TAT-N24
TAT-N24 is a cell-penetrating peptide and also an inhibitor of p55PIK. TAT-N24 disrupts the interactions between p55PIK and p53, PCNA or Rb, blocks the p53-dependent ubiquitin-mediated degradation process, and inhibits the nuclear translocation and phosphorylation of NF-κB p65. TAT-N24 enhances MMS-induced p53-dependent cell apoptosis, inhibits DNA synthesis, reduces the expression of Cyclin D1, and induces cell cycle arrest at the G0/G1 or S phase. TAT-N24 inhibits the activation of NLRP3 and NLRC4 inflammasomes, reduces the expression of ZBP1-PANoptosome components, and suppresses PANoptosis. TAT-N24 can be used in research related to leukemia, colon cancer, cervical cancer, liver cancer, corneal neovascularization, restenosis and acute glaucoma.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C198H313N63O56S3
- Molecular Weight:4568.19
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
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Help & FAQs
Biologische Aktivität
Beschreibung
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p55PIK |
p53 |
PCNA |
Rb |
NF-κB |
p65 |
Cyclin D1 |
NLRP3 |
NLRC4 |
In Vitro
TAT-N24 efficiently localizes to the nucleus of HeLa cells[1].
TAT-N24 (50-100 μg/mL; 24-72 h) inhibits the proliferation of HeLa cells in a time- and dose-dependent manner, with significant effects observed at 50 μg/mL and 100 μg/mL after 72 h[1].
TAT-N24 (50-100 μg/mL; 24-72 h) inhibits the proliferation of HepG2 cells in a time- and dose-dependent manner, with significant effects observed at 50 μg/mL and 100 μg/mL after 72 h[1].
TAT-N24 (120 μg/mL; 3 days) induces differentiation of HL60 human leukemia cells into the monocyte lineage, as shown by increased CD11b, CD14, CCL2, CCR, and CD163 expression, and synergizes with ATRA to enhance granulocytic marker expression[3].
TAT-N24 (10-100 μg/mL; 12-36 h) does not induce significant apoptosis in SW480 cells alone, but enhances MMS-induced p53-dependent apoptosis in a dose- and time-dependent manner, with maximum effects seen at ≥50 μg/mL TAT-N24 combined with 200 μM MMS over 36 h[1].
TAT-N24 alone downregulates p53 and p53-dependent apoptosis-related gene expression in SW480 cells, but acts synergistically with MMS to upregulate these genes, consistent with enhanced p53-dependent apoptosis[1].
TAT-N24 does not alter p53-dependent apoptosis-related gene expression in p53-null H1299 cells, either alone or in combination with MMS, confirming its gene-regulatory effects are p53-dependent[1].
TAT-N24 (120 μg/mL; 1-4 days) inhibits proliferation, induces G0/G1 cell cycle arrest, and reduces DNA synthesis in HL60 human leukemia cells when treated at 120 μg/mL for up to 4 days[3].
TAT-N24 (120 μg/mL; 3-48 hours) inhibits proliferation, induces megakaryocytic differentiation, and blocks p55PIK-mediated pro-proliferative signaling in K562 human chronic myeloid leukemia cells, with dose-dependent upregulation of TLR2 and TLR4 at 60-180 μg/mL[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HeLa cells
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Concentration:50 μg/mL; 100 μg/mL
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Incubation Time:24 h; 48 h; 72 h
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Result:Inhibited cell proliferation in a time- and dose-dependent manner.
Significantly reduced the number of viable cells at 72 h compared to untreated controls.
Reduced colony formation at 50 μg/mL and 100 μg/mL for 72 h.
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Cell Line:HepG2 cells
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Concentration:50 μg/mL; 100 μg/mL
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Incubation Time:24 h; 48 h; 72 h
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Result:Inhibited cell proliferation in a time- and dose-dependent manner.
Significantly reduced the number of viable cells at 72 h compared to untreated controls.
