VTose – Kimer Med continues work based on DRACO approach

The DRACO technology, pioneered by Todd Rider, is currently being continued and developed at Kimer Med, a New Zealand-based company, under a new name: the VTose project. Kimer Med, founded in 2020, is focused on expanding and refining the original concept, which aims to create a broad-spectrum antiviral drug capable of combating a wide range of dangerous viruses, including those causing diseases of major epidemic and pandemic significance.

Todd Rider’s Origins and Ideas

Todd Rider developed DRACO (Double-stranded RNA Activated Caspase Oligomerizer) as an innovative antiviral therapy based on the detection of double-stranded RNA, a characteristic of viruses replicating their genomes within host cells. DRACO’s mechanism of action is to selectively detect and induce apoptosis in infected cells while leaving healthy cells unharmed. This approach promises to treat a broad spectrum of viral diseases, overcoming the limitations of conventional therapies targeting single viruses.

Acquisition and development by Kimer Med – VTose project

Despite promising results from preliminary studies and mouse tests, work on Rider’s original DRACO stalled for many years due to insufficient funding and technological challenges. In 2020, Kimer Med launched the VTose project—an improved antivirus platform based on DRACO technology.

Kimer Med has invested significant financial and research resources to improve the underlying technology—particularly in terms of efficacy, safety, and scalability. VTose is now an advanced antiviral therapy capable of combating multiple viral families through a mechanism known as viral cytopathic effect (CPE) reduction.

Latest achievements and research results

In June 2023, Kimer Med announced that VTose demonstrated 100% efficacy in the laboratory against Dengue (DENV-2) and Zika (ZIKV) viruses, as confirmed by independent testing in laboratories in the U.S. Furthermore, the project extended its effectiveness against at least eleven viruses from different families, including influenza viruses and herpes simplex virus type 2 (HSV-2)—all of which confirmed the therapy’s low toxicity to healthy cells.

Financing and the Clinical Future

In March 2024, Kimer Med signed a contract worth up to $750,000 (NZ$1.3 million) with Battelle Memorial Institute, a global leader in independent research and development, to support the company in developing additional antiviral drug candidates based on its VTose technology.

Additionally, the company has secured significant funding of over NZ$14 million from private and institutional sources to advance its future clinical trials. Preparations are currently underway to advance the VTose project into early clinical trials (Phase I), which could represent a breakthrough in the treatment of viral infectious diseases on a global scale.

Development strategy and scientific cooperation

Kimer Med is focused on continuously improving the VTose formulation, expanding its delivery capabilities and improving its effectiveness against latent and difficult-to-control viruses. The company is also conducting in vivo studies in animal models and building partnerships with research institutions to accelerate the translation of this technology into the medical market.

Summary

The VTose project is currently the most important successor to Todd Rider’s DRACO technology. It is currently one of the most innovative approaches to treating a wide range of viral infections. Thanks to advanced research, solid financial support, and international research collaborations, VTose has a real chance of becoming a breakthrough drug that will provide effective therapy against many dangerous viruses, even those that have traditionally posed difficult challenges to medicine.


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Sources:

  • fightaging.org, 2024
  • Wikipedia, 2011
  • Kimer Med official announcements, recent years

The last step towards HIV cure – EBT-101 protein

EBT-101: Are we on the verge of finding a cure for HIV?

HIV, or human immunodeficiency virus, has shaped modern medicine and transformed the lives of countless people since its discovery in the early 1980s. Today, thanks to advances in antiretroviral medicine (ART), people with HIV can live long and healthy lives. However, even with daily medication, the virus lurks—like a cat in the shadows—ready to strike the moment we stop taking it.

What if we could banish the virus from hiding…for good? Meet EBT-101 , a novel gene-editing treatment that aims to cure HIV, not just control it. Sounds like science fiction? Scientists are testing it right now. Let’s take a closer look and learn more about this potential medical revolution.


Why is HIV so difficult to cure?

HIV is insidious. It not only circulates in the blood but also penetrates the DNA of immune cells, creating hidden “reservoirs.” As long as you take your medication daily, the virus remains inactive. But interrupt it for a moment, and HIV quickly reactivates.

That’s why it’s so hard to find a real cure for HIV: the virus is part of you, hidden, almost like a computer virus buried in your hard drive.


What makes the EBT-101 course unique?

EBT-101 is based on the wonder tool of modern genetics: CRISPR-Cas9 . Imagine super-precise scissors that can locate and cut the specific DNA fragments where HIV hides.

