SnowyWeather
Iron
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Introduction (Optional Read)
I've been looking around, and have found no discussion about this method on this forum and some other places I checked, so I thought I would spread the word. This is a reupload of my original thread on nutria.
Quick Disclaimer:
You cannot legally possess what is needed to carry this process out on a human, and you also cannot legally practice human trials yet.
I do not condone any illegal activity, and don't mean to promote it. This thread is purely to spread awareness for a potential new method.
Basic Iris Knowledge
All you really need to know:
Less iris melanin -> more light scattering -> blue or gray appearance
More melanin -> greater light absorption -> green, hazel, or brown appearance
AAV6
Around 2022, biologists began research on an experimental route that targets reducing melanin-producing cells in the iris (as an alternative to frying your irises with lasers). This method is known as the AAV-mediated melanocyte-targeted suicide gene approach.
They inject an adeno-associated virus (typically AAV6) into the anterior chamber that carries a gene (like herpes simplex virus thymidine kinase) under a melanocyte-specific promoter*. The virus only infects the iris stromal melanocytes*. Then you give a prodrug* like ganciclovir, which only becomes toxic inside those cells and triggers apoptosis*. The melanocytes die off, melanin drops, and the iris lightens (brown → lighter brown/grayish in the rabbit studies).
It’s been shown in Dutch Belted rabbits. Obviously visible lightening by day 28-35, then went stable after that, no uveitis or pressure spikes reported in the published work.
The process is even patented (US11400039B2), but it is currently still experimental, with zero human trials recorded so far.
patents.google.com
There are more sources out there if you want to research some more on your own.
Procedure [Projected for Human Trials]
Step 0: Preparation
Nobody can do this by themself, and no surgeon or biologist can legally offer this. You will need to find some surgeon off-market, or if you're a retard, ask a friend that you trust a lot.
Step 1: Localized injection
In the published protocol, researchers performed an intracameral injection: delivering roughly 50 microliters of the AAV6 vector, at a dose around 1×10¹² vector genomes, directly into the anterior chamber (see Figure 1d: [8] below) using a very fine 30-gauge needle. Obviously use anesthesia. I won't explain it here, do your own research for that, since that can be it's own thread in itself.
Step 2: Preventing Backflow (Pupil Control)
To keep the virus from drifting behind the iris into the posterior chamber, researchers applied topical pilocarpine (pupil restricting drug) before and after the injection, dosed up to four times a day for the first day post-op.
Step 3: Dosing & Bloodwork
This is where human trials would vary the most from the animal trials. Because the activator drug Ganciclovir or valganciclovir has an established human safety profile, which is much lower than rabbits.
Hypothetical dosing (more research should be implemented per person)
Step 4: Verifying containment
Researchers checked for off-target effects by examining tissue samples (hematoxylin and eosin staining) from both the treated eye and the untreated contralateral eye, and found no inflammatory infiltrate and no meaningful difference between the two — essentially a built-in control group (the animal's other eye) to confirm the treatment stayed localized and didn't provoke a broader immune reaction. Obviously this would only work if you operated on one eye, but you could alternatively go to a doctor and request examination if you wish.
Results
Because the dosing of the activator drug being so different between humans and the animals in the current public trials, results would be much less obvious. Here's a diagram of what the trials looked like when successful on the animal trials:
In humans, the results will be less potent, but still have a big impact.
Projected Human Trial Results:
Past MS 9 there is realistically no reason for you to consider this method.
The reason that the lower MS values see disproportionately more brightening is because with less melanin remaining, it creates the illusion that the trials are more effective.
Explanation [Biology]
Explanation [Chemistry]
Conclusion
As looksmaxxers we all need to band together and start creating viruses to inject into ourselves with for the benefit of humanity. Any looksmaxxer ready to ctb should donate their body to science and allow us to inject AAV6 into their eyes and begin human trials.
Introduction (Optional Read)
I've been looking around, and have found no discussion about this method on this forum and some other places I checked, so I thought I would spread the word. This is a reupload of my original thread on nutria.
Quick Disclaimer:
You cannot legally possess what is needed to carry this process out on a human, and you also cannot legally practice human trials yet.
I do not condone any illegal activity, and don't mean to promote it. This thread is purely to spread awareness for a potential new method.
