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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Just after breakfast, sitting in his laboratory at the University of Alicante, Francisco Mojica stared at his computer screen in dismay. It was the 1990s, and he had just created a database of DNA sequences of extreme bacteria—organisms that lived in conditions that would kill almost any other life. These bacteria inhabited salt-saturated lakes—organisms adapted to be “salt lovers,” as their scientific name, halobalilia, implied.labiotech+1
But instead of the usual, orderly DNA sequences he expected, Mojica stumbled upon something strange: regularly repeated DNA fragments, separated by spaces with ever-changing sequences . They were like repeated words in a strange verse—”word-space-word-space-word.” Interesting. Almost like an archive. But an archive of what?wikipedia
Little did he know that he had just discovered one of the most groundbreaking technologies that would fundamentally revolutionize medicine, agriculture, and biology over the next two decades.
First Spark: The Strange Sequence from 1987
The history of CRISPR (acronym for Clustered Regularly Interspaced Short Palindromic Repeats) begins earlier, in Japan.bitesizebio
In 1987, while working on the gene encoding alkaline phosphatase in E. coli , Japanese scientist Yoshizumi Ishino and his team had an unexpected surprise. While cloning DNA for an experiment, they stumbled upon fragments of DNA that were repeated—a highly unusual finding. These sequences were organized into clusters and were regularly distributed along the bacterial genome.biocompare+1
Ishino and his team published their observations, but their significance was never fully explored. This discovery languished in the scientific literature, like a hidden treasure waiting for adventurers.biocompare
The Key to the Puzzle: Francisco Mojica Discovers the Function
Flash forward to the year 2000. Francisco Mojica, now a researcher at the University of Alicante, was working on a different question: how do bacteria from extreme environments adapt to changes in salt concentration? But his curiosity quickly veered elsewhere.labiotech
Using access to growing genetic databases, he began comparing these strange, repetitive sequences Ishino had previously discovered. Imagine his surprise when he discovered that the same repeats appeared in the genomes of bacteria studied around the world—in microorganisms from the ocean, soil, and caves .biocompare
In 2000, he and his colleagues published work showing that this cluster was highly evolutionarily conserved—and therefore must have meant something important. Its very preservation over millions of years of evolution indicated that nature does nothing without reason.biocompare
But that was just the beginning.
Eureka Moment: Virus in Bacterial DNA
A few years later, while comparing databases, Mojica noticed something extraordinary: DNA fragments nested between repeats in the bacterial genome were identical to fragments of the genomes of viruses (bacteriophages) that attack bacteria .labiotech
Not just any fragments – but fragments of actual viruses infectious to those same bacteria!
It was an immediately logical presumption: if a bacterium stores fragments of a virus’s DNA in its cell, it must have acquired this genetic material somehow . And if it holds them, it must need them for something.labiotech
Mojica hypothesized: CRISPR is a bacteria’s adaptive immune system . Once a virus attacks a bacterium and it becomes infected, part of the virus’s genome is squeezed into the CRISPR archive. The next time the same virus tries to attack that bacterium (or its descendants), the immune system will “remember” it and attack it.wikipedia+1
Sounds almost like memory? Because that’s exactly what it is— biological, genetic memory .
A path through the groves of scientific journals
In 2003, Mojica wrote a paper proposing this theory. He submitted it to Nature , one of the world’s most prestigious scientific journals. It was rejected. He tried the Proceedings of the National Academy of Sciences . It was rejected.wikipedia
Nucleic Acids Research . Once again – refusal.wikipedia
He was frustrated, but he didn’t give up. The paper finally made it to the Journal of Molecular Evolution in February 2005. It wasn’t Nature, but it was a publication. Importantly, that same year, independently of Mojica’s work, another laboratory published similar findings.flagshippioneering+1
But something changed. Scientists began to listen.