But EBT-101 isn’t just about CRISPR therapy! Here’s what makes it so interesting:

  • Multiplex gene editing  : Most gene editing targets only one site. EBT-101 targets three places where HIV can hide in DNA. It’s like a triple-locked door—and three keys to ensure nothing escapes!
  • Long-term effects  : Animal studies indicate that a single dose of therapy can eliminate enough of the virus to permanently inactivate it.
  • AAV delivery  : The tool is introduced into the body using a harmless helper virus, known as  an adeno-associated virus (AAV)  , which sends gene-editing instructions directly to cells.

How do clinical trials work?

First step: safety first

Phase 1 clinical trials for EBT-101 began in 2022, meaning real people are already participating in the studies ( https://www.clinicaltrials.gov/study/NCT05144386 ). At this early clinical stage, the main questions are:

  • Is the treatment safe?
  • Does it cause any unexpected or dangerous side effects?
  • Can scientists test whether removing HIV from cells is effective?

Who can participate?

The first study involves HIV-1-infected adults whose viral load remained very stable for years on treatment. This is important because researchers need a clear, stable starting point to see if EBT-101 actually has an effect.

What will happen next?

If the study shows that EBT-101 is safe (does not cause serious side effects or “off-target” genetic modifications), the next steps will be to try to answer the following questions:

  • How well does the body cleanse itself of hidden HIV viruses?
  • Can you safely stop taking HIV medications without risking a viral relapse?
  • How long do the effects last?

Answering these questions will take several years and further studies in larger groups. A scientific breakthrough would be to discover that a single therapy proved effective in just a handful of people.


What are the biggest challenges for EBT-101?

Let’s be curious and honest—eliminating HIV isn’t as easy as cutting toast! Here are some of the serious challenges we face:

1. Completely reach all HIV reservoirs

HIV hides in many types of immune system cells, in various tissues—deep lymph nodes, the intestines, the brain. Therapy must find each infected cell to prevent the virus from spreading again. This “needle in a haystack” problem is one of the most difficult challenges in HIV research.

2. Avoiding side effects

CRISPR is very precise, but not perfect. If the gene-editing scissors make a mistake—cutting healthy human DNA instead of the virus itself—it could cause serious health risks, such as the development of cancer or other diseases. Clinical trials are closely monitored for these risks.

3. The body’s immune response

Introducing CRISPR tools and a carrier virus (even a harmless one like AAV) can attract the attention of the body’s defense mechanisms. If the immune system attacks the carrier system, the therapy may be less effective or trigger inflammation.

4. Durability: Is one dose enough?

Early research offers hope, but we don’t yet know whether a single treatment eliminates HIV for life or if the virus can return years later. Researchers will need to follow participants long-term to be sure.

5. Availability and cost

New, complex gene therapies are typically very expensive initially and may be limited to wealthy countries or well-funded research centers. Ensuring EBT-101 is available to all people living with HIV will be a major challenge in the future.

6. Ethical and Regulatory Obstacles

Because it involves editing the genome of human cells, strict ethical rules and debates apply. Long-term effects must be understood before widespread use is considered.


Where are we now and what awaits us?

Scientists around the world are eagerly watching the EBT-101 trials. If successful, they could pave the way not only to a cure for HIV but also for other diseases caused by viruses hidden in our DNA. Companies and universities are racing to improve gene-editing tools, reach more cells, and make the therapy safer and easier to administer.

EBT-101 is not yet a cure, but the idea of ​​curing HIV, rather than controlling the disease, could become a reality in our lifetime.


Summary: Hope on the Horizon

EBT-101 is one of the boldest ideas in modern medicine. Using CRISPR gene editing, it aims to find and remove the hidden HIV virus from human DNA, offering hope for a true, lasting cure. The path from the laboratory to the patient’s bedside is long, fraught with scientific puzzles and ethical questions, but each step brings us closer to a world where HIV no longer lurks in the shadows.

Could people with HIV really close this chapter of their lives forever? If so, EBT-101 could go down in history as a true medical miracle.

DRACO – widespread cure that occurs infected cell apotheosis

DRACO: The Discovery That Could Change Medicine: Todd Rider’s Incredible Story of Fighting Viruses

When a scientist comes up with an idea of killing all viruses during taking shower

How DRACO —Double-stranded RNA Activated Caspase Oligomerizer was invented?

It all started in the shower. Todd Rider, a bioengineer at MIT, had an epiphany—a shift in perspective that could revolutionize the entire field of viral medicine. It was the mid-2000s, and the world had no idea that the approach to treating viral infections was about to change. But first, it’s important to understand why this idea was so revolutionary.

