Stimulants NEW Pure Dopaminergic stimulant: Alpha-cyclopropyl-amphetamine!!! 🤓

[LikeADaVinci]

hi,

I’m interested in finding and experimenting with a purely dopaminergic releasing amphetamine drug, as it seems EVERY STIMULANT DRUG OF THE AMPHETAMINE CLASS RELEASES BOTH NOREPINEPHRINE AND DOPAMINE BOTH, (or rarely serotonin and dopamine (cyclazodone)), but that purely dopaminergic releasing agents or reuptake inhibitors are unknown …

So take UWA-101 for example, which is MDMA with an alpha-cyclopropyl moiety as opposed to the standard alpha methyl … this drug drops the activity at the NE receptor down to nothing while retaining the serotonergic activity (classic to methyenedioxy amphetamines) while causing a huge boost in dopaminergic affinity (something largely spared by MDMA naturally)

So the logic goes: what if we drop the methyenedioxy bridge in UWA-101 and demethylate the nitrogen (so it’s not neurotoxic) and simply have alpha-cyclopropyl-dextroamphetamine?

This can easily be made similar to PN2P with benzaldehyde and alpha-cyclopropylamine (I think?) to yield a precursor analguous to PN2P except with a cyclopeopyl moiety instead of methyl, that when reduced with sodium borohydride should yield the desired (R/S)-alpha-cyclopropyl-phenethylamine?

Going by structure activity logic, if the alpha cyclopropyl in UWA-101 vs MDMA drops the NE activity and drastically increased Dopaminergic activity, shouldn’t alpha-cyclopropylamphetamine follow suite and be a purely dopaminergic releasing agent with no NE (neuroepinephrine) receptor activity?

Wouldn’t that be the holy grail of amphetamines? No increase in blood pressure or heart rate (no strain on the cardiovascular system, no stress induced on the body) while offering purely pleasurable stimulation?

In thinking of synthesizing some and trying it out.

My only question is: is there any reason to think that methylcyclopropylamine wouldn’t bond with benzaldehyde at the mid-point carbon in between the amine and the cyclopropyl group?

Thanks!

If anyone else wants to help me out any synthesize this before I get a chance to (it will probably take me a year to find the time to complete this) could you please let me know of the result here on this thread or by PM?

Thanks!

Christopher Scott

 

[negrogesic]

Going by structure activity logic, if the alpha cyclopropyl in UWA-101 vs MDMA drops the NE activity and drastically increased Dopaminergic activity, shouldn’t alpha-cyclopropylamphetamine follow suite and be a purely dopaminergic releasing agent with no NE (neuroepinephrine) receptor activity?

Wouldn’t that be the holy grail of amphetamines? No increase in blood pressure or heart rate (no strain on the cardiovascular system, no stress induced on the body) while offering purely pleasurable stimulation?

Your underlying assumption is wrong. An amphetamine without ability to release norepinephrine wouldn't be the "holy grail of amphetamines". Norepinephrine (NE) release is important to the reinforcing effects of amphetamines, heightening arousal and alertness etc. Drugs that increase both dopamine and NE are generally more reinforcing than purely dopaminergic drugs, but this ratio (selectivity) is important. Overly selective dopamine releasers often have less reinforcing effects because they lack the full stimulant effects provided by NE release or reuptake.

As far as your proposed molecule (alpha-cyclopropylamphetamine) the overall bulkiness/steric hinderance of the cyclopropyl group would reduce the molecule’s ability to fit into the binding site of DAT as effectively as amphetamine/meth/aminorex etc. This would probably make it act more like a reuptake inhibitor, with the bulkiness causing it to block transporter reuptake, rather than promote release.

But again the underlying logic is flawed. An amphetamine analog that is purely dopaminergic would be less rewarding than one with ability to release NE. What the optimal rewarding DA:NE ratio is for releasing agents, I'm not sure. This optimal ratio has been better studied in reuptake inhibitors due to the massive amount of phenyltropanes created and the ability to fine tune DAT:NET:SERT selectivity in such reuptake inhibitors. Cocaine is near optimal, although there a few synthetic phenyltropanes that are supposedly more reinforcing in animal studies. The optimal ratio of DA:NE release might be something like methamphetamine or 4-MAR, but its hard to say because of the 5HT release factor with both those drugs, which of course changes the reinforcing properties (particularly euphoria). I've tried some quite selective dopamine reuptakers (like morphodrol) -- which when vaped had a very strong urge to redose despite producing marginal euphoria. That's why the lever pressing animal studies should be taken with a grain of salt, because some dopaminergic stimulants can be compulsively reinforcing, but not especially enjoyable.