Basic Iris Knowledge
All you really need to know:
Less iris melanin -> more light scattering -> blue or gray appearance
More melanin -> greater light absorption -> green, hazel, or brown appearance
Dark Irises are caused by one thing: Melanin
Found in skin, hair, and most importantly: Irises
There are different types, but the most relevant type of melanin to this thread is Eumelanin
Eumelanin:
Another type is Pheomelanin, which isn’t as important, but still feels a little relevant and is worth mentioning. Pheomelanin is common in green and hazel eyes. Just another obstacle to get to blue eyes
Importance of Melanin
Eye color isn’t a direct gene. You don’t just get the “Blue eye gene” or “green eye gene” from your parents. The gene only determines eumelanin and pheomelanin levels. Meaning that if you change the eumelanin or pheomelanin levels you store, your eyes will be lighter.
Found in skin, hair, and most importantly: Irises
There are different types, but the most relevant type of melanin to this thread is Eumelanin
Eumelanin:
- Two types: black eumelanin and brown eumelanin, most people have varying amounts of both
- Black hair means more black eumelanin, brown hair means more brown eumelanin
- Blonde hair is caused by no black eumelanin and a small amount of brown eumelanin
- This explains why blonde hair often comes with blue eyes: low eumelanin
Another type is Pheomelanin, which isn’t as important, but still feels a little relevant and is worth mentioning. Pheomelanin is common in green and hazel eyes. Just another obstacle to get to blue eyes
Importance of Melanin
Eye color isn’t a direct gene. You don’t just get the “Blue eye gene” or “green eye gene” from your parents. The gene only determines eumelanin and pheomelanin levels. Meaning that if you change the eumelanin or pheomelanin levels you store, your eyes will be lighter.
AAV6
Around 2022, biologists began research on an experimental route that targets reducing melanin-producing cells in the iris (as an alternative to frying your irises with lasers). This method is known as the AAV-mediated melanocyte-targeted suicide gene approach.
They inject an adeno-associated virus (typically AAV6) into the anterior chamber that carries a gene (like herpes simplex virus thymidine kinase) under a melanocyte-specific promoter*. The virus only infects the iris stromal melanocytes*. Then you give a prodrug* like ganciclovir, which only becomes toxic inside those cells and triggers apoptosis*. The melanocytes die off, melanin drops, and the iris lightens (brown → lighter brown/grayish in the rabbit studies).
- Melanocyte-Specific Promoter: A specialized DNA regulatory region that restricts gene expression primarily to pigment-producing cells and melanoma cells
- Iris Stromal Melanocytes: Specialized pigment cells located in the front layer of the eye's iris that produce melanin, control eye color, and absorb stray light (cells that determine your eye color)
- Prodrug: A pharmacologically inactive medication or compound that, after intake, is metabolized into a pharmacologically active drug
- Apoptosis: A programmed process of cell self destruction that eliminates damaged or unneeded cells
It’s been shown in Dutch Belted rabbits. Obviously visible lightening by day 28-35, then went stable after that, no uveitis or pressure spikes reported in the published work.
The process is even patented (US11400039B2), but it is currently still experimental, with zero human trials recorded so far.
Here's the patent if you want to read more about it yourself:
US11400039B2 - Changing eye color by gene transduction - Google Patents
A person's iris color can lighten, such as from brown to lighter brown, green, hazel, or blue, by introducing a melanocyte-killing agent through the cornea of the person's eye and contacting the anterior surface of the iris with the agent at a dose sufficient to kill melanocytes in the iris stroma.patents.google.com
There are more sources out there if you want to research some more on your own.
Procedure [Projected for Human Trials]
Step 0: Preparation
Nobody can do this by themself, and no surgeon or biologist can legally offer this. You will need to find some surgeon off-market, or if you're a retard, ask a friend that you trust a lot.
Step 1: Localized injection
In the published protocol, researchers performed an intracameral injection: delivering roughly 50 microliters of the AAV6 vector, at a dose around 1×10¹² vector genomes, directly into the anterior chamber (see Figure 1d: [8] below) using a very fine 30-gauge needle. Obviously use anesthesia. I won't explain it here, do your own research for that, since that can be it's own thread in itself.
Step 2: Preventing Backflow (Pupil Control)
To keep the virus from drifting behind the iris into the posterior chamber, researchers applied topical pilocarpine (pupil restricting drug) before and after the injection, dosed up to four times a day for the first day post-op.