A problem that has plagued scientists for decades

Imagine a doctor treating a patient with viral pneumonia. They have access to only a few drugs, each of which targets one specific virus or a small group of related viruses. If the patient has the flu, they use oseltamivir (known as Tamiflu). If it’s COVID-19, they use COVID-19 medications. If the cancer recurs immediately after surgery, they have to wait. This is precisely because antivirals are so specific . Business Insider

For decades, scientists have been searching for what Rider called “virus kryptonite”—a universal drug that would work against all, or almost all, viruses. The problem is that every virus is slightly different. Each evolves differently, each hides from the immune system in different ways. businessinsider

Todd Rider’s Perspective: A Breakthrough Idea

Todd Rider, a senior scientist at MIT Lincoln Laboratory, was born in 1986 and quickly found himself in the world of science. After completing his PhD in engineering at MIT in 1995, he supplemented his knowledge with courses in biology and biomedicine at Harvard Medical School. At MIT, he worked on a project of defense importance, which gave him access to top scientists, laboratories, and funding. businessinsider

But it was in the shower, pondering the problem of viral infections, that Rider came up with an idea that changed everything. Instead of attacking viruses directly—which would mean adapting to each virus individually—why not attack the characteristics common to ALL viruses? businessinsider

RNA with a Hook: How Viruses Give Themselves Away

Scientists have long known that when a virus infects a cell, it does something very distinctive: it produces long sequences of double-stranded RNA (dsRNA) . This is essentially “trace evidence” of the virus’s crime within the cell. pmc.ncbi.nlm.nih

Humans also have RNA, but the natural RNA in our cells isn’t double-stranded, and if it is, it’s in very short pieces (less than 24 base pairs). Viruses, on the other hand, produce long, characteristic helices of double-stranded RNA. This essentially serves as a warning signal to the cell’s natural defense system that something is wrong. Science

Cells have evolved over millions of years to recognize this signal. Many proteins in our bodies can “sense” this double-stranded RNA and trigger the process of cellular suicide— apoptosis . It’s a clever mechanism: if a cell knows it’s infected and the virus is replicating within it, it’s better for it to destroy itself than allow the virus to multiply and infect other cells. pmc.ncbi.nlm.nih+ 1

DRACO: Combining two revolutionary ideas

Todd Rider had a brilliant idea: what if he combined two things into one protein?

  1. dsRNA detector – part of the protein that recognizes the double-stranded RNA of the virus
  2. Cell suicide trigger – part of the protein that triggers apoptosis

Rider calls it DRACO —Double-stranded RNA Activated Caspase Oligomerizer. It sounds complicated, but the idea is elegant: pmc.ncbi.nlm.nih

  • “Double-stranded RNA” = double-stranded RNA
  • “Activated” = activated
  • “Caspase” = enzymes responsible for cell suicide
  • “Oligomerizer” = when multiple DRACO molecules attach to the same RNA, they form an assembly (oligomer)

How does it work in practice? When DRACO enters an infected cell (using a special transport peptide), it searches for the virus’s double-stranded RNA. Once it finds it, it attaches itself to it. When multiple DRACO molecules attach to the same RNA fragment, they form a structure that activates caspases —cell suicide enzymes. voanews+ 1

But—and this is important—DRACO contains a signal that enters the cell nucleus via a special active transport system, allowing it to act inside the cell .

Results that amazed the world of science

In 2011, Todd Rider and his team published groundbreaking research in the prestigious journal PLoS ONE. The results were astonishing: riderinstitute

In laboratory tests, DRACO has demonstrated effectiveness against 15 different viruses . Not just a few – but FIFTEEN! And not just in laboratory dishes, but also in live mice infected with influenza. voanews+ 1

Viruses tested include: riderinstitute+ 1

  • Dengue
  • H1N1 (flu)
  • Rhinovirus (cold)
  • Arenaviruses
  • Bunyavirus

Most importantly, DRACO only killed infected cells, leaving healthy cells virtually untouched . DRACO was tested in 11 different savanna cell types, and none of them showed significant toxicity. pmc.ncbi.nlm.nih

In vivo tests (on living organisms)

When scientists tested DRACO on mice infected with H1N1 flu, the results were spectacular. DRACO injection: voanews

  • It prevented infection (when administered before infection) – the protective effect lasted up to three weeks
  • Treated the infection – when given within the first three days of infection, it stopped the virus from replicating

Anthony Fauci, then director of the National Institute of Allergy and Infectious Diseases in the US, admitted that DRACO was “potentially” a breakthrough. voanews

