

A Brief History of Ivermectin
Ivermectin was developed from compounds isolated from the soil bacterium Streptomyces avermitilis by Satoshi Ōmura and William C. Campbell, who later shared the 2015 Nobel Prize in Physiology or Medicine for their work.
The drug quickly became one of the most successful antiparasitic medicines ever developed because of:
- broad-spectrum activity
- low cost
- relatively favorable safety profile
- effectiveness against multiple parasitic diseases
Today, hundreds of millions of doses are administered globally through public health programs.
Why Researchers Became Interested in Cancer
The interest in cancer research emerged when scientists noticed that ivermectin affects many cellular processes that cancer cells depend on.
Unlike conventional targeted therapies that focus on a single molecular target, ivermectin appears to influence multiple pathways simultaneously.
This is particularly interesting because cancer cells often develop resistance when only one pathway is blocked.
Cell Cycle Arrest
Cancer cells divide continuously and uncontrollably.
Several studies reviewed in the article found that ivermectin can stop cells during critical stages of division, particularly:
- G0/G1 phase
- G2/M phase
When cells become trapped at these checkpoints, they can no longer reproduce efficiently.
This effect has been observed in several cancer cell lines, including breast, ovarian, lung, and colorectal cancers.
Induction of Apoptosis
Apoptosis is the body's natural mechanism for eliminating damaged or abnormal cells.
Cancer cells frequently develop ways to avoid apoptosis, allowing them to survive longer than normal cells.
Laboratory studies suggest ivermectin can:
- activate caspases
- increase pro-apoptotic proteins
- reduce anti-apoptotic proteins
As a result, cancer cells become more likely to self-destruct.
Inhibition of Cancer Stem Cells
One of the most intriguing findings discussed in the review involves cancer stem cells.
These cells are believed to:
- initiate tumor formation
- drive metastasis
- contribute to treatment resistance
- cause tumor recurrence
Several studies suggest ivermectin may suppress stem-cell-related signaling pathways, potentially reducing the ability of tumors to regenerate after treatment.
Blocking Key Signaling Pathways
Cancer cells rely on numerous signaling networks to survive and spread.
The review describes ivermectin's effects on:
Akt/mTOR Pathway
Controls growth, metabolism, and survival.
Wnt/β-catenin Pathway
Important for stem-cell maintenance and tumor progression.
STAT3 Signaling
Frequently overactive in aggressive cancers.
PAK1 Signaling
Associated with invasion, migration, and metastasis.
YAP1 Signaling
Linked to uncontrolled tissue growth and drug resistance.
Because these pathways influence many tumor types, ivermectin has attracted attention as a potential multi-target therapy.
Effects on Tumor Metabolism
Cancer cells consume energy differently from normal cells.
Many tumors rely heavily on glucose metabolism, a phenomenon known as the Warburg effect.
Research reviewed in the paper suggests ivermectin may:
- alter glucose utilization
- interfere with mitochondrial function
- increase oxidative stress
These changes can place cancer cells under metabolic pressure.
Anti-Angiogenic Activity
Tumors need a blood supply to grow.
The review discusses evidence that ivermectin may suppress angiogenesis—the formation of new blood vessels.
Without adequate blood vessels, tumors struggle to obtain:
- oxygen
- nutrients
- growth factors
This could potentially slow tumor progression.
Antiviral Research
The review also discusses antiviral studies.
In laboratory experiments, ivermectin showed activity against:
- Dengue virus
- Zika virus
- Yellow fever virus
- West Nile virus
- HIV
- SARS-CoV-2
One proposed mechanism involves inhibition of the importin α/β transport system used by some viruses to move proteins into the cell nucleus.
The review presents ivermectin as a biologically active molecule with effects extending far beyond parasite control. Laboratory evidence suggests potential anticancer, anti-inflammatory, and antiviral properties through multiple molecular mechanisms.
Source: Full Review Article (PMC11008553)