Dr. Nocopes

Whatever is required.

[Dr. Nocopes @drnocopes]

you can now blast unlimited gear without any consequences and you are still afraid

nuked kidneys? ss-31 will reverse it

nuked liver? tudca and glutathione will reverse it

nuked heart? telmisartan and nebivolol will reverse it

mf blast and live your best life

god made you a subhuman, doesn't mean you have to accept it

[Dr. Nocopes @drnocopes]

imagine thinking TMG or boron are nootropics. the state of normie X

[Dr. Nocopes @drnocopes]

@morellifit semax is cope

[Dr. Nocopes @drnocopes]

@banay_john this

[Dr. Nocopes @drnocopes]

forgot one stripper

[Ábris Babicz | The Demi Cycle Protocol 🧬 @AbrisGains]

If peptides were strippers

-Semaglutide: Samantha. Every dad in the suburb secretly had a round with her. You leave skinny, sad, and shitting yourself in the Uber.

-Tirzepatide: Tiffany, Samantha’s hotter sister. (Samantha cries about it in the dressing room)

-Retatrutide: Rebecca, waist thinner than your arms, mildly schizophrenic

-Cagrilintide: Carly. Only shows up with Samantha. Doubles the bill but you still don’t know what she did.

-Survodutide: Sabrina, the suspiciously young German intern. “Starting next month” since 2023, still gets paid somehow.

-Mazdutide: Mazzy, Sabrina’s twin, dances in Shanghai. Their boss, Lilly still takes 30%.

-Liraglutide: Linda. Dayshift since 2010. Three kids. Needs you every single day.

-Exenatide: Lizzie. Her secret trick, the "Lizard spit" puts Pingpong shows in Bangkok to shame. “Retired” six times. Still on the Thursday night fluffer rotation.

-Amycretin: Amy, the new girl. Does oral, but not afraid of needles either. Can’t do the pole yet, but already has a waitlist.

-MariTide: Mariah. Shows up at the club only once a month. One round and you can't forget her for three weeks, but probably because you'll puke the whole time.

-BPC-157: Bonita. Fixed your knee, your gut and your marriage. FDA and ICE has been trying hard to deport her since 2023, she’s on stage every Friday anyway.

-TB-500: Tabitha, Bonita’s cousing from Cozumel. Their special two-girl show is called The Wolverine.

-Pentadeca Arginate: Penny. She's technically Bonita wearing a wig. Even thier tattoos are the same. “I’m a different person.” she swears.

-GHK-Cu: Giselle. Blue hair. Older guys' favourite, they claim her lap dance fixes up wrinkles. Still stings like a bitch every time she touches you.

-KPV: Kayla. Cleans up the mess after the other girls, yet still nobody tips her.

-VIP: Vanessa. VIP room only. Won’t dance for you unless your basement has mold.

-HGH: Heather. A fckin’ grand a night. Every regular has the same jaw.

-Ipamorelin: Ivy. Nursing student. Sweet, kind, vanilla only. Neither will she get you kicked out, nor will she do anything crazy.

-CJC-1295: CJ. Only dances in a pair with Ivy. If you book the long version she'll still be at your place next Thursday asking about breakfast.

-Sermorelin: Sarah. Your anti-aging doc’s favourite. $300/round. She talks about her ex for an hour. You probably won't come.

-Tesamorelin: Tess. Only touches your belly. Needs a prescription and your mortgage.

-GHRP-6: Gina. You leave her and drive straight to Taco Bell (every single time...)

-Hexarelin: Hailey. Hits hardest in the building. Two weeks later she won’t even look at you.

-IGF-1 LR3: Irina. Everything grows on her lap. Everything. Then you pass out and she takes your watch.

-Follistatin-344: Faith. $500 a dance. “I’ll make you a monster.” Nobody’s ever seen her face.

-AOD-9604: Ava, Australian. She promised a sweaty cardio session, you got a limp starfish. No one understands why she's till fully booked.

-Adipotide: Addy. Melts your fat, keeps your kidneys as a tip. Banned from every club in the states.

-MOTS-c: Marilyn, slim manic goth girl, always high on coke

-SS-31: Elle. Champagne room. $600. You walk out not sure anything happened.

-Epitalon: Katya, Russian, 48. ID says 25. Nobody checked.

-DSIP: Dee. Supposed to put you to sleep, yet it’s 3am and you’re wide awake texting Rebecca.

-Semax: Sasha, another Russian. Straight up the nose. You go home and finish your taxes.

-Selank: Svetlana, Sasha’s calm sister. Also up the nose. You end up crying about your mother-in-law.

-Dihexa: Dixie. Strongest bitch on the menu by a mile. Everyone’s scared of her. Nobody says why.

-Cerebrolysin: Celeste, Austrian. Made of pig brains. You book her ten nights in a row. You come out smarter and don’t ask questions.

-Melanotan II: Mel. Spray tan, random boners, six new moles, daddy issues.

-PT-141: Bree. She's into ladies. Every dude in the club booked her anyway. 45 minutes in you’re hard and puking at the same time.