Anyway alpha-cyclopropylamphetamine would be a crappy drug, and if anything it would likely be dopamine reuptake inhibitor given the constraints of the dopamine transporter.

Your whole premise of more dopamine = more fun is based on the simplistic view that society has on dopamine, whereby people think that dopamine = fun, but the reality is more complex than that. Why waste a year trying to figure out how to synthesize a drug based on that half-baked notion (especially given the lack of understanding of how ligands interact with the DAT, i.e., that adding a cyclopropyl group would actually turn it into a reuptake inhibitor, not a releasing agent).

This is why I presume you weren't actually planning on synthesizing this compound, because anyone capable of synthesizing such a thing would also have enough of a grasp on SAR to realize that it wouldn't even make sense to do so.

That said, some Chinese RC manufacturers have synthesized some pretty awful stuff just in an attempt to skirt the law. For instance, I was unfortunate enough to try 3F-PHP, which felt like a highly selective NE reuptaker. It was basically an anxiety attack in powder form.

 

[emkee_reinvented]

MDAI, very selective primarly for Serotonin.
A good name would be Serotonin Straightjacked.

Bit of balance is better.

 

[Skorpio]

Please don’t try to synthesize that compound. Your methods would not give you what you think (and if you have to ask, you probably shouldn’t be doing it).

 

[PenisEnvyThe3rd]

What about a dopamine reuptake inhibitor?

 

[WellTram]

I dont know but for the most pleasurable effects it should raise noradrenaline, serotonine and dopamine. For example, tramadol was made in hope to create functional stim-like painkiller and it release serotonine, it inhibits noradrenaline reuptake and raise dopamine by it's active opioid metabolite and in right dose it feels like something between low dose mdma and low dose meth but I am ultrarapid cyp2d6 metabolizer. I can do meth and after few hours take tramadol and it will feel like i did more meth lol. But I have luck that my antiseizure medication doesnt produce any psychoactive effects its like taking sugar pill which absolutely prevents seizures.

So the point of what I said is that for best euphoria u probably need dopamine, serotonine, noradrenaline and maybe some kind of hightened endogenous endorphine release or ingesting something acting on dopamine, serotonine, noradrenaline and opioid receptors but acting on opioid receptors is basically raising dopamine but not directly.

 

[PenisEnvyThe3rd]

hi,

I’m interested in finding and experimenting with a purely dopaminergic releasing amphetamine drug, as it seems EVERY STIMULANT DRUG OF THE AMPHETAMINE CLASS RELEASES BOTH NOREPINEPHRINE AND DOPAMINE BOTH, (or rarely serotonin and dopamine (cyclazodone)), but that purely dopaminergic releasing agents or reuptake inhibitors are unknown …

So take UWA-101 for example, which is MDMA with an alpha-cyclopropyl moiety as opposed to the standard alpha methyl … this drug drops the activity at the NE receptor down to nothing while retaining the serotonergic activity (classic to methyenedioxy amphetamines) while causing a huge boost in dopaminergic affinity (something largely spared by MDMA naturally)

So the logic goes: what if we drop the methyenedioxy bridge in UWA-101 and demethylate the nitrogen (so it’s not neurotoxic) and simply have alpha-cyclopropyl-dextroamphetamine?

This can easily be made similar to PN2P with benzaldehyde and alpha-cyclopropylamine (I think?) to yield a precursor analguous to PN2P except with a cyclopeopyl moiety instead of methyl, that when reduced with sodium borohydride should yield the desired (R/S)-alpha-cyclopropyl-phenethylamine?

Going by structure activity logic, if the alpha cyclopropyl in UWA-101 vs MDMA drops the NE activity and drastically increased Dopaminergic activity, shouldn’t alpha-cyclopropylamphetamine follow suite and be a purely dopaminergic releasing agent with no NE (neuroepinephrine) receptor activity?

Wouldn’t that be the holy grail of amphetamines? No increase in blood pressure or heart rate (no strain on the cardiovascular system, no stress induced on the body) while offering purely pleasurable stimulation?

