Matthew Spears

[Anagen💈 @anagenxyz]

Your follicles are not just growing hair. They are keeping time.

Every follicle on your head expresses the same core clock genes as the master pacemaker in your brain: BMAL1, CLOCK, PER, and CRY, wired into the same ~24 hour feedback loop.

Cut a human follicle out of the body, keep it alive in a dish, and its clock genes keep cycling on a ~24 hour rhythm for days (Al-Nuaimi 2014).

PER3 peaks just before you wake (Akashi 2010).

The readout is so reliable it was used to measure how far night-shift workers' internal clocks had slipped out of sync with their schedule.

These genes gate the hair cycle itself.

PER1 sits quiet while a hair grows, then climbs sharply as it shifts into regression. So researchers silenced it. 96 hours later, 71% of those follicles were still in the growth phase, versus 4% of controls (Al-Nuaimi 2014).

PER1 and BMAL1 are part of the molecular switch that ends a hair's growth.

In mice, the follicle's stem-cell pool is split into two camps at any given moment, sitting at opposite phases of the clock. Some primed to fire, some held in reserve (Janich 2011).

The clock controls the timing of growth.

Knock out that clock and the skin shows signs of premature ageing.

To be clear: no study shows that a few bad nights make you go bald.

But hair growth is not constant. It is a rhythm, and that rhythm is entrained to time.

[Anagen💈 @anagenxyz]

This bottle contains MINX, a proprietary smooth-release oral minoxidil we recently invented to treat hair loss.

We designed it with AI, then validated the drug's release profile in our wet lab. (1/11)

[Anagen💈 @anagenxyz]

A hair loss company just raised $100 million from Eli Lilly.

Lilly wrote a $40 million check itself.

The drug, ABS-201, is an AI-designed antibody that blocks the prolactin receptor.

The science is real. The data underneath the hype is the problem.

Prolactin is not just a pregnancy hormone. Your scalp follicles carry its receptor, and prolactin pushes them into the regression phase early (Foitzik 2006). In mice, knock that receptor out and they grow longer hair (Craven 2001).

So blocking it is a real idea. Follicles may stay in the growth phase longer, and it never touches DHT.

But here is what should slow you down.

We have been able to lower prolactin for decades. Cabergoline does it, cheaply, in a pill. It does not grow hair, because the prolactin that matters is made inside the follicle, not in your blood.

And this is not even AbSci's idea or the first prolactin receptor antibody to enter humans.

A company called Hope Medicine built the first prolactin-receptor antibody for hair, HMI-115, years ago.

Its entire efficacy case is one Phase 1b: 12 men, open label, no placebo, about 14 more hairs per cm2 versus baseline. Worse than Minoxidil.

Then they ran the real test. 192 men, randomized, placebo-controlled, hair count as the primary endpoint. It finished in November 2024.

The results have never been released.

And it is not that the company went dark. They published the same antibody's endometriosis trial in The Lancet last month. The hair trial, finished a year earlier, has said nothing.

When a company publishes one result and buries the other, the silent one is rarely the winner.

Meanwhile, AbSci's $100 million readout was a single dose in 32 volunteers. The endpoint was side effects from one dose. It has not measured hair on a single person.

And with a half-life over 65 days, one shot blocks prolactin across your body for months. If it were a blockbuster hair drug, there could have been growth benefits by month 3.

So no, it is not a scam. The target is real.

But it is a monoclonal antibody, too large to cross skin so you have to inject it, for a condition a $20 generic already treats, riding on a placebo-controlled trial nobody will show you.

The prolactin pathway is real. The hype is the product.

[Anagen💈 @anagenxyz]

Finasteride exists because of a village in the Dominican Republic.

In the 1970s, researchers found a cluster of genetically male children there, born unable to make DHT.

They grew up with small prostates. Full heads of hair. No acne.

The cause was a single missing enzyme: 5-alpha-reductase (5-ar) Type 2.

Merck saw the blueprint. Block that one enzyme. Shrink the prostate. Keep your hair.

That became finasteride. Proscar for the prostate in 1992. Propecia for hair in 1997.

The first drug ever built to lower DHT.

But there was a catch.

There are actually three forms of 5-ar. But for your hair, two matter: Type 1 and Type 2.

Type 1 is the more abundant one in your scalp. In balding follicles it runs about 4x higher than Type 2 (Sawaya 1997).

But Type 2 is the one we can actually prove matters.