Step 3: Dosing & Bloodwork
This is where human trials would vary the most from the animal trials. Because the activator drug Ganciclovir or valganciclovir has an established human safety profile, which is much lower than rabbits.
Hypothetical dosing (more research should be implemented per person)
- Low Dose: ~1–1.5 mg/kg IV, once daily, for 5 days
- Med Dose: ~2.5 mg/kg IV, once daily, for 5 days
- Max Dose: ~5 mg/kg IV, once daily, for 5 days (matching standard approved dosing, only reached if lower cohorts are clean)
Step 4: Verifying containment
Researchers checked for off-target effects by examining tissue samples (hematoxylin and eosin staining) from both the treated eye and the untreated contralateral eye, and found no inflammatory infiltrate and no meaningful difference between the two — essentially a built-in control group (the animal's other eye) to confirm the treatment stayed localized and didn't provoke a broader immune reaction. Obviously this would only work if you operated on one eye, but you could alternatively go to a doctor and request examination if you wish.
Results
This is the Martin-Schultz Scale, used for referencing eye color. This scale is commonly used in science, so its preferred to the 1998 Eye Color scale, which I see is more commonly used on these forums.
Because the dosing of the activator drug being so different between humans and the animals in the current public trials, results would be much less obvious. Here's a diagram of what the trials looked like when successful on the animal trials:
In humans, the results will be less potent, but still have a big impact.
Projected Human Trial Results:
Low Dose Result: ~MS 15-16
Med Does Result: ~MS 12-13
Max Dose Result: ~MS 9-11
Med Does Result: ~MS 12-13
Max Dose Result: ~MS 9-11
Low Dose Result: ~MS 11-12
Med Does Result: ~MS 9-10
Max Dose Result: ~MS 5-7
Med Does Result: ~MS 9-10
Max Dose Result: ~MS 5-7
Low Dose Result: ~MS 9-10
Med Does Result: ~MS 6-8
Max Dose Result: ~MS 3-5
Med Does Result: ~MS 6-8
Max Dose Result: ~MS 3-5
Low Dose Result: ~MS 7-8
Med Does Result: ~MS 4-6
Max Dose Result: ~MS 1-3
Med Does Result: ~MS 4-6
Max Dose Result: ~MS 1-3
Past MS 9 there is realistically no reason for you to consider this method.
The reason that the lower MS values see disproportionately more brightening is because with less melanin remaining, it creates the illusion that the trials are more effective.
Explanation [Biology]
As mentioned earlier, eye color isn't determined by a pigment that determines a specific eye color. Melanin cells (melanocytes) absorb light to make brown and black eyes. Blue and green eyes have less melanocytes, causing light to displace and scatter instead of being absorbed. Once enough melanocytes die and their melanin is cleared away, the underlying scattering effect becomes visible, brown eyes turn blue/green/hazel. In the rabbit study, this shifted iris color from brown toward blue with no observed inflammation.
The trick to doing this without harming the rest of the eye relies on an important part of melanocyte biology: melanocytes are essentially the only cells in the body that make heavy use of the enzyme tyrosinase, the rate-limiting step in melanin synthesis. Every melanocyte has active tyrosinase gene machinery while almost no other cell type does.
Once triggered, the affected melanocytes die via apoptosis. This matters biologically because apoptotic cells shrink, package themselves into membrane-bound fragments, and get quietly cleared by resident immune cells (efferocytosis) without causing inflammation. Consistent with this, tissue staining in the study showed no cellular infiltrate and no meaningful difference between the treated eye and the untreated control eye which is a sign the cell death was clean rather than damaging.
The trick to doing this without harming the rest of the eye relies on an important part of melanocyte biology: melanocytes are essentially the only cells in the body that make heavy use of the enzyme tyrosinase, the rate-limiting step in melanin synthesis. Every melanocyte has active tyrosinase gene machinery while almost no other cell type does.
Once triggered, the affected melanocytes die via apoptosis. This matters biologically because apoptotic cells shrink, package themselves into membrane-bound fragments, and get quietly cleared by resident immune cells (efferocytosis) without causing inflammation. Consistent with this, tissue staining in the study showed no cellular infiltrate and no meaningful difference between the treated eye and the untreated control eye which is a sign the cell death was clean rather than damaging.
Explanation [Chemistry]
There are really three chemical systems stacked on top of each other.