In thinking of synthesizing some and trying it out.

My only question is: is there any reason to think that methylcyclopropylamine wouldn’t bond with benzaldehyde at the mid-point carbon in between the amine and the cyclopropyl group?

Thanks!

If anyone else wants to help me out any synthesize this before I get a chance to (it will probably take me a year to find the time to complete this) could you please let me know of the result here on this thread or by PM?

Thanks!

Christopher Scott

Why not just supplement for its precursors and produce dopamine naturally?

 

[CarryBagMan]

Your underlying assumption is wrong. An amphetamine without ability to release norepinephrine wouldn't be the "holy grail of amphetamines". Norepinephrine (NE) release is important to the reinforcing effects of amphetamines, heightening arousal and alertness etc. Drugs that increase both dopamine and NE are generally more reinforcing than purely dopaminergic drugs, but this ratio (selectivity) is important. Overly selective dopamine releasers often have less reinforcing effects because they lack the full stimulant effects provided by NE release or reuptake.

As far as your proposed molecule (alpha-cyclopropylamphetamine) the overall bulkiness/steric hinderance of the cyclopropyl group would reduce the molecule’s ability to fit into the binding site of DAT as effectively as amphetamine/meth/aminorex etc. This would probably make it act more like a reuptake inhibitor, with the bulkiness causing it to block transporter reuptake, rather than promote release.

But again the underlying logic is flawed. An amphetamine analog that is purely dopaminergic would be less rewarding than one with ability to release NE. What the optimal rewarding DA:NE ratio is for releasing agents, I'm not sure. This optimal ratio has been better studied in reuptake inhibitors due to the massive amount of phenyltropanes created and the ability to fine tune DAT:NET:SERT selectivity in such reuptake inhibitors. Cocaine is near optimal, although there a few synthetic phenyltropanes that are supposedly more reinforcing in animal studies. The optimal ratio of DA:NE release might be something like methamphetamine or 4-MAR, but its hard to say because of the 5HT release factor with both those drugs, which of course changes the reinforcing properties (particularly euphoria). I've tried some quite selective dopamine reuptakers (like morphodrol) -- which when vaped had a very strong urge to redose despite producing marginal euphoria. That's why the lever pressing animal studies should be taken with a grain of salt, because some dopaminergic stimulants can be compulsively reinforcing, but not especially enjoyable.

Anyway alpha-cyclopropylamphetamine would be a crappy drug, and if anything it would likely be dopamine reuptake inhibitor given the constraints of the dopamine transporter.

Your whole premise of more dopamine = more fun is based on the simplistic view that society has on dopamine, whereby people think that dopamine = fun, but the reality is more complex than that. Why waste a year trying to figure out how to synthesize a drug based on that half-baked notion (especially given the lack of understanding of how ligands interact with the DAT, i.e., that adding a cyclopropyl group would actually turn it into a reuptake inhibitor, not a releasing agent).

This is why I presume you weren't actually planning on synthesizing this compound, because anyone capable of synthesizing such a thing would also have enough of a grasp on SAR to realize that it wouldn't even make sense to do so.

That said, some Chinese RC manufacturers have synthesized some pretty awful stuff just in an attempt to skirt the law. For instance, I was unfortunate enough to try 3F-PHP, which felt like a highly selective NE reuptaker. It was basically an anxiety attack in powder form.

Could this be why purely dopaminergic drugs for Parkinson's like L-Dopa would probably not be satisfactory for a stimulant chaser?? Yeah it's pure dopamine , but nothing else. Could make you more randy possibly, but not pleasurably reinforcing or euphoric.

 

[TheLightBringer]

Could this be why purely dopaminergic drugs for Parkinson's like L-Dopa would probably not be satisfactory for a stimulant chaser?? Yeah it's pure dopamine , but nothing else. Could make you more randy possibly, but not pleasurably reinforcing or euphoric.

Ive always wondered if co-administering selective DRIs and NRIs would produce a euphoria similar to a proper NDRI. Like say one took modafinil + atomoxetine and added a TAAR1 agonist like 3-methoxy-tyramine. Would this produce a more typical stimulant euphoria?

