1. Cytoskeleton Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR Apoptosis
  2. Integrin FAK mTOR Apoptosis
  3. T7 Peptide

T7 Peptide is a protein synthesis inhibitor and anti-angiogenic agent, with a Kd of 10 nM for human transferrin receptor. T7 Peptide inhibits the phosphorylation of focal adhesion kinase, the activation of phosphatidylinositol 3-kinase and Akt, the kinase activity of mTOR, as well as the phosphorylation of 4E-BP1 in endothelial cells. T7 Peptide induces G0/G1 cell cycle arrest, apoptosis and protective autophagy in hepatocellular carcinoma cells, and suppresses tumor growth in mouse models. T7 Peptide is applicable to research related to cancer, glioblastoma, hepatocellular carcinoma and glioma.

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T7 Peptide

T7 Peptide Chemical Structure

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Description

T7 Peptide is a protein synthesis inhibitor and anti-angiogenic agent, with a Kd of 10 nM for human transferrin receptor. T7 Peptide inhibits the phosphorylation of focal adhesion kinase, the activation of phosphatidylinositol 3-kinase and Akt, the kinase activity of mTOR, as well as the phosphorylation of 4E-BP1 in endothelial cells. T7 Peptide induces G0/G1 cell cycle arrest, apoptosis and protective autophagy in hepatocellular carcinoma cells, and suppresses tumor growth in mouse models. T7 Peptide is applicable to research related to cancer, glioblastoma, hepatocellular carcinoma and glioma[1][2][3][4].

IC50 & Target

αvβ3

 

In Vitro

T7 peptide (4.5 μM; 21 h) specifically inhibits cap-dependent translation in C-PAE cells without affecting cap-independent translation[1].
T7 peptide (4.5 μM) inhibits total protein synthesis in MLEC-wt cells[1].
T7 peptide (4.5 μM) does not inhibit total protein synthesis in MLEC-β3 null cells, indicating dependence on αVβ3 integrin for this activity[1].
T7 peptide (4.5 μM) does not inhibit total protein synthesis in MEF-wt cells, indicating αVβ3 integrin expression is essential but not sufficient for this activity[1].
T7 peptide (4.5 μM) does not inhibit total protein synthesis in non-endothelial cell lines, demonstrating endothelial cell specificity for this activity[1].
The T7 peptide (0.25-2 μM; 6-24 h) significantly reduces viability of Huh-7 and Hep3B human HCC cells in a concentration- and time-dependent manner, but has minimal effect on normal human liver L-02 cells[3].
The T7 peptide (0.25-1 μM; 24 h) induces significant apoptosis (both early and late) in Huh-7 and Hep3B human HCC cells[3].
The T7 peptide (0.25-1 μM; 24 h) induces G0/G1 cell cycle arrest in Huh-7 and Hep3B human HCC cells[3].
The T7 peptide (0.5-1 μM; 24 h) upregulates pro-apoptotic Bax, Fas, and FasL and downregulates anti-apoptotic Bcl-2 in a concentration-dependent manner in Huh-7 and Hep3B human HCC cells[3].
The T7 peptide (0.5-1 μM; 24 h) induces autophagy in Huh-7 and Hep3B human HCC cells by upregulating Beclin-1, Atg5, and LC3-II in a concentration-dependent manner[3].
The T7 peptide (1 μM; 24 h) has enhanced apoptotic effect in Huh-7 and Hep3B human HCC cells when autophagy is inhibited[3].
The T7 peptide (0.5-1 μM; 24 h) induces autophagy in Huh-7 and Hep3B human HCC cells via inhibition of the Akt/mTOR signaling pathway, and co-treatment with Akt/mTOR inhibitors enhances this autophagic response[3].
T7 peptide (5 μM; 2 h at 37 °C) modified LDL shows enhanced cellular uptake in bEnd.3 and C6 cells via synergistic mediation by TfR and LDLR[4].
T7 peptide (0.5-6% molar ratio; 4 h at 37 °C) modification enhances BBB penetration and subsequent C6 glioma cell uptake, with optimal efficacy observed at a 4% molar ratio of T7 to LDL[4].

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

Cell Viability Assay[3]

Cell Line: human hepatocellular carcinoma (HCC) Huh-7, Hep3B cells; normal human liver L-02 cells
Concentration: 0.25-2 μM (24 h); 1 μM (6, 12, 24 h)
Incubation Time: 24 h (0.25, 0.5, 1, 2 μM); 6 h, 12 h, 24 h (1 μM)
Result: Significantly decreased viability of Huh-7 and Hep3B cells in a concentration- and time-dependent manner.
Had little effect on viability of L-02 cells.

Apoptosis Analysis[3]

Cell Line: human HCC Huh-7, Hep3B cells
Concentration: 0.25-1 μM
Incubation Time: 24 h
Result: Significantly enhanced apoptotic cell death, with increases in both early and late apoptosis in Huh-7 and Hep3B cells.

Cell Cycle Analysis[3]

Cell Line: human HCC Huh-7, Hep3B cells
Concentration: 0.25-1 μM
Incubation Time: 24 h
Result: Arrested cells in the G0/G1 phase, with corresponding decreases in S phase and G2/M phase populations.

Western Blot Analysis[3]

Cell Line: human HCC Huh-7, Hep3B cells
Concentration: 0.5-1 μM
Incubation Time: 24 h
Result: Upregulated expression of Bax, Fas, and FasL, and downregulated expression of Bcl-2 in a concentration-dependent manner.
In Vivo

The T7 peptide (2.5-5 mg/kg; i.p.; every other day) dose-dependently suppresses Hep3B xenograft tumor growth in nude mice, achieving a ~27% tumor cell apoptotic rate at the 5 mg/kg dose via pathways involving reduced Akt/mTOR phosphorylation, increased Bax expression, and decreased Bcl-2 expression[3].
T7 peptide (4% molar ratio; 0.5 mg/kg; intravenous tail vein injection) conjugation to LDL particles enhances accumulation in intracranial glioma tissue in female ICR mice bearing C6 glioma[4].

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

Animal Model: BALB/c athymic nude (male, 5-6 weeks old, 18-22 g, Hep3B human HCC cells xenograft)[3]
Dosage: 2.5 mg/kg; 5 mg/kg
Administration: i.p.; every other day;30 days
Result: Suppressed Hep3B xenograft tumor growth with tumor growth at day 35.
Increased tumor tissue apoptotic.
Upregulated Bax protein expression at both doses.
Downregulated Bcl-2 protein expression at both doses.
Reduced phosphorylated Akt (Ser473) and phosphorylated mTOR (Ser2448) levels at both doses, with no significant change in total Akt or mTOR protein levels.
Caused no obvious mouse weight loss with either dose.
Molecular Weight

3018.36

Formula

C137H189N33O39S3

Sequence

Thr-Met-Pro-Phe-Leu-Phe-Cys-Asn-Val-Asn-Asp-Val-Cys-Asn-Phe-Ala-Ser-Arg-Asn-Asp-Tyr-Ser-Tyr-Trp-Leu (Disulfide bridge: Cys7-Cys13)

Sequence Shortening

TMPFLFCNVNDVCNFASRNDYSYWL (Disulfide bridge: Cys7-Cys13)

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
References
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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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T7 Peptide
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HY-P10323
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