Experimental Proof: Horvath and Siksnys Show It Works
Although Mojica proposed the hypothesis, experimental evidence came from a completely different direction – from laboratories that were studying… ferments for yogurt production.pmc.ncbi.nlm.nih
In 2005, Philippe Horvath’s team at Danisco (yes, the dairy giant!) investigated how Streptococcus thermophilus bacteria – used to produce yogurt and cheese – could be resistant to infectious viruses (bacteriophages).pmc.ncbi.nlm.nih
Horvath and his colleagues demonstrated experimentally what Mojica had proposed theoretically: when S. thermophilus was infected with a new bacteriophage, the bacterium integrated new sequences derived from the phage’s genome directly into its CRISPR region of DNA . Even better, the next time the same phage tried to infect descendants of that bacterium, they were resistant.pmc.ncbi.nlm.nih
This was not just a theory – it was experimental proof of a working biological immune system.pmc.ncbi.nlm.nih
Separately, that same year, Vytautas Siksnys from Lithuania published a paper showing that the CRISPR system from one bacterium ( S. thermophilus ) could be transferred to a completely different species— E. coli —and it would work there. This was important because it demonstrated the universality of the system.flagshippioneering
2006-2011: Developing the Foundation
In the following years, scientists around the world began to study CRISPR in more detail. Fiona Barrangou and others demonstrated exactly how CRISPR works—how bacteria “learn” to recognize viruses and use this knowledge to protect themselves.nature
Several variants of CRISPR systems have been discovered – CRISPR-Cas9 , CRISPR-Cas12a , and others. Each system had its own Cas proteins – enzymes that perform the actual “cutting” of DNA.pmc.ncbi.nlm.nih
It turned out that Cas9 , from Streptococcus pyogenes (the bacterium that causes angina), was particularly remarkable. When prompted by guide RNA, it would precisely cut DNA exactly where instructed.pmc.ncbi.nlm.nih
By 2011, scientists knew almost everything they needed to know about CRISPR in nature. But no one had yet considered: what if, instead of letting bacteria do what they do naturally, we scientists taught Cas9 to do what we wanted?
The San Juan Meeting and the History That Was Written
In 2011, at a scientific conference in San Juan, Puerto Rico, two scientists from different sides of the Atlantic met by chance.pmc.ncbi.nlm.nih
Jennifer Doudna , a protein structuralist at the University of California, Berkeley, specialized in studying biological mechanisms at the molecular level. Emmanuelle Charpentier , a microbiologist at Umeå University in Sweden, also studied bacterial immune systems.innovativegenomics+1
They talked about CRISPR. Doudna was fascinated; Charpentier was an expert. They decided to collaborate.pmc.ncbi.nlm.nih
2011: Charpentier Discovers the Third Missing Piece
Before Doudna and Charpentier deepened their collaboration, Charpentier had made a significant discovery in her Umeå lab. She was studying CRISPR with Streptococcus pyogenes and discovered something that would change everything.mpg
It turned out that in addition to krRNA (CRISPR RNA) and Cas9, there was a third, critically important component: tracrRNA (trans-activating crRNA) . This was a small but crucial RNA molecule.pmc.ncbi.nlm.nih+1
This was a groundbreaking observation because the tracrRNA turned out to be a “bridge”—it connected Cas9 to the krRNA in such a way that Cas9 knew where to look and where to cut.pmc.ncbi.nlm.nih
2012: The Turning Point When Nature Became a Tool
Now Doudna and Charpentier had all the pieces of the puzzle. In their UC Berkeley/Umeå lab, they worked together (communicating across the ocean) to assemble CRISPR-Cas9 into something that could be a controllable tool.embryo.asu
Their key contribution was elegant: instead of using two separate RNA molecules (krRNA and tracrRNA), they combined them into a single molecule , which they called single guide RNA (sgRNA) .embryo.asu
Why was this important? Because it simplified the technology. Instead of programming two different RNAs, scientists now had to program just one. It was like going from using a computer with two buttons to one with a single large button labeled with what you wanted to do.mpg+1
Experiment: Testing in Dish
In their experiment, Doudna, Charpentier and their team (including Martin Jinek and Michael Hauer from Berkeley, and Krzysztof Chylinski and Ines Fonfara from Umeå) set up a laboratory scene:embryo.asu
They produced pure Cas9 protein – an enzyme not yet “programmed”embryo.asu
They created guide RNA that could program Cas9 to search for a specific DNA sequence.embryo.asu
They combined them in a laboratory tube – along with the target DNAembryo.asu
And they waited.