I assume its more complex than that, but still curious. Maybe a modafinil + atomoxetine + kanna + TAAR1 agonist together would produce a decent mimic of a triple reuptake inhibitor

 

[Allylbenzene]

Ive always wondered if co-administering selective DRIs and NRIs
...
I assume its more complex than that, but still curious. Maybe a modafinil + atomoxetine + kanna + TAAR1 agonist together would produce a decent mimic of a triple reuptake inhibitor

That's how you'd recreate most drugs. MDMA needs an alpha-2 adrenergic & Imidazoline-1 agonist though so low-dose clonidine or possibly agmatine works. Agmatine adds some 5-HT2A activity also.

An LSD mix is also plausible by combining both botanicals and supplements to hit 5-HT1-7, D1-5 and adrenergic α1,2 & ß1,2. Plus a 5-HT3 antagonist for additional synergy.

 

[N0ph0n0]

Sounds like ass, it would feel really flat and boring.

 

[TheLightBringer]

That's how you'd recreate most drugs. MDMA needs an alpha-2 adrenergic & Imidazoline-1 agonist though so low-dose clonidine or possibly agmatine works. Agmatine adds some 5-HT2A activity also.

An LSD mix is also plausible by combining both botanicals and supplements to hit 5-HT1-7, D1-5 and adrenergic α1,2 & ß1,2. Plus a 5-HT3 antagonist for additional synergy.

I think it could work for some substances but some molecules simply have a too complex pharmacological profile.

Like the MDMA experience people have replicated using a SERT releaser + low dose NDRA + barely threshold dose of a psych, maybe even add on agmatine or a threshold dose clonidine like you said for a2 agonism and use some SubQ oxytocin and Im sure no one would be able to tell the experiences apart reliably.

But replicating the pharmacological profile of LSD using botanicals and supplements and still have it feel like a proper LSD experience seems out of reach. At that point youd have to take an actual psychedelic to replicate an actual psychedelic, in which case the experience would likely produce a different qualia due to the nature of the varied experience with different scaffolds of 5ht2a agonists. Monoamine releasers are generally more straightforward

 

[TheLightBringer]

@Allylbenzene But on another note Im still really fascinated by trying to replicate the experience of substances using others, I wonder to what extend one could replicate say 3-MeO-PCP or Alcohol with other drugs.

 

[Allylbenzene]

I think it could work for some substances but some molecules simply have a too complex pharmacological profile.

It depends how you interpret the pharmacological mechanisms and their upstream and downstream relations. If you look at the downstream effects of 5-HT2A activation for example this can be more-or-less recreated. One such downstream effect is the release of psychoactive endocannabinoids.

Alcohol is relatively straightforward when you factor in the GABA, cannabinoid & NMDA actions and DRI/opioidergic metabolites (tetrahydroisoquinolines).

Like the MDMA experience people have replicated using a SERT releaser + low dose NDRA + barely threshold dose of a psych, maybe even add on agmatine or a threshold dose clonidine like you said for a2 agonism and use some SubQ oxytocin and Im sure no one would be able to tell the experiences apart reliably.

I'd say that the MDMA effect can be recreated in multiple different pharmacological ways using various types of substances. Eg just because MDMA acts like an SRI doesn't mean an SRI is required. But some elements might be key to the MDMA effect eg DRI, 5-HT2A & α2-adrenergic agonism.

But replicating the pharmacological profile of LSD using botanicals and supplements and still have it feel like a proper LSD experience seems out of reach.

A mix of botanical & supplement ligands for each of the 5-HT receptors, D1-5 and adrenergic receptors is feasible. This was explored back in 2010. Alternatively the wide variety of LSA adducts (which isn't an option for some people).

At that point youd have to take an actual psychedelic to replicate an actual psychedelic

Based on what I wrote above, only the 5-HT2A activator and LSA would be considered a "psychedelic". Agmatine activates 5-HT2A (and mimics the key ketamine MOA) so it counts as a sort of disassociative psychedelic. This post covers that in more detail.

 

[TheLightBringer]

It depends how you interpret the pharmacological mechanisms and their upstream and downstream relations. If you look at the downstream effects of 5-HT2A activation for example this can be more-or-less recreated. One such downstream effect is the release of psychoactive endocannabinoids.

Alcohol is relatively straightforward when you factor in the GABA, cannabinoid & NMDA actions and DRI/opioidergic metabolites (tetrahydroisoquinolines).

