Delving into the Latest Updates on Azurin-p28 with Synapse

Overview

Basic Info

Drug Type

Synthetic peptide

Synonyms

Azurin p28

Target

p53

Action

modulators

Mechanism

p53 modulators(Tumor protein p53 modulators)

Therapeutic Areas

Neoplasms

Active Indication

Neoplasms

Inactive Indication

Brain CancerCentral Nervous System NeoplasmsChoroid Plexus Neoplasms+ [7]

Originator Organization

University of Illinois

Active Organization

Southern Research Institute

Inactive Organization

National Cancer Institute

CDG Therapeutics, Inc.

University of Illinois

+ [1]

Drug Highest PhasePreclinical

First Approval Date-

RegulationOrphan Drug (United States)

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Structure/Sequence

Molecular FormulaC122H197N31O47S2

InChIKeyRFGPECAMUVWTJN-AWHPYGDNSA-N

CAS Registry897026-25-4

Sequence Code 165904

Source: *****

This phase I trial studies the side effects and best dose of azurin-derived cell-penetrating peptide p28 (p28) in treating patients with recurrent or progressive central nervous system tumors. Drugs used in chemotherapy, such as azurin-derived cell-penetrating peptide p28, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing.

Start Date01 Aug 2013

Sponsor / Collaborator

National Cancer Institute

NCT00914914

/ CompletedPhase 1

A Phase I Trial of p28 (Cell Penetrating Peptide) in the Treatment of Refractory Solid Tumors

The purpose of this study is to evaluate the safety of an experimental drug (p28) as a treatment for certain advanced cancers which express a protein called p53 and which have not responded to prior treatment.

Start Date01 Apr 2009

Sponsor / Collaborator

CDG Therapeutics, Inc.

100 Clinical Results associated with Azurin-p28

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100 Translational Medicine associated with Azurin-p28

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100 Patents (Medical) associated with Azurin-p28

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44

Literatures (Medical) associated with Azurin-p28

02 Sep 2024·Toxicology Research

Design and computational analysis of a novel Leptulipin-p28 fusion protein as a multitarget anticancer therapy in breast cancer

Article

Author: Nadeem, Tariq ; Bashir, Hamid ; Rehman, Hafiz Muhammad ; Khalid, Sania ; Al-Qassab, Yasamin ; Fatima, Tehreem ; Mubasher, Mian Muhammad ; Ahmad, Irfan ; Kalsoom, Maria

AbstractThe search for novel therapeutic agents to treat breast cancer has compelled the development of fusion proteins that synergize the functional benefits of different bioactive peptides. Leptulipin, derived from scorpion venom, exhibits antitumor properties. On the other hand, p28, a peptide from the bacterial protein azurin, enhances cell penetration. The current study investigated the design and computational evaluation of a Leptulipin-p28 fusion protein for breast cancer treatment. The amino acid sequences of Leptulipin and p28 were joined via a rigid linker to maintain structural and functional integrity. Secondary and tertiary structure predictions were performed using online servers of GOR-IV and I-TASSER. Physicochemical properties and solubility were analyzed using ProtParam and Protein-Sol. Validation and quality assessment of the fusion protein were confirmed through Rampage and ERRAT2. Finally, the fusion protein was docked with 2 receptors (VEGFR and Cadherin) and docked complexes were simulated on GROMACS. The Leptulipin-p28 fusion protein exhibited a stable structure exhibiting a high quality score of 92 on ERRAT and Ramachandran plot analysis highlighting 76.3% of residues in the favorable region. Docking studies with VEGFR and Cadherin receptors followed by 100 ns simulations on GROMACS showed stable complex formation. Molecular dynamics simulations confirmed the stability and robust interaction of the fusion protein-receptor complexes over time. The computational analysis indicates that the Leptulipin-p28 fusion protein holds promise as a multitarget therapeutic agent in breast cancer. The current findings warrant further investigation through in vitro and in vivo studies to validate the current outcomes.