What happened: Cas9 precisely cut the DNA exactly where the guide RNA told it to . Not just anywhere—right there.embryo.asu
But that wasn’t the goal. Doudna and Charpentier were pursuing something much bigger: demonstrating that the CRISPR-Cas9 system can be programmed like a hyper-precise tool that scientists can target to ANY DNA sequence .embryo.asu
When Doudna and Charpentier showed they could program five different guide RNAs, each targeting a different site in the DNA, the idea was clear: It could work for any sequence a scientist wanted to edit .embryo.asu
Science Publication: The Moment When Everything Changed
Their manuscript reached the editorial office of Science in 2012.pmc.ncbi.nlm.nih
In the June 2013 issue of Science , an article was published: “RNA-guided genetic engineering of human pluripotent stem cells.” The title didn’t sound revolutionary, but its content was incredible.pmc.ncbi.nlm.nih
The article included a detailed description of the three CRISPR-Cas9 components:pmc.ncbi.nlm.nih
Cas9 protein (enzyme)
crRNA (lead part)
tracrRNA (connector)
And importantly , they showed how all three could work together as a programmed, precise DNA editing tool .pmc.ncbi.nlm.nih
But that was only part of it. Doudna and Charpentier proposed something radical: What if scientists could use this system not only in bacteria, but also in eukaryotic cells—like human cells?pmc.ncbi.nlm.nih
The scientific world reacted with madness.
The Year After: Feng Zhang and the First Editions in Mammalian Cells
In 2013, just a few months after Doudna-Charpentier’s publication, Feng Zhang of the MIT Broad Institute published his own paper in Science .embryo.asu
Zhang took the CRISPR-Cas9 described by Doudna and Charpentier and demonstrated that it could be delivered into living mouse and human cells and edit their genome .embryo.asu
It was a massively important demonstration. Theoretically, it worked in a tube. But would it work in living cells? Yes, and Zhang is proof.embryo.asu
Now scientists had not only a conceptual tool, but a practical tool.
Revolution: Six Months, Thousands of Articles
Six months after Doudna-Charpentier’s publication, dozens of labs around the world had already begun experimenting with CRISPR-Cas9.news.berkeley
Here’s why CRISPR was so transformative compared to previous technologies (such as ZFNs – Zinc Finger Nucleases, and TALENs – Transcription Activator-Like Effector Nucleases):ijisrt
aspect
ZFN
LANGUAGES
CRISPR-Cas9
Ease of design
Very difficult, requires protein engineering
Difficult, but easier than ZFN
Very easy – just change the RNA
Time to act
Weeks/months
Days/weeks
Hours/days
Cost
Dear
Easy
Very cheap
Precision
High
High
High
Versatility
Limited to certain sequences
More universal
Universal
Multiplex (multiple targets at once)
Difficult
Difficult
Easy
Scientists could now take any DNA sequence – from a human gene, mitochondrial DNA, bacteria, plants – and program Cas9 to cut it in hours.news.berkeley
It was like going from handwriting every letter of a document to having a golden pen that could write whatever you wanted.
First Triumphs: 2013-2015
By 2015, CRISPR-Cas9 had already been used to:
Gene editing in mouse cells – creating disease modelsaddgene
Mutation Repair – Scientists Worked on Serum Fibrosis and Beta-Thaliasiaaddgene
Gene function research – blocking genes to see what they doaddgene
Plant resistance formations – plants resistant to drought or diseaseaddgene
In 2015, Science named CRISPR its “Breakthrough of the Year” – the only laboratory tool to win this prestigious award.bitesizebio
Parallel History: The Battle for Patents
While Doudna and Charpentier published their results in Science , almost simultaneously, Zhang at MIT/Broad Institute was also working on the CRISPR project. The result: a patent controversy exists today.insights
Doudna and Charpentier filed their patent application in March 2013, but with priority from May 2012.insights
Zhang submitted his application in October 2013, but with priority from December 2012.insights
Zhang received the first patent – the U.S. Patent and Trademark Office granted him Patent No. 8,697,359 in April 2015. But Doudna and Charpentier also hold patents (European and other).broadinstitute+1
In the world of medicine and business – where patents mean money – this battle continues to this day.
