Could Leronlimab be the wonder molecule that STOPS cancer?

Could Leronlimab be the wonder molecule that stops cancer from spreading?

Why? What is the mechanism?

Let's unpack the mystery and simplify it for easy understanding.

What we're talking about in particular is metastatic triple-negative breast cancer (mTNBC) — aka the most aggressive, hardest-to-treat form of breast cancer, and stage 4, meaning the cancer is in its late stage. It has already spread to other organs like the brain, lungs, or liver.

The condition is as close to a death sentence as in the past, until now!

Aggressive Chemotherapy and Radiation treatment, in some instances, may slow down but never guarantee healing. In some cases, it may even hasten the victim's demise.

Cancer may have finally met its terminator years into trial with numerous subjects. Stage 4 cancer patients who were given months to live were enrolled in the study of Leronlimab months after being subjected to a previous scientific trial study; with Leronlimab, they recovered and are now cancer-free—3 YEARS later!

So, could this biotech company with 22¢/share valued stock hold the cure?

We're talking about Cytodyn's Leronlimab. #CancerBreakthrough #Biotech #Leronlimab #Cytodyn #CYDY

🧬 Most available Cancer Drugs may slow cancer growth but do not guarantee complete remission.

CytoDyn's Leronlimab: drug tested on 30 Metastatic Triple-Negative Breast Cancer (mTNBC) patients revealed promising results.

All subjects had a history of failed cancer treatments.

Their previous treatment results have only a median survival of 6.6 months.

After switching the 19 patients to another trial test with higher Leronlimab doses (525–700mg)

Results: Median survival jumps to 12+ months!

Progression-free: 6.1 months. 2025 update: Some terminal patients are still alive three years later!

Alive 36+ months later. ZERO signs of cancer. Leronlimab is NOT slowing cancer but rather ERASING it.

The question remains: Is this a functional cure for stage 4 mTNBC?

Leronlimab might be shutting cancer down completely.

Let us examine the possibility based on the trial results:

🧠 What could be Leronlimab's mechanism of action?

When a benign Cancer (tumor) undergoes a malignant transformation, the cancer breaks out of the original tumor. It mutates and spreads, invading the rest of the body like a wildfire spreading through houses in one community. As the cancer mutates, it could become malignant and rapidly spread to other organs via the bloodstream or lymph system through its unique chemical pathways.

The question remains: Is this a functional cure for stage 4 mTNBC?

How does Leronlimab possibly shut cancer down completely?

Radical cancer cells may initially spread undetected and undisturbed by the victim's T-cells (the body's defense system). As they develop undetected by the victim's defense, the cancer cells actively seek a chemokine receptor (CCR5) to access and spread to another cell.

This receptor, CCR5, is a chemokine receptor involved in cell signaling. CCR5 signaling promotes cancer cell migration and invasion, contributing to the metastatic spread of cancer.

Not only that, but cancer cells exploit CCR5 to suppress the victim's immune system (Tumor Microenvironment: CCR5 signaling influences the tumor microenvironment by recruiting immune and stromal cells and by inducing immunosuppressive polarization of macrophages). The recruitment of immunosuppressive cells like T-regulatory cells or Myeloid-Derived Suppressor Cells (MDSCs) enhances the tumor's ability, as a destructively invasive cell, to disguise itself as a non-intruder (suppressed gene expression), avoiding detection from T-cells, therefore gaining the ability to proliferate, thus spreading aggressively (metastasizing) to other organs.

A mechanism that protects the tumor from being identified as a cancer cell by the lymphocytes (Memory T-cells).

However, in an event (such as low-dose chemo) that may trigger exposure (unmasking) of the disguised cancer cells, the memory T-cells, once they are exposed and already recognized by the cancer victim's T-cells (defense system leukocytes), become activated to attack the unmasked cancer cells.

The administration of Leronlimab, an antibody that blocks CCR5, triggers immunomodulation response, a mechanism that alters the immune environment, and perhaps -- and this has yet to be investigated -- the Leronlimab, a humanized IgG4 monoclonal antibody (mAb) molecule, and with the aid of a trigger (e.g., with low dose chemo) exposes the cancer cells gene expression allowing the Lymphocytes (Memory T-cells) to identify and remember cancer cells as the intruder, which, in response, may activate the victims natural killer (NK) cells to become hostile to cancer. Granting that the victim's immune system is healthy and active, it is safe to assume that these NK cells can effectively attack and destroy the cancer cells.

