 缓解 PAI-1 介导的 Furin 抑制作用，促进 MT1-MMP 成熟，激活 NOTCH1 信号通路，抑制增殖并诱导细胞凋亡 (apoptosis)。TM5614 sodium 在小鼠骨骼肌损伤模型中促进骨骼肌再生并缓解炎症。TM5614 sodium 可用于骨骼肌损伤诱导的炎症、慢性髓系白血病相关研究。

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TM5614 sodium

TM5614 sodium Chemical Structure

CAS No. : 1247823-40-0

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TM5614 sodium 相关抗体

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MMP-1 MMP-2 MMP-3 MMP-8 MMP-9 MMP-13 MMP-14 MMP-17 ADAM10 ADAM17 MMP-7 MMP-12 MMP-10 MMP ADAM8 MMP-19

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

TM5614 sodium is an orally active and specific PAI-1 inhibitor with an IC50 of <6.95 μM. TM5614 sodium blocks the interaction between PAI-1 and serine proteases or LRP-1, and enhances plasmin generation. TM5614 sodium restores macrophage efferocytosis and promotes macrophage polarization. TM5614 sodium alleviates PAI-1-mediated inhibition of Furin, promotes MT1-MMP maturation, activates the NOTCH1 signaling pathway, inhibits proliferation and induces apoptosis. TM5614 sodium promotes skeletal muscle regeneration and alleviates inflammation in a mouse model of skeletal muscle injury. TM5614 sodium can be used in research on skeletal muscle injury-induced inflammation and chronic myeloid leukemia[1][2].

体外研究
(In Vitro)

TM5614 sodium (2 h) 可通过依赖 LRP-1 的机制增强小鼠骨髓来源 CCR2+Ly6C+ 巨噬细胞及 J774.1-GFP 细胞的胞葬作用[1]。
TM5614 (62.7 μM; 72 h) sodium 可通过抑制增殖、诱导凋亡及调控 Furin/NICD 信号通路，对 PAI-1/K562-1 和 PAI-1/K562-2 慢性髓系白血病细胞发挥直接抗肿瘤作用[2]。
TM5614 sodium 上调 Furin 的蛋白表达水平，提高细胞表面e MT1-MMP 的表达水平[2]。

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

TM5614 sodium 相关抗体:

Apoptosis Analysis[2]

Cell Line: PAI-1/K562-1 and PAI-1/K562-2 cells
Concentration: 62.7 μM
Incubation Time: 72 h
Result: Significantly increased the proportion of early and late apoptosis.
体内研究
(In Vivo)

TM5614 (10 mg/kg；口服；每日；连续 3-7 天) sodium 可通过下调促炎细胞因子表达、上调抗炎细胞因子表达并加速组织修复，在心脏毒素 (CTX) 诱导的小鼠骨骼肌损伤模型中促进骨骼肌再生并缓解炎症，增强巨噬细胞的吞噬活性 (作为胞葬作用的替代指标)，使巨噬细胞的葡聚糖摄取量提升 14.5 个百分点[1]。

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

Animal Model: C57BL/6J (12- to 20-week-old male; CTX-induced skeletal muscle injury)[1]
Dosage: 10 mg/kg
Administration: p.o.; daily; 7 consecutive days/ daily; 3 consecutive days
Result: Reduced relative mRNA expression of pro-inflammatory cytokines TNF-α, IL-1β, IFN-γ, and CCL2 in injured TA muscle on day 4 post-CTX injection.
Increased relative mRNA expression of anti-inflammatory cytokine IL-10 in injured TA muscle on day 4 post-CTX injection.
Accelerated disappearance of EBD blue staining in injured TA muscle by day 8 post-CTX injection.
Increased number of mature/restored skeletal myofibers in injured TA muscle by day 8 post-CTX injection.
Increased the percentage of CD45+CD11b+ macrophages in injured TA muscle that took up TRITC-labeled dextran from 23.9% to 38.4%.
分子量

424.81

Formula

C23H14ClN2NaO3
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

TM5614 sodium 相关分类

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  • 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:

TM56141247823-40-0TM 5614TM-5614PAI-1Ser/Thr ProteaseFurinMMPNotchApoptosisPlasminogen activator inhibitor-1Serine proteasesSerine endopeptidasesThreonine proteasesMatrix metalloproteinasesPAI-1/K562-2 cellschronic myeloid leukemiaLRP-1J774.1-GFP cellsPAI-1/K562-1 cellsmacrophage polarizationCTX-induced mouse skeletal muscle injury modelmurine bone marrow-derived CCR2+Ly6C+ macrophagesmacrophage efferocytosisInhibitorinhibitorinhibit

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