Kp7-6 - CAS:629628-53-1

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Kp7-6

目录号 : KM2318 CAS No. : 629628-53-1 纯度 : 98%

Data Sheet 产品使用指南

Kp7-6，一种 Fas 模拟肽，是一种 Fas/FasL 拮抗剂。Kp7-6 保护细胞免受 Fas 介导的细胞凋亡，并保护小鼠免受 Fas 介导的肝损伤。

规格	价格	是否有货	数量
1mg		In-stock
5mg		In-stock
10mg		In-stock

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生物活性

Kp7-6, a Fas mimetic peptide, is a Fas/FasL antagonist. Kp7-6 protects cells from Fas-mediated apoptosis, and protects mice from Fas-mediated hepatic injury.

体外研究

Kp7-6 (1 h, 0.1-5 mM) can dose dependently inhibit apoptosis of CM cells, RINm5F cells, and isolated mouse pancreatic beta cells induced by human islet amyloid peptide (hA), and has stronger activity in cultured insulinoma cell lines.
Kp7-6 (5 mM) can inhibit the activation of hA induced activated caspase-8, phosphorylated JNK1, and activated caspase-3 in isolated mouse islets when used as a pretreatment or post-treatment.
Kp7-6 (300 μM; 2 h) can effectively inhibit the binding of FasL to Fas receptor in solid-phase ELISA experiments.
Kp7-6 (12.5-100 μM; 300 s) can specifically bind to FasL (Kd=11.2 μM) and Fas (Kd=13.2 μM) with similar affinity.
Kp7-6 (0-1000 μM; 25 h) can dose dependently protect Jurkat cells from FasL induced cytotoxicity, with a cell survival rate of>90% at a concentration of 1000 μM, and no toxicity when acting alone on Jurkat cells.
Kp7-6 (0-1000 μg/mL; 3 h) can dose dependently inhibit FasL induced apoptosis in Jurkat cells.
Kp7-6 (1 mM; 2 h) can activate the NF - κ B signaling pathway (via I κ B α phosphorylation) in Jurkat cells stimulated by FasL, and inhibit the phosphorylation of ERK1/2 without altering the activation level of JNK.

Apoptosis Analysis

Cell Line:

CM insulinoma cells, RINm5F insulinoma cells, isolated murine islet β-cells

Concentration:

0.1 mM, 0.5 mM, 1 mM, 5 mM, 10 mM

Incubation Time:

1 hour

Result:

Dose-dependently suppressed hA-evoked apoptosis.
Partially but significantly suppressed apoptosis in CM and RINm5F cells at 0.5-1 mM.
Completely suppressed apoptosis in both cell lines at 5 mM.
Exhibited more potent protective effect in cultured cell lines than in isolated islets.
Effectively inhibited apoptosis in all three β-cell systems.
Showed similar rescue effect between cultured cell lines and islet β-cells.

Cell Cytotoxicity Assay

Cell Line:	Jurkat cells
Concentration:	10, 100, 1000 μM
Incubation Time:	1 h (preincubation with FasL); 24 h (incubation with cells before [³H]thymidine pulsing)
Result:	Showed dose-dependent inhibitory activity against FasL-induced cytotoxicity. Protected >90% of Jurkat cells from Fas-mediated cytotoxicity at the highest tested concentration. Did not mediate cytotoxicity to Jurkat cells at the tested concentrations.

Apoptosis Analysis

Cell Line:	Jurkat cells
Concentration:	300, 1000 μg/mL
Incubation Time:	3 hours
Result:	Dose-dependently reduced the percentage of annexin V-positive apoptotic Jurkat cells treated with FasL. Reduced apoptotic cells to 31.5% at 300 μg/mL, and to 21.5% at 1000 μg/mL, compared to 49.6% apoptotic cells with FasL alone.

Western Blot Analysis

Cell Line:	Jurkat cells
Concentration:	1 mM
Incubation Time:	2 h (preincubation with cells before FasL treatment)
Result:	Enhanced phosphorylation of IκBα in the presence of FasL at 5 min. Significantly inhibited phosphorylation of ERK1/2 at 5-30 min compared to treatment with FasL alone. Had no effect on JNK activation.

体内研究

Kp7-6 (3 mg per mouse; i.p.); A single dose can significantly alleviate the liver injury induced by ConA in C57BL-6 mice, which can be verified by the decrease in serum ALT and AST activity.
Kp7-6 (100 mg/kg; i.p.; daily administration) can reduce the level of FasL in tumor tissue, increase the infiltration of CD8+Fas+T cells, and significantly reduce the tumor weight of Rip1-Tag2 pancreatic neuroendocrine tumor mice.

Animal Model:	C57BL-6 (8-week-old)
Dosage:	3 mg per mouse
Administration:	i.p.; single dose
Result:	Reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities significantly (P < 0.01 vs. Con A-treated mice).

Animal Model:	Rip1-Tag2 (C57BL/6 background; 12 weeks old; spontaneous pancreatic neuroendocrine tumor model)
Dosage:	100 mg/kg
Administration:	i.p.; daily
Result:	Significantly reduced tumor FasL levels compared to vehicle controls. Increased infiltration of CD8+Fas+ T cells in tumor tissues compared to vehicle controls. Significantly decreased tumor weight compared to vehicle controls. Left ACSS2 expression in tumor tissues unchanged compared to vehicle controls.

分子式

C₄₈H₅₆N₁₀O₁₅S

分子量

1077.15

CAS号

629628-53-1

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Sealed storage, away from moisture

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

溶解性数据

In Vitro:

DMSO : 100 mg/mL (92.84 mM; Need ultrasonic)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	0.9284 mL	4.6419 mL	9.2838 mL
5 mM	0.1857 mL	0.9284 mL	1.8568 mL
10 mM	0.0928 mL	0.4642 mL	0.9284 mL

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用；以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

1.

请依序添加每种溶剂： 10% DMSO → 40% PEG300 → 5% Tween-80 → 45% saline

Solubility: ≥ 2.5 mg/mL (2.32 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (2.32 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。
2.

请依序添加每种溶剂： 10% DMSO → 90% (20% SBE-β-CD in saline)

Solubility: ≥ 2.5 mg/mL (2.32 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (2.32 mM，饱和度未知) 的澄清溶液。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。
3.

请依序添加每种溶剂： 10% DMSO → 90% corn oil

Solubility: ≥ 2.5 mg/mL (2.32 mM); Clear solution

此方案可获得 ≥ 2.5 mg/mL (2.32 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。