PPAP HCl - A Functional Stimulant Without the Push?

Introduction

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Recently, when reading random publications (as one does), I stumbled upon a very interesting compound called PPAP HCl (1-Phenyl-2-propylaminopentane). It is an experimental compound related to selegiline, also known as L-deprenyl, which again is structurally related to amphetamine. The mechanisms are very different, but the subjective target can overlap: more drive, more focus, and less friction.

PPAP introduced me to a class called monoaminergic activity enhancers, which I initially thought was just another way of saying MAOIs. It is not. The difference is what made it interesting enough that curiosity won.

First, I’ll briefly explain amphetamine and selegiline, as they are relevant compounds with major differences but still key similarities. Feel free to skip to the PPAP section if you’re familiar with them.

Amphetamine

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Amphetamine is a powerful recreational and medical stimulant. I think of it as a forceful motivational drug: whatever you do can start feeling important and rewarding. That can help with work, but your brain does not cleanly separate good productivity from garbage productivity. It is not uncommon to become extremely productive at being unproductive. I once spent about 12 hours straight playing Minesweeper. I have also spent an entire night researching Norwegian law, calculating and graphing estimated blood concentrations of amphetamine so I could figure out when I could legally drive.

The point being, amphetamine makes everything feel good and productive. Doing work feels good; scrolling on Reddit instead also feels good. You’re giving your brain false signals for what’s important. It is both a releaser and reuptake inhibitor, which in layman’s terms means it releases dopamine while also interfering with its normal recycling.

Think of it like this: you have a bucket with a fixed amount of water, slowly draining and refilling to maintain balance. When you do something rewarding, like playing video games, the water level rises. Then it returns towards normal when you get bored. Amphetamine rapidly increases the water and blocks the drainage at the same time.

Selegiline

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Selegiline is a lesser-known drug, commonly used to treat Parkinson’s disease and sometimes prescribed off-label for depression. It’s also pretty popular in biohacker and high-performer circles for its dopamine-preserving effects. I haven’t personally tried it, but it’s one of those compounds that keeps showing up in nootropic stacks and biohacking protocols.

It belongs to a class called MAO inhibitors. Specifically, it irreversibly inhibits MAO-B, an enzyme involved in breaking down dopamine. Going back to the water analogy: if amphetamine floods the trough and blocks the drain, selegiline interferes with the filter inside the tank. More dopamine survives each signal, without the same forced release. Structurally, it is basically methamphetamine with a propargyl group bolted onto the nitrogen. That little triple-bonded carbon tail is the “warhead”: it forms a covalent bond with the enzyme, and the body has to synthesize more enzyme before activity fully returns.

At lower prescribed doses, selegiline is more selective for MAO-B. At higher exposure it can lose that selectivity and affect MAO-A as well, which creates a much broader interaction profile. It also metabolizes into l-methamphetamine and l-amphetamine. These are weaker stimulant enantiomers than the recreational versions, but they can still show up on drug tests, which is a fun conversation to have with your employer.

MAO inhibitors can have serious and long-lasting interactions with medications and, depending on the drug and exposure, tyramine-rich foods. This background is here to explain why PPAP caught my attention, not to suggest experimenting with an MAOI.

1-Phenyl-2-propylaminopentane

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Now finally, PPAP. The idea that interested me was that it might behave more like an amplifier than a shove. You could take it, lie in bed, and wait for an amphetamine-style high that never arrives. At least subjectively, it seemed to need some natural push—something interesting enough to engage with—before I noticed anything.

When I was experimenting with PPAP, I did that exact thing (well, YouTube instead of TikTok—fuck TikTok). I took 20 mg orally, waited, and thought it was bunk. Useless crap. Didn’t feel anything. Even though I knew the proposed mechanism, I was still disappointed.

On a later workday I took roughly 50 mg. I had basically forgotten about it by the time I started working. After a while, I noticed I was completely immersed. Normally, I’d switch between tasks, take mini breaks, check my phone, and generally bounce around like most people do. This time I had stayed with the same problem until I randomly checked the clock.

I wouldn’t say it impaired multitasking exactly, but it heavily quieted background noise and external distractions. It made me very goal-oriented and gave me crazy tunnel vision. Again, this wasn’t really something I noticed until my colleague knocked on my door and told me it was lunchtime.

Wow, I’d really stayed on topic for several hours without any distractions or disruptions.

My usual workflow is scattered. I start doing one thing, then a random thought appears out of nowhere and I have to switch tasks. On PPAP, it felt like my focus narrowed down to ONE task.

The cleanest way I can put it: PPAP makes effort feel good. Not the task—the effort itself. It won’t turn boring shit into something fun the way amphetamine will; it only enhances what’s already there. Doomscrolling doesn’t get any more rewarding, but actually grinding through work does. So there’s a real catch: with no baseline of interest, there’s nothing for it to grab onto.