Funding disappears – a story of disappointment

Science rarely follows genius. After initial successes and enthusiasm, challenges arose. Todd Rider was working at Draper Laboratory when management changed. Unfortunately, the new management had no interest in continuing DRACO research. businessinsider

In 2014, Rider received a $2 million grant from the Templeton Foundation, but Draper Lab ultimately withdrew from the project. Undeterred, Rider tried crowdfunding on Indiegogo in 2015, hoping to raise $90,000. The campaign failed – it raised far too little. businessinsider

Since December 2015, research on DRACO has practically ground to a halt. For seven years, nothing. businessinsider

Resurrection: Kimer Med Takes the Flag

In August 2020, as the world grappled with the COVID-19 pandemic, New Zealand biotech company Kimer Med decided to take on the challenge. The company’s founders—scientists with both scientific and business experience—decided to revive this technology.

Instead of simply copying DRACO Rider, Kimer Med went further. They developed their own platform, which they called VTose . This was a significant step forward: kimermed

Kimer Med Progress: VTose Better Than Original

In June 2023, Kimer Med announced that its VTose antivirus showed 100% effectiveness in laboratory tests against two viruses:

  • Dengue (type 2) – 100% reduction of cytopathic effect (CPE) – i.e. 100% destruction of viruses
  • Zika – 100% Fightaging Reduction

But that was just the beginning. Over the following months, Kimer Med tested VTose against an increasing number of viruses, and the results were impressive. As the company’s scientists themselves say :

“Since its launch in 2020, Kimer Med has developed innovative antivirals demonstrating efficacy against 11 different viruses, including all four Dengue serotypes, Zika virus, and Herpes Simplex 2 (HSV-2).”

Agreement with Battelle Memorial Institute

In March 2024, Kimer Med signed an agreement with Battelle Memorial Institute (the world’s largest independent research and development organization) worth up to $750,000 USD (NZ$1.3 million) . The agreement focused on developing new antiviral candidates targeting alphaviruses , a family of viruses that pose a public health threat .

How It Works at the Molecular Level: Entering the Protein Kingdom

To truly understand why DRACO is so sophisticated, you have to delve deeper into cellular biology.

Slippage recognition

DRACO uses a protein called PKR (Protein Kinase R) or RNaseL as a detector of double-stranded RNA. These proteins evolved in higher organisms to be sensitive to long dsRNA sequences—characteristic of viruses but not naturally occurring in healthy cells.

When PKR or RNaseL attaches to the viral dsRNA, they undergo structural changes – they begin to aggregate, forming clusters (oligomers). 2025.igem

Cascade of Death – Caspase Oligomerization

The second part of DRACO contains a domain associated with Apaf1 and caspase – proteins responsible for programmed cellular suicide.

When multiple DRACO molecules assemble on the same dsRNA fragment, their caspase domains converge and initiate the activation process. The caspases begin to autoactivate—they degrade each other, creating a proteolytic avalanche. This cascade leads to irreversible cell damage. Science

In short : the virus may have dragged the cell into its own death, but now the cell is commemorating suicide—and DRACO is urging it to express this decision through apoptosis. voanews

Specificity: Why Healthy Cells Are Safe

This is a key element. Healthy cells don’t produce long dsRNA fragments. Even if they do produce short fragments (under 24 base pairs), they are too short for DRACO to bind effectively. pmc.ncbi.nlm.nih+ 1

Therefore, DRACO remains completely inert in healthy cells but deadly to infected cells. pmc.ncbi.nlm.nih+ 1

Challenges and Limitations: This is not magic

Scientists always want to be honest – DRACO is not a cure for all viruses.

Not all viruses produce dsRNA

DRACO only works on viruses that produce long sequences of double-stranded RNA. However, there are viruses that don’t. Some strains of hantavirus and many plant viruses are among them. But the good news is that most viruses that infect humans produce dsRNA . voanews

Virus Resistance – An Evolutionary Game

Viruses are incredibly adaptable. Over millions of years, they have evolved mechanisms to evade the cell’s natural defenses. For example, Ebola produces a protein called VP35, which sequesters (hides) dsRNA from the cell’s defense system. If the virus became resistant to DRACO by increasing its production of such proteins, it would theoretically be possible. reddit

However—and this is important—Rider argues that DRACO attacks the cell, not the virus itself directly. The virus can’t “mutate” its escape route from apoptosis as easily as it can mutate its surface proteins. To resist DRACO, the virus would have to mitigate its natural replication process—and this could lose its infectious potential. reddit

Mobile Delivery: The Logistics Problem

For DRACO to work, it must get inside the cell. This requires special transport peptides (PTDs – protein transduction domains). In current laboratory conditions, it works perfectly, but in the whole organism? It’s more complicated. Kimer Med and other teams are working on better ways to deliver DRACO to infected cells. fightaging+ 1

Endogenous retroviruses and genetic elements

The question scientists have been asking: What about viruses embedded in our DNA? The human genome contains many endogenous retroviruses and transposons (elements of DNA that can replicate themselves). Could DRACO kill them?