A Dramatic Turning: The Nobel Prize in 2020
In a year when the world was grappling with COVID-19, the Swedish Academy of Sciences awarded the 2020 Nobel Prize in Chemistry to exactly two women: Emmanuelle Charpentier and Jennifer Doudna “for developing a method for genome editing.”Nobel Prize
This was historic. It was the first time the Nobel Prize in Chemistry was awarded solely to two women . Charpentier and Doudna were pioneers not only in science but also in gender equality in science.pmc.ncbi.nlm.nih
During her Nobel speech, Doudna expressed her gratitude to Charpentier: “Without her commitment and vision, this would not have been possible.”
From 2013 to 2025: How Far We’ve Come
Fast forward to today. Since the first Science article in 2012, CRISPR has gone from a laboratory curiosity to a real-world tool in medicine:
2019 : First CRISPR clinical trial in sickle cell patients in the USpmc.ncbi.nlm.nih
2023 : FDA approves the first CRISPR-Cas9-based drug for sickle cell disease and thalassemia – Casgevypmc.ncbi.nlm.nih
2024 : More than 1,500 CRISPR clinical trials worldwideinnovationhub
2025 : CRISPR-edited cells are now being delivered to patients who say they “feel like new people”innovationhub
Summary: How Bacteria Taught Us to Heal
The story of CRISPR is a story of discovery that began with curiosity—why do bacteria have these strange DNA repeats?—and led to a medical revolution.
From Yoshizumi Ishino in 1987 discovering the mysterious sequences, to Francisco Mojica understanding their function, to Jennifer Doudna and Emmanuelle Charpentier seeing that the bacterial immune system could be a tool for humanity – each step has been extraordinary.mdpi+4
What bacteria have developed over millions of years of evolution—a self-defense system against viruses—has taught us how to treat human genetic diseases. Nature is our best engineer. We just had to pay attention.pmc.ncbi.nlm.nih+1
Today, in 2025, CRISPR is beyond the “can work” stage and entering the “actually works in patients” stage. This journey from infectious discovery to reliable medical tool took 38 years. But the wait was worth it.
Sources and References
– MDPI: CRISPR-Cas: Converting A Bacterial Defence Mechanism into A State-of-the-Art Genetic Manipulation Tool (2019)mdpi – PMC/NIH: CRISPR-Cas9: From a bacterial immune system to genome-edited human cells in clinical trials (2017)pmc.ncbi.nlm.nih – BioCompare: The History and Evolution of CRISPR (2021)biocompare – Lab Biotechnology EU: Francis Mojica, the Spanish Scientist Who Discovered CRISPR (2022)labiotech – Bitwise Bio: A Brief History of CRISPR-Cas9 Genome-Editing Tools (2024)bitesizebio– Wikipedia: Francisco Mojicawikipedia – Innovative Genomics Institute: Jennifer Doudna and Emmanuelle Charpentier – Behind the Development of CRISPR (2025)innovativegenomics – Flagship Pioneering: A History of CRISPR (2020)flagshippioneering – PMC/NIH: Nobel Prize 2020 in Chemistry honors CRISPR (2020)pmc.ncbi.nlm.nih – PMC/NIH: Breaker of chains (2021)pmc.ncbi.nlm.nih – ASU Embryo Project: Jennifer Doudna and Emmanuelle Charpentier’s Experiment (2017)embryo.asu – Broad Institute: Statements and background on CRISPR patent process (2025)broadinstitute – CRISPR Therapeutics: Dr. Emmanuelle Charpentiercrisprtx – Insights.bio: Revolutionizing genome editing with CRISPR/Cas9: patent dispute (2015)insights – Max Planck Institute: Emmanuelle Charpentier: An artist in gene editing (2017)mpg – Nobel Prize Official: Jennifer A. Doudna (2018)Nobel Prize – PMC/NIH: The genome-editing decade (2021)pmc.ncbi.nlm.nih – PMC/NIH: Blossom of CRISPR technologies and applications (2018)pmc.ncbi.nlm.nih – International Journal of Innovation and Scientific Research: Comparative Review of ZFN, TALEN, and CRISPR/Cas9ijisrt – UC Berkeley News: How CRISPR worksnews.berkeley – AddGene: CRISPR History and Development for Genome Engineering (2024)addgene – Innovation Hub: The Breakthrough of CRISPR (2023ub: The Breakthrough of CRISPR (2023)pmc.ncbi.nlm.nih
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?
dsRNA detector – part of the protein that recognizes the double-stranded RNA of the virus
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
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
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:
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.