I also recorded taking as much as 100 mg, which was a very high amount in my own history. At that point the tunnel vision became extreme. I’m usually aware of every conversation and movement around the office, but I barely noticed people entering my room. Not exaggerating.

But more definitely wasn’t better. At 100 mg my focus actually got worse instead of sharper, and I ended up overstimulated, a little anxious, and with a mouth so dry it was genuinely annoying. Somewhere around 50 mg is my sweet spot—past that I’m just paying costs with nothing extra to show for it.

Another thing I noticed, which also happens to me on amphetamines, was losing any sense of how much time had passed. I’d work on a problem for hours, then suddenly notice I was thirsty, needed the restroom, had missed a call, or had otherwise ignored my body. The one time I accidentally stayed at work for two extra hours was after taking PPAP after lunch.

My notes contain several experiences between 30 and 60 mg. I am recording that because it is part of the history, not because it is a sensible range for anyone else. I used PPAP too inconsistently to say anything meaningful about tolerance or withdrawal.

For me, it did not push me to start working. It made it easier to continue once I had started. I did not see an obvious change in my sleep, blood pressure, or heart rate records, but that is one person’s noisy data with plenty of confounders—not evidence of no effect.

The compound I keep getting asked about is BPAP, PPAP’s close cousin. I’ve never actually tried it. From what I remember it’s less selective and also enhances serotonin activity, so I’d expect a broader, murkier effect rather than PPAP’s very clean, dopamine-flavoured focus. I don’t have an obvious use case in mind, but I’m curious enough that I’ll probably get around to it eventually.

What the research actually shows

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Human research is the missing piece.

The major 1992 PPAP paper described transporter experiments and several animal models. The authors reported effects on learning, retention, locomotion, and tetrabenazine-induced behavioural changes, then proposed possible clinical uses. Interesting, yes. Evidence that PPAP treats ADHD, depression, or cognitive problems in humans? No.

In July 2026, a larger in vitro transporter study profiled PPAP alongside amphetamine, MDMA, and dozens of emerging stimulants. This is much more useful than an anecdote for describing what PPAP did in that assay, but it still does not tell us a safe human dose, real-world toxicity, or what somebody will feel.

PPAP had a DAT IC50 in the same range as amphetamine in this experiment, while much higher concentrations were needed to inhibit NET and especially SERT. That gives PPAP a very DAT-selective inhibition profile in this assay. It does not prove that PPAP “ignores serotonin,” lacks cardiovascular effects, or is more potent or safer in humans.

The toxicity prediction

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I also ran PPAP through ProTox 3.0. The full prediction report is available here for transparency.

I originally gave the model’s predicted LD50, toxicity class, and target probabilities more attention than they deserved. They are computational guesses, not measurements, and they cannot establish a human safety margin. The honest conclusion from that PDF is not “PPAP looks safe.” It is that a prediction tool produced hypotheses which would need actual toxicology data.

Final thoughts

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PPAP did not make me want to work. It made it weirdly difficult to stop once I had begun. That difference is the entire reason I still think about it.

The proposed activity-enhancer mechanism makes me wonder whether this whole class deserves serious attention in ADHD and cognitive research. And I’ll say the quiet part out loud: I genuinely believe PPAP could be one of the most promising ADHD compounds I’ve come across—and with strikingly low abuse potential. Everything about how it feels points that way. There’s no rush, no high, no kick to chase; it doesn’t reward you just for taking it, it won’t make wasting time fun, and pushing the dose only makes things worse. That’s the opposite of how something addictive behaves.

To be clear, that’s a belief, not a finding. I could be overfitting a single very subjective experience, and the transporter data does not fix that. But it’s what I actually think, and this post was never pretending to be anything other than my experience.

I cannot say anything solid about tolerance, withdrawal, long-term effects, or human toxicity. “Different from classic stimulants” does not automatically mean safe. That said—gut, not data—I’d bet it’s nowhere near as toxic as a lot of what we prescribe today, Adderall included. Until there is real human evidence, this stays what it always was: an interesting compound, an unusually focused day at work, and a sample size of one.

I’ve now put roughly 10 g through myself over about a year, and it’s easily one of the most powerful substances I’ve ever used—not in a knock-you-flat way, but in how completely it rewires my relationship with work.

I’d describe it as: “seems like bunk, let’s just try to get some work done.. oh shit. I’m locked the fuck in”. I also feel like it has a slight mood-boosting effect outside of work, but again, just my experience. Someone once asked if it makes sex better and honestly I’ve got no idea—I’m not sure I’ve ever been intimate on it. I could see it going either way: either completely locked in, or too robotic and detached to care. Probably very individual, like most of this. It gave me a flow state I haven’t had in years, and it’s becoming one of my favourite research chemicals.

— Henrik (co-authored under the influence of its subject)