13 Oct 2023·ACS Pharmacology & Translational Science

Novel Inhibitor of Mixed-Lineage Kinase Domain-Like Protein: The Antifibrotic Effects of a Necroptosis Antagonist

Article

Author: Bae, Sang Hyun ; Kwon, Ye-Mi ; Park, Sunyou ; Jun, Dae Won ; Lee, Jung Yeol ; Choi, Myeong A. ; Kim, Hye Young ; Hong, Eunmi ; Lee, Seung Min ; Lee, Ju Yeon ; Lee, A. Hyeon ; Park, Gye Ryeol ; Lee, Ji Hoon ; Oh, Ju Hee ; Park, Jin-wan

The pseudokinase mixed-lineage kinase domain-like protein plays a crucial role in programmed cell death via necroptosis. We developed a novel mixed-lineage kinase domain-like inhibitor, P28, which demonstrated potent necroptosis inhibition and antifibrotic effects. P28 treatment directly inhibited mixed-lineage kinase domain-like phosphorylation and oligomerization after necroptosis induction, inhibited immune cell death after necroptosis, and reduced the expression of adhesion molecules. Additionally, P28 treatment reduced the level of activation of hepatic stellate cells and the expression of hepatic fibrosis markers induced by necroptosis stimulation. Unlike the necrosulfonamide treatment, the P28 treatment did not induce cytotoxicity. Finally, the cysteine covalent bonding of P28 was confirmed by liquid chromatography-tandem mass spectrometry.

01 Jul 2023·Molecular Cell

Glucose-induced CRL4COP1-p53 axis amplifies glycometabolism to drive tumorigenesis

Article

Author: Chen, Xing ; Huang, Niu ; Wang, Fengchao ; Zhang, Xiaozhe ; Zhao, Li ; Chen, Hao ; Luo, Yifan ; Su, Yang ; Xiao, Yihang ; Chow, Billy Kwok Chong ; Rao, Feng ; Wu, Mingxuan ; Wei, Xiayun ; Jin, Wenfei ; Zhang, Hongyun ; Fu, Qiuyu ; Nie, Siyue ; Zhang, Peitao ; Ren, Yan ; Wang, Huifang ; Pu, Weijie ; Hao, Yi ; Lin, Hong ; Zhang, Keren

The diabetes-cancer association remains underexplained. Here, we describe a glucose-signaling axis that reinforces glucose uptake and glycolysis to consolidate the Warburg effect and overcome tumor suppression. Specifically, glucose-dependent CK2 O-GlcNAcylation impedes its phosphorylation of CSN2, a modification required for the deneddylase CSN to sequester Cullin RING ligase 4 (CRL4). Glucose, therefore, elicits CSN-CRL4 dissociation to assemble the CRL4^COP1 E3 ligase, which targets p53 to derepress glycolytic enzymes. A genetic or pharmacologic disruption of the O-GlcNAc-CK2-CSN2-CRL4^COP1 axis abrogates glucose-induced p53 degradation and cancer cell proliferation. Diet-induced overnutrition upregulates the CRL4^COP1-p53 axis to promote PyMT-induced mammary tumorigenesis in wild type but not in mammary-gland-specific p53 knockout mice. These effects of overnutrition are reversed by P28, an investigational peptide inhibitor of COP1-p53 interaction. Thus, glycometabolism self-amplifies via a glucose-induced post-translational modification cascade culminating in CRL4^COP1-mediated p53 degradation. Such mutation-independent p53 checkpoint bypass may represent the carcinogenic origin and targetable vulnerability of hyperglycemia-driven cancer.

100 Deals associated with Azurin-p28

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R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Choroid Plexus Neoplasms	Discovery	United States	National Cancer Institute	01 Aug 2013
Gliosarcoma	Discovery	United States	National Cancer Institute	01 Aug 2013
Medulloblastoma	Discovery	United States	National Cancer Institute	01 Aug 2013
Oligodendroglioma	Discovery	United States	National Cancer Institute	01 Aug 2013
Solid tumor	Discovery	United States	CDG Therapeutics, Inc.	01 Apr 2009
Solid tumor	Discovery	United States	Dr. Tapas K. Das Gupta	01 Apr 2009
Brain Cancer	Discovery	-	National Cancer Institute	-
Brain Cancer	Discovery	-	University of Illinois	-
Brain Cancer	Discovery	-	CDG Therapeutics, Inc.	-
Central Nervous System Neoplasms	Discovery	United States	-	-

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