1: The delivery vehicle (AAV6 capsid)
AAV (adeno-associated virus) is a small, non-enveloped virus: a protein shell (capsid) built from repeating viral proteins, packaging a single strand of DNA about 4.7 kilobases long. The patent describing this method specifies the recombinant AAV can use either an AAV1 or an AAV6 capsid protein. Critically, it's recombinant meaning the genes that let the natural virus replicate itself have been stripped out and replaced with the therapeutic DNA cassette.
AAV (adeno-associated virus) is a small, non-enveloped virus: a protein shell (capsid) built from repeating viral proteins, packaging a single strand of DNA about 4.7 kilobases long. The patent describing this method specifies the recombinant AAV can use either an AAV1 or an AAV6 capsid protein. Critically, it's recombinant meaning the genes that let the natural virus replicate itself have been stripped out and replaced with the therapeutic DNA cassette.
This means:
- It can't reproduce itself or spread as an infection.
- It doesn't insert into your chromosomes, it persists in the cell nucleus as a small circular loop of DNA (an episome), separate from your genome, avoiding the mutation risk that comes with viruses that integrate.
- AAV6's capsid chemistry gives it a particular binding affinity for cell-surface sugars, which helps determine which tissues it enters efficiently which is part of why this serotype was chosen for ocular work.
2) Tyrosinase Promoter
Inside that DNA payload sits a promoter sequence cloned from the tyrosinase gene. The design links a suicide gene to a promoter for tyrosinase, so the gene is only active in the presence of the transcription factors melanocytes naturally produce. Even if the virus happens to enter a non-melanocyte cell nearby, the payload gene stays silent there, because that cell lacks the melanocyte-specific transcriptional machinery needed to activate the promoter. This is the first layer of chemical selectivity.
Inside that DNA payload sits a promoter sequence cloned from the tyrosinase gene. The design links a suicide gene to a promoter for tyrosinase, so the gene is only active in the presence of the transcription factors melanocytes naturally produce. Even if the virus happens to enter a non-melanocyte cell nearby, the payload gene stays silent there, because that cell lacks the melanocyte-specific transcriptional machinery needed to activate the promoter. This is the first layer of chemical selectivity.
3) The trigger (HSVtk + ganciclovir)
The gene sitting behind that promoter encodes herpes simplex virus thymidine kinase (HSVtk) is an enzyme that, together with a nucleoside analog drug forms the core "suicide gene" system. Human thymidine kinase is picky about what it will phosphorylate, but HSVtk is much less picky.
The gene sitting behind that promoter encodes herpes simplex virus thymidine kinase (HSVtk) is an enzyme that, together with a nucleoside analog drug forms the core "suicide gene" system. Human thymidine kinase is picky about what it will phosphorylate, but HSVtk is much less picky.
When ganciclovir (a synthetic molecule that structurally resembles the DNA building block guanosine) enters a cell expressing HSVtk, the enzyme phosphorylates it into ganciclovir-monophosphate. Host cell enzymes then add two more phosphates, producing ganciclovir-triphosphate, which is a molecule now similar enough to a real nucleotide that DNA polymerase mistakenly incorporates it into newly replicating DNA. But ganciclovir's chemical structure lacks the normal connection point needed to keep extending the DNA strand, so it acts as a chain terminator, jamming DNA replication and accumulating unrepairable damage. The cell's internal damage-sensing pathways respond by triggering apoptosis.
This gives a second, independent layer of selectivity on top of the promoter lock: only cells that got transduced by the virus, AND have the promoter switched on, AND are then exposed to ganciclovir will make the toxic metabolite.
It's important to note that the phosphorylated ganciclovir can leak into neighboring cells through gap junctions, which can be useful for cleaning up a slightly wider patch of tissue without needing every single cell to be individually transduced.
This gives a second, independent layer of selectivity on top of the promoter lock: only cells that got transduced by the virus, AND have the promoter switched on, AND are then exposed to ganciclovir will make the toxic metabolite.
It's important to note that the phosphorylated ganciclovir can leak into neighboring cells through gap junctions, which can be useful for cleaning up a slightly wider patch of tissue without needing every single cell to be individually transduced.
Conclusion
As looksmaxxers we all need to band together and start creating viruses to inject into ourselves with for the benefit of humanity. Any looksmaxxer ready to ctb should donate their body to science and allow us to inject AAV6 into their eyes and begin human trials.
