Description

Product Description

Bortezomib is a synthetic boronic acid dipeptide and one of the first-in-class reversible inhibitors of the 26S proteasome. The 26S proteasome is responsible for the degradation of ubiquitinated intracellular proteins, a process critical for maintaining cellular homeostasis. By disrupting this process, Bortezomib induces the accumulation of regulatory proteins involved in apoptosis, cell cycle arrest, and immune responses, making it an essential compound in mechanistic oncology and cell biology research.

In molecular and biochemical studies, Bortezomib has been extensively used to investigate pathways such as NF-κB inhibition, mitochondrial apoptotic signaling, and endoplasmic reticulum stress response. Its mechanism of action involves reversible covalent binding to the threonine residue in the proteasome’s catalytic site, leading to blockade of proteolytic activity.

Researchers employ Bortezomib to study tumor cell apoptosis, autophagy regulation, and metabolic stress. It is also utilized to explore proteostasis disorders, including neurodegeneration and inflammatory conditions, where proteasomal dysfunction is implicated.

Research Background and Relevance

The ubiquitin–proteasome pathway (UPP) is fundamental for cellular quality control. Bortezomib’s discovery revolutionized cancer pharmacology research by proving that targeted proteasome inhibition could selectively induce apoptosis in malignant cells. It has since become a vital molecular probe for dissecting intracellular degradation processes and protein turnover mechanisms.

In oncology research, Bortezomib has shown notable effects in multiple myeloma and lymphoma models, where inhibition of proteasomal degradation prevents NF-κB activation—one of the most critical survival pathways in tumor cells. This mechanism has inspired a wide range of investigations into protein homeostasis, cellular stress responses, and targeted drug design.

Biochemical and Cellular Effects

At the cellular level, Bortezomib causes accumulation of misfolded proteins, leading to endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR). This stress triggers pro-apoptotic factors, such as CHOP and caspase-12, resulting in programmed cell death.

Bortezomib also affects key signaling molecules including:

• NF-κB pathway: Suppresses activation through inhibition of IκB degradation.

• p53 pathway: Stabilizes p53 protein, enhancing transcription of apoptosis-related genes.

• JNK and MAPK pathways: Alters signaling dynamics contributing to apoptosis and oxidative stress.

These properties make it an ideal molecule for studying proteasome function, apoptosis, and signaling regulation in cancer cell biology.

Product Specifications

Mechanism of Action

Bortezomib targets the chymotrypsin-like activity of the 26S proteasome. The proteasome’s β5 subunit contains a threonine residue that serves as the nucleophile for proteolytic cleavage. Bortezomib forms a reversible covalent bond with this residue, effectively blocking proteasomal degradation of ubiquitinated proteins.

Proteasome Inhibition and Apoptosis

When the proteasome is inhibited, accumulation of defective and regulatory proteins triggers stress signals and apoptosis. Key downstream effects include:

• Activation of caspases-3, -8, and -9.

• Upregulation of pro-apoptotic proteins such as Bax and PUMA.

• Inhibition of anti-apoptotic proteins including Bcl-2 and Mcl-1.

• Suppression of NF-κB–dependent transcription of survival genes.

Cell Cycle Arrest

Bortezomib also halts the cell cycle in G2/M phase by preventing degradation of cyclins and checkpoint proteins. This mechanism provides valuable insight for cell cycle and mitotic regulation research.

Anti-Angiogenic and Immune Modulation Research

Bortezomib downregulates VEGF expression and endothelial proliferation, contributing to anti-angiogenic effects observed in tumor models. Moreover, its immune-modulating activities make it a useful compound for exploring T-cell activation and cytokine secretion pathways.

Side Effects

In laboratory research, Bortezomib may induce several concentration-dependent cytotoxic effects:

• Mitochondrial depolarization and ROS accumulation.

• ER stress and unfolded protein response.

• Impaired proteostasis and cell cycle dysregulation.

• Apoptosis in proliferative cell populations.

Researchers should handle this compound with appropriate biosafety precautions. It is not intended for human or veterinary administration.

Keywords

Bortezomib, CAS 179324-69-7, proteasome inhibitor, PS-341, NF-κB inhibition, apoptosis research, protein degradation, cancer pharmacology, tumor signaling, cell cycle arrest, oncology reagent, high purity compound.

Shipping Guarantee

All Bortezomib shipments are handled using validated cold-chain logistics to preserve compound integrity. Each package is sealed in moisture-proof containers with secondary protective wrapping and continuous temperature monitoring. Products are shipped via express international couriers with full tracking and insurance coverage.

Trade Assurance

We Bortezomib ensure product authenticity, verified ≥99% purity, and compliance with analytical standards (HPLC, MS, and NMR). Each batch is supplied with a Certificate of Analysis (CoA). Our trade assurance policy guarantees replacement or refund for any deviation from listed specifications.

Payment Support

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Disclaimer

All Bortezomib products are intended for laboratory research use only and not for human or veterinary use. They are not drugs, medical devices, or diagnostic tools. Researchers must handle materials according to institutional chemical and biosafety regulations. The information provided is for scientific reference only and does not imply therapeutic efficacy or regulatory approval.