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Cell Line:SW480 cells
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Concentration:10 μg/mL (in combination with 200 μM MMS); 50 μg/mL (in combination with 200 μM MMS); 100 μg/mL (alone); 10-90 μg/mL (in combination with 200 μM MMS); combined with 100, 200, 300 μM MMS
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Incubation Time:36 h (10 μg/mL + MMS); 12 h, 24 h, 36 h (50 μg/mL + MMS); 36 h (10-90 μg/mL + MMS); 36 h (TAT-N24 + 100, 200, 300 μM MMS)
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Result:Did not induce significant apoptosis when used alone at 100 μg/mL.
Doubled the apoptosis rate induced by 200 μM MMS at 10 μg/mL.
Achieved maximum enhancement of MMS-induced apoptosis at concentrations ≥50 μg/mL with 200 μM MMS.
Increased synergistic effect on MMS-induced apoptosis over 12-36 h of incubation.
Showed most pronounced enhancement of MMS-induced apoptosis at lower MMS concentrations (100-200 μM).
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Cell Line:human HL60 leukemia cells
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Concentration:120 μg/mL
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Incubation Time:1-4 days (cell counting); 48 h (cell cycle and DNA synthesis assays)
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Result:Reduced HL60 cell number by 45% compared to the control fusion protein after 4 days.
Induced cell cycle arrest at the G0/G1 transition, with 63.5% of cells in G0/G1 phase (compared to 51.4% in control cells), and decreased the percentage of cells in S phase to 23.7% and G2/M phase to 12.8%.
Reduced DNA synthesis, with only 45.2% of cells testing BrdU-positive (compared to 69.1% in control cells), and reduced BrdU fluorescence intensity to 0.37 times that of control cells.
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Cell Line:human HL60 leukemia cells
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Concentration:120 μg/mL
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Incubation Time:3 days
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Result:Increased the percentage of CD11b-positive HL60 cells to 26.2% (compared to 5.4% in control fusion protein-treated cells) and increased CD11b mRNA expression by 6.8-fold.
Strongly increased the percentage of CD14-positive cells to 46.5% (compared to 7.3% in control fusion protein-treated cells).
Upregulated mRNA expression of monocyte lineage markers CCL2, CCR, and CD163 by 3.3-, 2.8-, and 4.4-fold, respectively, while only slightly increasing granulocyte marker CD38 mRNA expression (3.1-fold).
When combined with ATRA, synergistically increased CD11b-positive cells to 70.4% (compared to 18.1% with TAT-N24 alone and 31.7% with ATRA alone), but did not further increase CD14-positive cell percentage beyond levels seen with TAT-N24 alone.
In Vivo
TAT-N24 (2 mg per 200 mL lipid emulsion; i.v.; every 2 days; 10-14 days) reduces HL60 leukemia xenograft tumor weight by 54% in athymic nude mice, inhibits tumor cell DNA synthesis, and induces differentiation, with no observed significant toxicity[3].
TAT-N24 (2 mg per 200 mL lipid emulsion; i.v.; every 2 days; 10-14 days) inhibits K562 leukemia xenograft growth and induces tumor cell differentiation via upregulation of TLR2 and TLR4 in athymic nude mice[3].
TAT-N24 (10 mg; local application via pluronic gel; single dose; immediately post-injury) reduces balloon injury-induced neointimal formation and VSMC proliferation in Rattus norvegicus carotid arteries[4].
TAT-N24 (2 μg; intravitreal; single injection) protects retinal ganglion cells from acute glaucoma-induced death by inhibiting ZBP1-PANoptosome-mediated PANoptosis, suppressing NLRP3 and NLRC4 inflammasome activation, reducing microglial activation, and attenuating pyroptosis, apoptosis, and necroptosis[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (female, 8-12 weeks old, 180-200 g, corneal suture model)[2]
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Dosage:0.9%
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Administration:topical; six times daily; 7 consecutive days
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Result:Reduced corneal neovascularization area scores and grade scores on days 3 and 7 compared to untreated models.
Decreased corneal inflammatory cell infiltration and neovascularization on days 3 and 7.
