Description

Product Description

ATWLPPRAANLLMAAS is a synthetic chimeric peptide designed to interfere with tumor angiogenesis and malignant cell growth. As a multifunctional bioactive peptide, ATWLPPRAANLLMAAS demonstrates a significant ability to suppress tumorigenic processes in hepatocellular carcinoma and other solid tumors.

Structurally, ATWLPPRAANLLMAAS integrates multiple amino acid sequences associated with anti-angiogenic and pro-apoptotic signaling pathways. By targeting the molecular mechanisms governing endothelial proliferation and vascular formation, it effectively disrupts tumor vascularization—an essential step for cancer growth and metastasis.

Research has shown that ATWLPPRAANLLMAAS can inhibit the proliferation, viability, migration, and invasion of hepatocellular carcinoma cells (HepG2, Huh7, and related lines). Its anti-tumor effect is closely linked to the activation of apoptotic signaling cascades, including upregulation of caspase-3 and -9, suppression of Bcl-2 expression, and promotion of mitochondrial membrane potential loss.

Beyond its direct cytotoxic effects, ATWLPPRAANLLMAAS modulates tumor microenvironmental factors, reducing the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMP-2, MMP-9). These molecular modulations inhibit extracellular matrix degradation and angiogenesis, thereby preventing tumor metastasis.

Given its stability and potency, ATWLPPRAANLLMAAS is a valuable tool in preclinical studies exploring novel anti-angiogenic therapies, tumor suppression mechanisms, and apoptosis induction. It provides a unique model for the design of peptide-based therapeutics targeting multiple tumor pathways.

Product Specifications

Mechanism of Action

ATWLPPRAANLLMAAS acts primarily through anti-angiogenic and pro-apoptotic mechanisms. By targeting endothelial and tumor cells simultaneously, it disrupts the vascular network essential for tumor growth. The peptide downregulates VEGF and MMPs, blocking angiogenesis and tumor invasion.

It also activates intrinsic apoptotic pathways, causing mitochondrial dysfunction, reactive oxygen species (ROS) accumulation, and activation of caspase cascades. These processes collectively lead to programmed cell death in tumor cells, without significantly affecting normal tissues.

Additionally, ATWLPPRAANLLMAAS modulates key signaling pathways such as PI3K/Akt, MAPK/ERK, and NF-κB, contributing to its broad-spectrum anticancer effects. This multifaceted mechanism makes it an attractive subject for peptide drug design and targeted cancer therapy research.

Side Effects

In experimental research, ATWLPPRAANLLMAAS has not demonstrated toxicity to normal cell lines at standard working concentrations. However, as an apoptosis-inducing peptide, it may cause mitochondrial stress and oxidative imbalance in non-target cells at high doses.

Potential experimental observations include:

• Temporary mitochondrial depolarization in non-cancerous cells

• Mild cytotoxicity at concentrations exceeding 100 μM

• Minor inflammatory responses in long-term culture systems

Further in vivo evaluation is recommended to fully characterize its safety profile, biodistribution, and immunogenicity.

Disclaimer

This product is for research use only. It is not intended for diagnostic, therapeutic, or human use.

Keywords

ATWLPPRAANLLMAAS, Anti-Angiogenic Peptide, Anti-Tumor Peptide, Apoptosis Inducer, Cancer Research, VEGF Inhibitor, Angiogenesis Blocker, Peptide Therapeutics, Hepatocellular Carcinoma, MMP Inhibition

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