Patent problem – Rider held patents on DRACO from MIT. This hindered the work of other scientists until the patents expired or were abandoned. kimermed
The Competition Virus – Other approaches (small molecules, monoclonal antibodies) have received more attention and funding. marketshaping.uchicago
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
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.
The story starts since CRISPR–Cas9 discovery. Noticed and appreciated by Emmanuelle Charpentier. After spending years working on Streptococcus pneumoniae bacteria defense mechanisms against antibiotics. She discovered an RNA that controls the synthesis of a class of molecules that are important in pro-life and self-defense processes. The though she spotted on was a patterned stretch of DNA called CRISPR in the genome of some bacteria, where it serves as part of a defense system against viruses. By copying part of an invading virus’ DNA and inserting it into that stretch, bacteria are able to recognize the virus if it invades again, and attack it by cutting its DNA. Different CRISPR systems have different ways of organizing that attack; all of the systems known at the time involved an RNA molecule called CRISPR RNA. Using bioinformatics in collaboration with Jörg Vogel they’ve noticed a dependency between used programmed sequence RNA and result on the genome. That showed up 3 main elements of this method tracrRNA, CRISPR RNA and the Cas9 protein which was noticed in 2005 by lexander Bolotin, French National Institute for Agricultural Research (INRA). But the first scientist that totticed CRISPR was . Also the coded part of the RNA (crRNA) was traced by John van der Oost from Netherlands this time using E-scherichia coli bacteria. The next breakthrough was made in 2008 by Marraffini and Sontheimer from USA. They evidenced that using CRISPR technique works not as RNA suppressor but in fact targets DNA. The next discovery belonged again to Emmanuelle Charpentier. She noticed tracrRNA forms a duplex with crRNA, and that it is this duplex that guides Cas9 to its targets. In thge summer of 2009 together with Elitza Deltcheva made and successful experiment of editing DNA. Another step was achieved in 2011 by Virginijus Siksnys from Lithuania. The team “transplanted” CRISPR into the bacteria which does not contain a Type II system – E. coli. The experiment wass succesful – the CRISPR unit turned out to be autonomous. They also successfully made experiments with programmed crRNA part. But the real use was done by Feng Zhang from Broad Institute of MIT that have demonstrated targeted genome erase in human and mouse cells.
Welcome to my blog about herbs and health. Today I would like to talk about antiviral herbs, i.e. plants that have the ability to destroy or inhibit the development of viruses in the body. In the era of the coronavirus pandemic and frequent respiratory infections, it is worth knowing natural ways to strengthen immunity and protect against diseases.
Antiviral herbs are plants that contain active substances with virucidal or virostatic activity. Some of them are effective against specific types of viruses, such as influenza, herpes or hepatitis, others have a broad spectrum of activity and can fight various pathogens. Antiviral herbs can be used both prophylactically and therapeutically, in the form of infusions, tinctures, syrups, oils or ointments.
Based on the website https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032839/, several groups of antiviral herbs can be distinguished:
– Herbs containing flavonoids – are plant compounds with strong antioxidant and anti-inflammatory properties. Flavonoids inhibit the multiplication of viruses by blocking their entry into cells or interfering with their replication. Examples of herbs rich in flavonoids are: **Baikal skullcap**, **chamomile**, **purple echinacea**, **elderberry**, **green tea** or **lemon**.
– Herbs containing terpenoids – are plant compounds with a variety of chemical structure and biological properties. Terpenoids exhibit antiviral activity by damaging the lipid membrane of the virus or inhibiting its enzymes. Examples of herbs rich in terpenoids are: **oregano**, **thyme**, **rosemary**, **lavender**, **sage** and **mint**.
– Herbs containing alkaloids – are plant compounds with a characteristic nitrogen structure and a strong pharmacological effect. Alkaloids have antiviral effects by affecting cell metabolism or blocking virus receptors. Examples of herbs rich in alkaloids include: **St. John’s wort**, **licorice**, **chili peppers**, **ginger** and **turmeric**.
