1. Apoptosis Cell Cycle/DNA Damage NF-κB MAPK/ERK Pathway
  2. Apoptosis PERK NF-κB Caspase JNK
  3. Kp7-6

Kp7-6 is a Fas mimetic peptide and also a Fas/FasL antagonist. Kp7-6 specifically binds to Fas and FasL, disrupts receptor complexes, and blocks downstream apoptosis signaling pathways. Kp7-6 inhibits the phosphorylation of ERK1-2, induces the phosphorylation of IκBα, and activates NF-κB. Kp7-6 inhibits the activation of caspase-8, caspase-3 and JNK, and suppresses human amylin-induced β-cell apoptosis. Kp7-6 inhibits FasL-induced lymphoid cytotoxicity and apoptosis. Kp7-6 reduces local tumor FasL expression, increases CD8+Fas+ T cell infiltration, and decreases tumor volume in pancreatic neuroendocrine tumor models. Kp7-6 prevents concanavalin A-induced liver injury in mice. Kp7-6 is applicable to research related to type 2 diabetes, concanavalin A-induced hepatitis and pancreatic neuroendocrine tumors.

For research use only. We do not sell to patients.

Custom Peptide Synthesis

Kp7-6

Kp7-6 Chemical Structure

CAS No. : 629628-53-1

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Based on 2 publication(s) in Google Scholar

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Description

Kp7-6 is a Fas mimetic peptide and also a Fas/FasL antagonist. Kp7-6 specifically binds to Fas and FasL, disrupts receptor complexes, and blocks downstream apoptosis signaling pathways. Kp7-6 inhibits the phosphorylation of ERK1-2, induces the phosphorylation of IκBα, and activates NF-κB. Kp7-6 inhibits the activation of caspase-8, caspase-3 and JNK, and suppresses human amylin-induced β-cell apoptosis. Kp7-6 inhibits FasL-induced lymphoid cytotoxicity and apoptosis. Kp7-6 reduces local tumor FasL expression, increases CD8+Fas+ T cell infiltration, and decreases tumor volume in pancreatic neuroendocrine tumor models. Kp7-6 prevents concanavalin A-induced liver injury in mice. Kp7-6 is applicable to research related to type 2 diabetes, concanavalin A-induced hepatitis and pancreatic neuroendocrine tumors[1][2][3].

In Vitro

Kp7-6 (1 h, 0.1-5 mM) dose-dependently inhibits apoptosis of CM cells, RINm5F cells and isolated mouse islet β-cells induced by human islet amyloid polypeptide (hA), with stronger activity in cultured insulinoma cell lines[1].
Kp7-6 (5 mM) inhibits the activation of hA-induced active caspase-8, phosphorylated JNK1 and active caspase-3 in isolated mouse islets when used as a pre-treatment or post-treatment[1].
Kp7-6 (300 μM; 2 h) potently inhibits the binding of FasL to Fas receptors in solid-phase ELISA assays[2].
Kp7-6 (12.5-100 μM; 300 s) binds specifically to FasL (Kd = 11.2 μM) and Fas (Kd = 13.2 μM) with comparable affinity[2].
Kp7-6 (0-1000 μM; 25 h) dose-dependently protects Jurkat cells against FasL-induced cytotoxicity, with a cell survival rate of >90% at the concentration of 1000 μM, and exhibits no toxicity when applied alone to Jurkat cells[2].
Kp7-6 (0-1000 μg/mL; 3 h) dose-dependently inhibits FasL-induced apoptosis in Jurkat cells[2].
Kp7-6 (1 mM; 2 h) activates the NF-κB signaling pathway (via IκBα phosphorylation) in FasL-stimulated Jurkat cells, inhibits ERK1/2 phosphorylation, and does not alter the activation level of JNK[2].

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

Apoptosis Analysis[1]

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 h
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[2]

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[2]

Cell Line: Jurkat cells
Concentration: 300, 1000 μg/mL
Incubation Time: 3 h
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[2]

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.
In Vivo

Kp7-6 (3 mg per mouse; i.p.; single dose) significantly reduces Con A-induced liver injury in C57BL-6 mice, as measured by decreased serum ALT and AST activities[2].
Kp7-6 (100 mg/kg; i.p.; daily) reduces tumor FasL levels, increases CD8+Fas+ T cell infiltration, and significantly decreases tumor weight in Rip1-Tag2 pancreatic neuroendocrine tumor mice[3].

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

Animal Model: C57BL-6 (8-week-old)[2]
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)[3]
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.
Molecular Weight

1077.15

Formula

C48H56N10O15S2

CAS No.
Appearance

Solid

Color

White to off-white

Sequence

Tyr-Cys-Asp-Glu-His-Phe-Cys-Tyr (Disulfide bridge:Cys2-Cys7)

Sequence Shortening

YCDEHFCY (Disulfide bridge:Cys2-Cys7)

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Sealed storage, away from moisture

Powder -80°C 2 years
-20°C 1 year

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (92.84 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 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
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

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

    This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

    Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
  • Protocol 2

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

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

    This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

    Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration: mg/mL
Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation

Purity: 99.28%

References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 0.9284 mL 4.6419 mL 9.2838 mL 23.2094 mL
5 mM 0.1857 mL 0.9284 mL 1.8568 mL 4.6419 mL
10 mM 0.0928 mL 0.4642 mL 0.9284 mL 2.3209 mL
15 mM 0.0619 mL 0.3095 mL 0.6189 mL 1.5473 mL
20 mM 0.0464 mL 0.2321 mL 0.4642 mL 1.1605 mL
25 mM 0.0371 mL 0.1857 mL 0.3714 mL 0.9284 mL
30 mM 0.0309 mL 0.1547 mL 0.3095 mL 0.7736 mL
40 mM 0.0232 mL 0.1160 mL 0.2321 mL 0.5802 mL
50 mM 0.0186 mL 0.0928 mL 0.1857 mL 0.4642 mL
60 mM 0.0155 mL 0.0774 mL 0.1547 mL 0.3868 mL
80 mM 0.0116 mL 0.0580 mL 0.1160 mL 0.2901 mL
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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.

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