Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
Phenothiazines, such as prochlorperazine...

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates these...

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

Chemotherapy-Induced Nausea and Vomiting: 5-HT₃ Receptor Antagonists

5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...

Inhibitors of Viral Protein Synthesis

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Post-operative venous thromboembolism in advanced epithelial ovarian cancer: risk factors, tumor gene expression, and survival.

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society·2026

Same author

Does lung adenocarcinoma subtyping offer clinical benefits?-a retrospective population-based cohort study from Sweden.

Annals of translational medicine·2026

Same author

Recent survival trends in the most fatal cancers in the Nordic countries: gains in some but not in all.

Acta oncologica (Stockholm, Sweden)·2026

Same author

Fully intravenous split-dose administration of the oncolytic adenovirus TILT-123 in advanced solid tumors.

Molecular therapy : the journal of the American Society of Gene Therapy·2026

Same author

Familial risks in prostate cancer between brothers and half-brothers as clues to germline genetic and environmental causes.

Familial cancer·2026

Same author

<i>Alistipes</i> and <i>Eggerthella</i> shape the response to oncolytic adenovirus therapy in mice and humans through short-chain fatty acid metabolism.

Oncoimmunology·2026

Search research articles

Related Experiment Video

Updated: Jul 18, 2026

Combined Genetic and Chemical Capsid Modifications of Adenovirus-Based Gene Transfer Vectors for Shielding and Targeting

Combined Genetic and Chemical Capsid Modifications of Adenovirus-Based Gene Transfer Vectors for Shielding and Targeting

Published on: October 26, 2018

Chlorpromazine and apigenin reduce adenovirus replication and decrease replication associated toxicity.

Anna Kanerva¹, Mari Raki, Tuuli Ranki

¹Cancer Gene Therapy Group, Rational Drug Design Program and Haartman Institute, University of Helsinki, Finland.

The Journal of Gene Medicine

|December 7, 2006

Summary

Chlorpromazine and apigenin reduce adenovirus replication and toxicity in vitro and in vivo. These compounds may serve as a safety switch for oncolytic adenovirus therapy and treat systemic adenoviral infections.

More Related Videos

An Efficient Method for Adenovirus Production

An Efficient Method for Adenovirus Production

Published on: June 10, 2021

Adenofection: A Method for Studying the Role of Molecular Chaperones in Cellular Morphodynamics by Depletion-Rescue Experiments

Adenofection: A Method for Studying the Role of Molecular Chaperones in Cellular Morphodynamics by Depletion-Rescue Experiments

Published on: September 16, 2016

Related Experiment Videos

Last Updated: Jul 18, 2026

Combined Genetic and Chemical Capsid Modifications of Adenovirus-Based Gene Transfer Vectors for Shielding and Targeting

Combined Genetic and Chemical Capsid Modifications of Adenovirus-Based Gene Transfer Vectors for Shielding and Targeting

Published on: October 26, 2018

An Efficient Method for Adenovirus Production

An Efficient Method for Adenovirus Production

Published on: June 10, 2021

Adenofection: A Method for Studying the Role of Molecular Chaperones in Cellular Morphodynamics by Depletion-Rescue Experiments

Adenofection: A Method for Studying the Role of Molecular Chaperones in Cellular Morphodynamics by Depletion-Rescue Experiments

Published on: September 16, 2016

Area of Science:

Oncolytic virotherapy
Pharmacology

Background:

Adenoviruses can cause severe toxicity, particularly in immunocompromised individuals.
While oncolytic adenoviruses show promise for cancer treatment, managing potential toxicity is crucial.

Purpose of the Study:

To investigate the effects of chlorpromazine and apigenin on adenovirus replication and toxicity.
To evaluate these agents as potential safety mechanisms for oncolytic adenovirus therapy.

Main Methods:

Assessed in vitro replication of oncolytic and wild-type adenoviruses in various cell types and liver samples.
Evaluated in vitro cell killing efficacy and in vivo efficacy, replication, and liver toxicity in the presence of chlorpromazine and apigenin.

Main Results:

Both chlorpromazine and apigenin demonstrated significant reduction in adenovirus replication and associated toxicity, both in vitro and in vivo.
Effective doses were found to be within predicted safe levels for human use.

Conclusions:

Chlorpromazine and apigenin may act as a safety switch to mitigate adenovirus replication-associated side effects during oncolytic therapy.
These compounds show potential for treating systemic adenoviral infections in immunosuppressed patients.