– Herbs containing glycosides – are plant compounds consisting of a sugar and non-saccharide part. Glycosides have an antiviral effect by activating the immune system or inhibiting the synthesis of viral proteins. Examples of herbs rich in glycosides are: **aloe**, **garlic**, **cinnamon**, **clove** or **calendula**.
Antiviral herbs can be used alone or combined in herbal blends for a synergistic effect. However, it is important not to exceed the recommended doses and duration of use, as some of
Natural antiviral herbs are:
1. **Oregano** – this popular kitchen spice has not only a deep flavor, but also strong antiviral properties. It contains a substance called **carvacrol**, which destroys the cell membranes of viruses and inhibits their multiplication. Oregano oil is effective against norovirus, herpes and respiratory viruses. It can be used orally or topically, but be careful because it is very irritating. You can also drink an infusion of dried oregano or add it to dishes.
2. **Garlic** (Allium sativum)- this vegetable has been known for its health-promoting properties for centuries. It contains a compound called **allicin**, which has the ability to destroy viruses and other pathogens. Garlic fights flu viruses, pneumonia, rotavirus and HIV. It is best eaten raw, after chopping or mashing it, which releases allicin. You can also prepare a mixture of garlic and honey or tincture of garlic and alcohol.
3. Cistus ** – is a plant with small pink flowers that grows in the Mediterranean. It is rich in **polyphenols**, which have strong antioxidant and antiviral properties. Cistus inhibits the multiplication of influenza, herpes, HIV and HPV viruses. You can drink an infusion of dried cistus leaves or use the extract of this plant in the form of capsules or syrup.
4. **Elderberry** – is a plant with dark berries and white inflorescences, which grows in Europe and North America. It contains **anthocyanins**, which give it its color and have anti-inflammatory, antibacterial and antiviral properties. Elderberry destroys influenza, cold and bird flu viruses. You can consume elderberry juice or syrup or drink an infusion of dried flowers.
5. **Lucorice** (Glycyrrhiza glabra) – is a plant with sweet roots that comes from Asia. It contains a substance called **glycyrrhizin**, which has anti-inflammatory, immunostimulating and antiviral properties. Licorice inhibits the replication of influenza, hepatitis C, HIV and SARS-CoV-2 viruses. You can drink an infusion of dried licorice roots or use the extract in the form of tablets or lozenges.
6.**Black-caraway** (Nigella sativa) – is an indigenous nutrient-rich herbaceous plant found around the world. The plant has various recognition in different languages e.g., black cumin, black seed, black-caraway (English), Habbah Al-Sauda, seed of blessing (Arabic), chernushka (Russian), çörekotu (Turkish). N. sativa has attracted the attention of many healers in ancient civilizations and researchers in recent times. Since ancient times, it is used in different forms to treat illness, including asthma, hypertension, diabetes, inflammation, cough, bronchitis, headache, eczema, fever, dizziness, and influenza
7.**Cinnamon** (Cinnamomum zeylanicum and C. cassia) – Cinnamon bark contains cinnamaldehyde, cinnamic acid, cinnamyl alcohol, coumarin, and eugenol as the major components (Usta et al., 2003). In addition to its proven health beneficiary effects, cinnamon may also protect the body against viral infections. Premanathan et al. (2000) reported that cinnamon bark was highly effective against HIV-1 and HIV-2, where they halt viral DNA replication machinery through the inhibition of HIV protease, integrase, and reverse transcriptase. They also inhibited vpr, sp1-related genes expression (cell cycle arrest), Tat, Rev, and glycosylation. Cinnamaldehyde derived from bark of cinnamon exhibited both in-vitro and in-vivo inhibitory effects against highly pathogenic influenza, Sendai virus, and HSV-1 virus by inhibiting viral protein synthesis at the post-transcriptional level
As you can see, nature has given us many plants and herbs
Viruses are like the fast engineers that can cleverly take over whole machinery and use it for their purpose. Clever able to mutate bad virus gets into the cell and replicates making the cell die. The whole specs of virus is that it needs a cell to replicate.
There are milions of viruses all over the world. Varing in kinds they have one thing in common. As they exist outside the cell the they are called as virons are build as core RNA or DNA molecules , a proten coat called capsid, that surrounds and protects genetic material. Sometimes additionelly the protein is also covered by such called envelope of lipids.