In other words, by blocking CCR5, Leronlimab blocks the cancer path, thus preventing its spread while empowering the victim's immune system to attack and destroy the cancer cells' ability to mutate more effectively.

Blocking CCR5 is like fireproofing/blocking the fire exit, stopping cancer from escaping and spreading while allowing the firefighters to use fire retardants effectively to suppress the fire.

So, with the introduction of Leronlimab, a few things happen:

Research has shown multiple key properties of the CCR5's role in cancer:

The CCR5 receptor on cancer cells potentially plays a role in the migration and invasion of cells into the bloodstream, which may lead to metastasis of breast, prostate, and colon cancer.

*Blocking the CCR5 receptor on Tregs also turns on anti-tumor fighting properties, restoring immune function.

*CCR5/CCL5 interaction blockage synergized with chemotherapy and controlled cancer progression.

*Chemotherapy traditionally increases the expression of CCR5, so blocking CCR5 is expected to reduce the levels of invasion and metastasis.

*Animal studies revealed a significant decrease in angiogenesis following the administration of leronlimab.

*The CCR5 receptor has been shown to play an integral role in macrophage repolarization due to macrophage plasticity.

Cancer Cells stop spreading.

Cancer cells have become more identifiable and managed with small doses of chemotherapeutic agents.

When administered, these small doses of chemotherapy are not meant to kill cancer. Instead, they expose the cancer-causing cells (which have the genomic sequencing ability to hide their expression via the epigenetic layer to avoid detection and attack by the host antibody) to be easily identified and attacked by the (T-cells) victim's antibody. This scenario is called immunomodulation.

The chances of completely eradicating the cancer-causing cells became higher. An action similar to uprooting the source.

Since the immune system can better recognize and destroy cancer-causing and damaged cells, the victim's immune system, including phagocytes, can effectively consume the damaged cells (phagocytosis) and allow mitochondrial repair.

Mitochondrial repair is a crucial regenerative process contributing to cell recovery, particularly in damage or injury scenarios.

Mitochondria, the "powerhouses" of cells, play a vital role in energy production and various other cellular processes, and their repair and maintenance are essential for overall tissue health and regeneration.

Before testing humans, Leronlimab was tested in mice with human breast cancer cells injected into them (they use special immune-deficient mice so the human cancer doesn't get rejected).

What happened?

Leronlimab cut the spread of breast cancer by 98–99.6%.

Returning to the fire scenario --- "the cancer tried to spread… and failed."

That's why the results were remarkable when tested in Humans!

What is now revealed from CytoDyn's human trials of 30 patients with stage 4 mTNBC.

*Most had failed other treatments

*Many had cancer in their brain, liver, and lungs

*Small group now alive 36+ months later and cancer-free

That's what we're looking at here — not just a drug that slows cancer, but one that may restore the system's balance.

Cancer spreads using CCR5. Leronlimab blocks it.

Stops cancer invasion.

It makes chemo work better.

Massive impact in stopping metastasis.

A Mice study revealed lung tumors cut by 98%.

In a human study?

Early signs unbelievably prove that it may be doing what other anti-cancer drugs have not been able to achieve, which is the destruction of cancer cells without the massive side effects common to oncology drugs currently on the market.

Leronlimab isn't just another drug — it's a whole new way to fight cancer.

And guess what?

The world will soon witness the presentation of accurate long-term survival data from actual humans on May 15 at ESMO.

European Society for Medical Oncology (ESMO) is a professional organization for medical oncology.

With more than 40,000 members representing oncology professionals from over 177 countries worldwide, ESMO was founded in 1975.

So yeah… 22¢ today might be the deal of the decade.

By Joel Inocencio, BSN, RN

Disclosure 🩺
The writer is a 30+ year nurse (ER, Oncology, Radiology, Geriatrics, Urology) and Senior Home Care consultant. Invested in $CYDY for 5+ years. Independent researcher focused on Cancer, HIV, Vaccines, and Aging. This is not financial or medical advice. Always consult a professional.
#Disclosure #Biotech

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