1. Apoptosis
  2. MDM-2/p53
  3. ReACp53

ReACp53 

Cat. No.: HY-P0121 Purity: 99.65%
Handling Instructions

ReACp53 could inhibit p53 amyloid formation and rescue p53 function in cancer cell lines.

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

Custom Peptide Synthesis

ReACp53 Chemical Structure

ReACp53 Chemical Structure

Size Price Stock Quantity
1 mg USD 95 In-stock
Estimated Time of Arrival: December 31
5 mg USD 290 In-stock
Estimated Time of Arrival: December 31
10 mg USD 430 In-stock
Estimated Time of Arrival: December 31
25 mg USD 770 In-stock
Estimated Time of Arrival: December 31
50 mg USD 1250 In-stock
Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

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Description

ReACp53 could inhibit p53 amyloid formation and rescue p53 function in cancer cell lines.

IC50 & Target

p53 amyloid formation[1].

In Vitro

ReACp53 penetrates into HGSOC primary cancer cells and converts mutant p53 from a punctate state into soluble WT-like p53. ReACp53 also induces cancer cell death, cell cycle arrest and results in p53 degradation. ReACp53 specifically affects cell viability and proliferation of cancer cells bearing mutant p53 but not wild type when grown as organoids[1].

In Vivo

Only mutant p53-bearing tumors in the ReACp53-treated mice cohorts are 80-90% smaller in weight than the control cohort, confirming the ability of ReACp53 to limit tumor proliferation and shrink tumors. A significant reduction of Ki67 positive cells is evident in ReACp53-treated OVCAR3 xenografts, indicative of a reduced proliferative index. Similar results are observed in the minimal residual disease model. In the paradigm, administration of ReACp53 results in a significant increase in p21 and MDM2 transcription in OVCAR3 but not MCF7 xenografts. A significantly increased population is also found in G0/G1 phase, supporting proliferative arrest upon ReACp53 administration in vivo[1].

Molecular Weight

2617.13

Formula

C₁₀₈H₂₀₆N₅₂O₂₄

Sequence

H-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Pro-Ile-Leu-Thr-Arg-Ile-Thr-Leu-Glu-OH

Sequence Shortening

HRRRRRRRRRRPILTRITLE-OH

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -80°C 2 years
  -20°C 1 year
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : ≥ 50 mg/mL (19.10 mM)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 0.3821 mL 1.9105 mL 3.8210 mL
5 mM 0.0764 mL 0.3821 mL 0.7642 mL
10 mM 0.0382 mL 0.1910 mL 0.3821 mL
*Please refer to the solubility information to select the appropriate solvent.
References
Animal Administration
[1]

Mice[1]
In the minimal residual disease model, three cohorts of mice (n=3) are injected with a matrigel/OVCAR3 (p53 mutant) suspension on one flank and with a matrigel/MCF7 (WT p53) suspension on the other flank. Treatment is started the same day. In both models, the treatment phase consist of three weeks of daily IP injections with 15 mg/kg of ReACp53, sequence-scrambled control peptide or vehicle alone[1].

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

References
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Keywords:

ReACp53ReACp 53ReACp-53MDM-2/p53Inhibitorinhibitorinhibit

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ReACp53
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HY-P0121
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