Yes I agree the perceived effect would be easily near identically replicated using a moderate dose of a GABA-A agonist and a threshold/light dose of an NMDA antagonist. As for recreating all of the pharmacological profile Nachr, 5ht3, Ca2+ and glycine would have to be taken into consideration as well. Im sure Im even missing some of its active sites I didnt mention.

I'd say that the MDMA effect can be recreated in multiple different pharmacological ways using various types of substances. Eg just because MDMA acts like an SRI doesn't mean an SRI is required. But some elements might be key to the MDMA effect eg DRI, 5-HT2A & α2-adrenergic agonism.

Also true but taking its whole pharmacological action into consideration oxytocin, Sert release and other things would be required

A mix of botanical & supplement ligands for each of the 5-HT receptors, D1-5 and adrenergic receptors is feasible. This was explored back in 2010. Alternatively the wide variety of LSA adducts (which isn't an option for some people).

The thing is I just dont see anything replicating the hallucinogenic and headspace effect of a potent 5ht2a agonist like LSD unless sufficiently potent itself. Thats why stacking multiple weak 5htx agonists and Dopamine and adrenergic agonists will not yield a cumulative effect that matches the LSD experience

Based on what I wrote above, only the 5-HT2A activator and LSA would be considered a "psychedelic". Agmatine activates 5-HT2A (and mimics the key ketamine MOA) so it counts as a sort of disassociative psychedelic. This post covers that in more detail.

Again agmatine cannot give the LSD experience, I dont see anyone being given agmatine + a bunch of supplements and saying the experience is just as intense as an LSD trip.

People responding to his post also seem to agree on my opinion:

”I take 3 grams of agmatine a day and I only notice huge appetite, super strong weed highs, better performance working out, and a kind of dull feeling like clonidine but not that bad.

Agmatine is a 5ht2a antagonist... and antagonist at all other ion receptor sights. It is not psychedelic, and its shared MOA with ketamine at mTOR has nothing to do with ket's psychedelic actions.

This is pretty silly honestly I think you've fooled yourself by reading about it and misunderstanding. It may be helpful for your cognition by its actions at a2-adrenergic. Be careful of the lowered blood pressure.”

And this guy who took 25 grams:
”After using agmatine in a variety of doses, situations, and timings I decided to finish off my tub that had about 25 grams left all at once just because I megadose things a lot (just out of sheer curiosity) and doses anywhere up to 10g had produced no effects. Still nothing. Not psychoactive in the least at any level for me.

Whenever I'm researching any substance, there's always one person who has insane things go say about it. Like the one doctor who used niacin on all of his patients for every psychological aiilment and cured everything from depression to schizophrenia. Or the person on longecity who claimed large doses of Bacopa Monnieri were making animals follow them through the forest and experiencing euphoria as powerful as MDMA. Etc. You can find extraordinary claims on any substance if you try hard enough, and often there's a hint of mania in the post that is extolling its virtues.”

 

[TheLightBringer]

I feel like were steering greatly off topic though, Id love to continue this discussion in DMs if youre interested

 

[Allylbenzene]

The thing is I just dont see anything replicating the hallucinogenic and headspace effect of a potent 5ht2a agonist like LSD unless sufficiently potent itself.

Besides the LSA adducts the allylbenzenes are ideal candidates. Interestingly LSD seems more potent at HT1a than 2a. The contribution of its non-HT2a properties is often under-appreciated. Earlier I forgot to mention it's activation of TrkB which is the receptor for BDNF. There are many TrkB/pro-BDNF options besides LSD.

Again agmatine cannot give the LSD experience

I never said it could. It's used as part of a well-designed combo like how Shulgin used BP medication (imidazoline/α2-adrenergic agonists) in his psychoactive combos. Agmatine shares imidazoline and a2-adrenergic agonism.