Lowered fluorescence intensity of HIF-1α and NF-κB p65 in corneal tissue on days 3 and 7.
Reduced mRNA levels of HIF-1α, VEGF-A, NF-κB p65, TNF-α, IL-1β, and IL-6 in treated corneal tissue on days 3 and 7.
Decreased protein levels of HIF-1α and NF-κB p65 in treated corneal tissue compared to untreated models.
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Animal Model:Athymic nude (male, 8-10 weeks old, 22-24 g, HL60 cell subcutaneous xenograft)[3]
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Dosage:2 mg per 200 mL lipid emulsion
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Administration:i.v.; every 2 days; 10-14 days
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Result:Reduced mean xenograft tumor weight by 54% compared to the control fusion protein.
Decreased DNA synthesis in tumor xenografts.
Induced expression of the differentiation marker Cd11b in tumor tissue.
Caused no significant changes in mouse appearance, weight, serum glucose levels, or hepatic enzyme activities.
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Animal Model:Athymic nude (male, 8-10 weeks old, 22-24 g, K562 cell subcutaneous xenograft)[3]
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Dosage:2 mg per 200 mL lipid emulsion
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Administration:i.v.; every 2 days; 10-14 days
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Result:Inhibited growth of K562 tumor xenografts.
Induced expression of the differentiation markers TLR2 and TLR4 in tumor tissue.
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Animal Model:Sprague-Dawley (adult male, 250-300 g, balloon dilation injury of left common carotid artery)[4]
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Dosage:10 mg
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Administration:local application via pluronic gel; single dose; immediately post-injury
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Result:Reduced neointimal formation, decreasing the intima-to-media ratio and intimal area relative to control.
Reduced the number of PCNA-positive cells (a marker of VSMC proliferation).
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Animal Model:C57BL/6 (adult female, 6-8 weeks old, acute ocular hypertension-induced acute glaucoma model)[5]
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Dosage:2 μg
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Administration:intravitreal; single injection
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Result:Mitigated reductions in ganglion cell layer and overall retinal thickness caused by acute ocular hypertension injury.
Preserved the number of retinal ganglion cells identified by Brn3a and RBPMS staining.
Reduced retinal apoptotic cell count measured by TUNEL staining.
Decreased acute ocular hypertension-induced upregulation of pyroptosis-associated proteins (NLRP3, NLRC4, ASC, GSDMD, Caspase-1, IL-1β) and GSDMD mRNA.
Inhibited microglial activation measured by Iba1-positive staining intensity.
Attenuated acute ocular hypertension-induced changes in apoptosis-associated markers (decreased Bcl-2/Bax ratio, elevated cleaved-Caspase-3).
Suppressed acute ocular hypertension-induced upregulation of necroptosis-associated molecules (RIPK1, RIPK3, MLKL mRNA and protein, phosphorylated RIPK1, RIPK3, MLKL).
Reduced acute ocular hypertension-induced upregulation of ZBP1-PANoptosome components (ZBP1, Caspase-8 mRNA and protein, RIPK1, RIPK3).
Chemical Information
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Molecular Weight 4568.19
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Formel C198H313N63O56S3
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Sequence
Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Met-Asp-Arg-Asp-Asp-Ala-Asp-Trp-Arg-Glu-Val-Met-Met-Pro-Tyr-Ser-Thr-Glu-Leu-Ile-Phe-Tyr-Ile-Glu
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Sequence Shortening
YGRKKRRQRRRMDRDDADWREVMMPYSTELIFYIE
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[2]. Huang J, et al. A cell-permeable peptide inhibitor of p55PIK signaling alleviates suture-induced corneal neovascularization and inflammation. Heliyon. 2023 Apr;9(4):e14869. [Content Brief]
[5]. Li F, et al. TAT-N24 enhances retinal ganglion cell survival by suppressing ZBP1-PANoptosome-mediated PANoptosis in an acute glaucoma mouse model. Experimental eye research. 2025 Feb;251:110244. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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