Rider’s answer: Infected cells produce a LOT of dsRNA. Endogenous genetic elements produce very little. Therefore, DRACO would be more sensitive to the large amounts of dsRNA typical of an active infection. reddit

The Future: Will It Be “Pandemic Fear”?

Not just one medicine, but a family of medicines

Kimer Med itself is changing the narrative somewhat. Instead of talking about one universal DRACO that treats all viruses, the companies are talking about a family of broad-spectrum antivirals . Each would potentially target a group of viruses—all flaviviruses (Dengue, Zika), all herpesviruses , etc.

This is still a huge advance. Instead of waiting years to develop drugs specific to each virus, we could have a platform on which we can quickly build variants for new threats. marketshaping.uchicago

Pandemic preparedness

Experts point out that such platforms could be crucial for future pandemic preparedness. Pandemics like COVID-19, or worse, could recur every 33-50 years. If we have the DRACO platform, we could potentially deploy antivirus in weeks, not years. marketshaping.uchicago

Clinical Phases: Human Trials

Both Todd Rider (if he returns to the project) and Kimer Med are talking about clinical trials. But that could take time. It usually takes years—safety studies, efficacy tests, regulatory approvals. Rider predicted in 2011 that it could take “at least a decade.” Now, in 2025, we know it can sometimes be longer. voanews

However, the outlook for Kimer Med and similar companies is optimistic. They are in the preclinical testing phase and have already demonstrated in vitro safety and activity against many viruses .

Why didn’t this happen earlier?

The question on many minds: why did we wait so long? Why didn’t Todd Rider receive the funding he needed?

There are several reasons:

  1. Risks of early research – Venture capitalists want to see evidence, and Rider had it, but they still needed animal testing, and then clinical trials. That’s a lot of money with no guarantee of success.
  2. Patent problem – Rider held patents on DRACO from MIT. This hindered the work of other scientists until the patents expired or were abandoned. kimermed
  3. The Competition Virus – Other approaches (small molecules, monoclonal antibodies) have received more attention and funding. marketshaping.uchicago
  4. Funding Science – Sometimes great ideas wait years for the right entrepreneur or investor to believe in the vision .

Summary: A new era in the fight against viruses?

Todd Rider’s DRACO was—and still is—one of the most promising ideas in viral medicine in the last few decades. Instead of searching for virus after virus, he combined the cell’s natural defense mechanisms with artificial intelligence. The result? A potentially universal cure for many viral infections.

Although Rider’s main project fell somewhat flat due to lack of funding, its spirit lives on at Kimer Med and likely in other labs around the world. Scientists acknowledge that DRACO was “optimal for further development.” businessinsider

Will we have universal antiviruses within the next decade? There’s hope. The world has experienced COVID-19 and knows that flaws in our pandemic preparedness are unacceptable. DRACO and its derivatives could be part of the answer.

Todd Rider had an idea in the shower. Now it’s time for the world to finally listen.


Sources and references

– Wikipedia, artykuł o DRACOwikipedia​
– Badania z PMC: Broad-Spectrum Antiviral Therapeutics (2011)pmc.ncbi.nlm.nih​
– Business Insider: Todd Rider Is Crowdfunding His DRACO Antiviral Research (2015)businessinsider​
– VOA News: Drug Compound Wipes Out Multiple Viral Infectionsvoanews​
– Publikacja naukowca z Rider Institute: pone.0022572riderinstitute​
– MIT News: New drug could cure nearly any viral infection (2011)news.mit​
– Kimer Med: Why now? Why us? How long? How much? (2024)kimermed​
– iGEM 2025 Kyoto: Design – COCCO2025.igem​
– Science.org: DRACOs: New Antivirals Against Pretty Much Everything? (2011)science​
– Fight Aging: An Update on Kimer Med, Improving on the DRACO Antiviral (2024)fightaging​
– Market Shaping, University of Chicago: Transforming Pandemic Preparedness with Platform-Based Antivirals (2025)marketshaping.uchicago​
– Reddit AMA: Dr. Todd Rider on DRACO (Q&A o oporze wirusów)reddit​

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