Shulgin report from this BL thread:

8.0 mg 2C-B-fly and 2.0 mg of rilmenidine at 12:30 pm; cannabis vapor at 4:00: The result was spectacular. I got a +4 experience from a pure imidazoline blood pressure medication! It is probably the entactogenic core of MDMA. I tend to think of the effects of MDMA as sweeter and gentler than this, but this was much stronger than any MDMA I have previously experienced. It turns out that 2.0 mg of rilmenidine is a very high dose. This is much more intense than the 0.2 mg of clonidine. Probably 1.0 mg would be adequate, and more comparable to a typical dose of MDMA. It also las ted longer than MDMA.... I took cannabis vapor. Within minutes my heart opened and the rilmenidine fully blossomed. At this point I could not feel the cannabis at all, although I had taken it only a few minutes before. I was astonished by the experience. Not because it worked, I had already seen the clonidine work. I was astonished by the depth of the experience, and I remained astonished for two weeks. I was ecstatic. Not ecstatic because it worked, rather the mental state was ecstatic, somewhat un-sober. I recalled Martin Ball calling 5-MeO-DMT the “crown jewel of the entheogens”. I felt that rilmenidine must also be a crown jewel. I described the state with superlatives.... Qualitatively, it is very hard to characterize the rilmenidine state, apart from the depth of it. At 3:52 hours she asked me how I feel, and I responded “It is like a peaceful lake, it feels eternal... in a peaceful sense”. Perhaps most telling, just 25 minutes after taking the cannabis, 3:55 hours after 36 taking the rilmenidine, I spoke to my wife about what for me were the core issues in our relationship. These are things that are very hard to discuss because they are painful, and discussion tends to lead to anger. But we discussed it peacefully. I expressed my sadness with tears. I believe this capacity for calm contemplation and discussion of painful personal issues is a core feature of the entactogenic state of MDMA, and here I was experiencing it with blood pressure medication.... For me it’s really, astonishingly among the best psychedelic experiences I’ve ever had. Unbelievable. (Shulgin 2016) Pharm 2, p. 26-27

Relevant paper on recreating MDMA:

Abstract: The drug MDMA, commonly known as ecstasy, produces a specific and distinct open hearted mental state, which led to the creation of a new pharmacological class, “entactogens”. Extensive literature on its mechanisms of action has come to characterize MDMA as a “messy” drug with multiple mechanisms, but the consensus is that the distinctive entactogenic effects arise from the release of neurotransmitters, primarily serotonin. I propose an alternative hypothesis:

• The entactogenic mental state is due to the simultaneous direct activation of imidazoline-1 (I1) and serotonin-2 (5-HT2) receptors by MDMA.
...
For example, the blood pressure medications rilmenidine and moxonidine are selective for imidazoline-1 and can be used to test the hypothesis that the entactogenic mental effects of MDMA are due to loading the imidazoline-1 mental organ into consciousness.

https://doi.org/10.1016/j.mehy.2015.12.018

People responding to his post also seem to agree on my opinion

I mentioned that post for the agmatine 5-HT2A info and it's ketamine-like MOA. The commentary is of little relevance since they're either misinformed or using it for different reasons.

I feel like were steering greatly off topic though, Id love to continue this discussion in DMs if youre interested

I reckon it's OT as OP was about making a "purely dopaminergic amphetamine" without any noradrenaline (NRI) effects, ie questioning the relevance of it's NRI MOA. In hindsight he also overlooked the role of adrenaline, histamine & VMAT in amphetamines effects.

 

[CarryBagMan]

@Allylbenzene But on another note Im still really fascinated by trying to replicate the experience of substances using others, I wonder to what extend one could replicate say 3-MeO-PCP or Alcohol with other drugs.

All these things would also need to efficiently pass thru the Blood-Brain Barrier as well correct ? Some do a better job than others. It would just seem like taking a grab-bag approach (a little of this, a little of that) would just be inefficient in how our bodies break everything down.

 

[Allylbenzene]

It would just seem like taking a grab-bag approach (a little of this, a little of that) would just be inefficient in how our bodies break everything down.

You're choosing from existing psychoactive substances. Eg for alcohol: a GABAergic, cannabinoid, opioidergic & dopaminergic (for the tetrahydroisoquinolines formed). MDMA might involve kanna alkaloids, agmatine, hordenine etc.

 

[Allylbenzene]

This thread was originally about UWA-101.
This is UWA-001 (alpha-phenyl-MDMA), active at 5-HT2A, SERT and NAT.

It has a 5-HT2A receptor affinity of 1.2 μM (~10-fold increase compared to MDMA), 1.3 μM for the serotonin transporter (~4-fold decrease compared to MDMA), 13.4 μM for the norepinephrine transporter (~26-fold increase compared to MDMA) and virtually no affinity for the dopamine transporter (>50 μM).

— 10.1096/fj.11-195016