Men born without Type 2 barely bald. And it sits in the dermal papilla, the cell that shrinks the follicle, whereas most of Type 1 sits in your oil glands (Bayne 1999).

No one has ever been found who was born without Type 1. That experiment does not exist in humans.

So this does not clear Type 1. It just means Type 2 is the one with the proof.

Finasteride blocks Type 2, and almost only Type 2. It is a near-pure Type 2 inhibitor. That is exactly why it works.

But that selectivity leaves Type 1 running, and it caps serum DHT at about 70%, because Type 1 makes the rest.

A decade later came dutasteride. Avodart, 2002.

It blocks both enzymes, and it blocks Type 2 harder than finasteride does.

So it suppresses DHT far more deeply, about 95% versus finasteride's 71% in a head to head. And in direct trials, dutasteride grows more hair.

How much of that edge is the deeper Type 2 block versus the added Type 1 block? No trial has cleanly separated the two variables yet, or a third unknown.

But the result is the same: more of the DHT signal off.

Finasteride blocks the enzyme that starts balding.

Dutasteride blocks the same one more strongly, plus the more abundant one finasteride leaves behind.

[Anagen💈 @anagenxyz]

Sublingual minoxidil is the most overhyped product in hair care right now.

This is the post no one in hair wants to write, because everyone wants to sell you standard oral minoxidil with a fancy upcharge.

Sublingual minoxidil has the same peak timing as standard oral minoxidil:

> Standard oral minoxidil: ~30 minutes
> Sublingual minoxidil: ~30 minutes
> MINX: 8 - 10 hours

Sublingual minoxidil shows a 3x higher peak blood level as MINX:

> 5mg Standard oral minoxidil: ~37 ng/mL
> 5mg Sublingual minoxidil: ~18 ng/mL
> 5mg MINX: ~6.5 ng/mL

Only one shows signs of prolonged release. It’s not sublingual minoxidil.

For prolonged release, you want three things:

> A very delayed peak.
> A very low peak.
> The same area under the curve as a standard dose.

Sublingual minoxidil does not do that in any study or blood test published as of today.

The worst part is that standard oral minoxidil is being marketed as sublingual.

Telehealths are saying, “Just put it under your tongue.”

It does not work. Under your tongue, standard oral minoxidil takes 10 to 30 minutes to dissolve, MAX.

For sublingual to actually work as a smooth release product, you’d need it to dissolve for hours, not minutes.

That is the bar: delayed peak, lower peak, same exposure.

As far as we can tell, MINX is the only hair-loss product on the market that has shown that in human data.

[Matthew Spears @looking4copes]

@JeffVincint It matters because you are a fraud. You are giving people false hope and it is wrong.

[Matthew Spears @looking4copes]

@JeffVincint I’m saying you made the whole thing up. Almost everything you just said is gibberish. I’m saying you didn’t make ethosomes at all. You simply mixed a gel together and posted a picture, claiming you made ethosomes.

[Matthew Spears @looking4copes]

@JeffVincint From mixing. This is exactly what it looks like when you incorporate air into a gel mixture. Ethosomes are not that big. It’s very easy to fact check this.

[Matthew Spears @looking4copes]

@JeffVincint I have made ethosomes before. They aren’t some kind of advanced delivery system. High schoolers can make them. They are not visible to naked eye. You show a picture of air bubbles and claim they are ethosomes.

[Matthew Spears @looking4copes]

@JeffVincint Please address this. These are clearly not ethosomes as ethosomes can barely be seen with the naked eye. These are large air bubbles. You should know this.

[Matthew Spears @looking4copes]

@RBrokeman @JeffVincint So? This is always the case with new treatments. Yet new drugs get approved every year.

[Matthew Spears @looking4copes]

@RBrokeman @JeffVincint Why would anyone boycott a hair growth cosmetic?

[Matthew Spears @looking4copes]

@JeffVincint This just looks like air bubbles, not ethosomes.

[Matthew Spears @looking4copes]

@JeffVincint How long does this study run?

[Matthew Spears @looking4copes]

@JeffVincint I want to dunk my head in this

[Matthew Spears @looking4copes]

@JeffVincint I hope your topical is not Calcitrol. It has been tried before.

[Matthew Spears @looking4copes]

@JeffVincint What does this mean?

[Matthew Spears @looking4copes]

@JeffVincint Any idea how affordable this will be?

[Matthew Spears @looking4copes]

@JeffVincint Can you elaborate? I don’t follow.

[Matthew Spears @looking4copes]

@JeffVincint Fuck it’s over. You had a nice run Jeff.