-Kisspeptin: Kissy. Flirts with you, your balls wake up, then she asks if you want kids.

-Oxytocin: Olive. Hugs only. Yu start crying, then you propose her.

-hCG: Chelsea. Every TRT guy pays her monthly so his balls won’t shrink.

-Triptorelin: Trish. One night only. Your boys come back online. Book her twice and you’re castrated.

-Insulin: Ingrid. Can't live without her, but can also kill you by Tuesday. Bodybuilders book her anyway. Bring gummy bears (not medical advice)

-EPO: Erin. Every cyclist’s girlfriend in 1998. Turns your blood into ketchup. You die in your sleep. Banned from the club, still hides in the basement for some reason.

-MK-677: Misty. Not even a stripper, she just snuck in through the kitchen. Don't try to approach her or else you'll wake up bloated, with numb hands and an empty fridge.

-Orforglipron: Olivia. Oral only. Fake ID. Does half of what the needle girls do.

-NAD+: Nadia. 20 minutes of dying, then the best you’ve felt in years. $400 a drip.

-5-Amino-1MQ: Mina. “Melts fat.” Every review is from a guy named Dave.

-SLU-PP-332: Lulu. “Exercise in a pill.” Never seen a gym. Neither have her customers.

-Bimagrumab: Bimi. Too big for the door. Keeps your muscle before Samantha would take the rest.

[Dr. Nocopes @drnocopes]

mf still debating GHK-Cu, ngmi.

[Greg O'Gallagher @gregogallagher]

There’s a ton of hype around GHK-Cu right now, both topical and injectable.

But the evidence is still very limited.

Meanwhile, most people are overlooking one of the most powerful, well-researched anti-aging topicals we have: tretinoin.

Tretinoin is a prescription-strength vitamin A derivative with decades of clinical research behind it.

It increases skin cell turnover, stimulates collagen production, improves skin texture, reduces fine lines, and helps reverse signs of sun damage.

Over time, it can even increase the thickness of the skin’s deeper layers.

The catch? It takes consistency. You’ll typically need 3–6 months to see meaningful improvements, with benefits continuing beyond that.

You also need to introduce it gradually, manage irritation, and be diligent about sun protection.

It’s not some exciting new peptide. It’s a proven treatment that’s been around for decades.

The best tools aren’t the newest or trendiest. They’re the ones with the strongest evidence.

[Dr. Nocopes @drnocopes]

@NapoleonBased fluvoxamine + memantine

[Dr. Nocopes @drnocopes]

btw this stack nukes any addiction because it targets the root cause.

[Dr. Nocopes @drnocopes]

how to nuke porn addiction permanently stack

• cariprazine
• bupropion
• fluvoxamine

here's how they work

porn addiction is not a moral failing, it is a structural hijacking of the mesolimbic reward circuitry. chronic supraphysiological visual novelty triggers massive ventral striatal dopamine spikes that accumulate deltafosb, downregulate postsynaptic d2/d3 receptors, and uncouple prefrontal executive control (hypofrontality).

quitting with "willpower" fails because you are left with a hypodopaminergic baseline where only extreme digital novelty can register a signal, while conditioned cues instantly fire d3-mediated craving loops.

cariprazine is a third-generation dopamine receptor partial agonist with a sub-nanomolar affinity for the d3 receptor (ki = 0.085 nm) that is nearly 10x higher than its affinity for d2, and actually exceeds the binding affinity of endogenous dopamine itself. in the nucleus accumbens and islands of calleja, d3 receptors are the exact molecular switches that govern cue-induced craving and conditioned incentive salience ("wanting").

because cariprazine acts as a partial agonist (~30-40% intrinsic activity) with an ultra-long half-life via its active metabolite didesmethyl-cariprazine (ddcpa, 1-3 weeks), it acts as a permanent molecular clamp on d3 receptors. during baseline hypodopaminergic states, it provides enough intrinsic tonic stimulation to erase anhedonia and withdrawal apathy.

the moment a porn cue or intrusive thought attempts to fire a massive phasic dopamine spike, cariprazine physically blocks endogenous dopamine from binding d3, completely flatlining the cue-induced craving spike before it can escalate into compulsion.

bupropion provides the tonic catecholaminergic drive and cholinergic circuit-breaker required to redirect focus into productive work. it inhibits the dopamine transporter (dat) and norepinephrine transporter (net), restoring baseline tonic dopamine and norepinephrine levels in the dorsolateral prefrontal cortex (dlpfc) to reverse hypofrontality and restore top-down executive impulse control.

bupropion and its primary metabolite hydroxybupropion act as potent non-competitive antagonists at neuronal α3β4 and α4β2 nicotinic acetylcholine receptors (nachrs) located on ventral tegmental area (vta) dopaminergic terminals. conditioned visual triggers rely on mesopontine cholinergic inputs firing these exact nicotinic receptors to trigger burst-firing dopamine release in the striatum. blocking α3β4 and α4β2 severs the Pavlovian link between an environmental trigger and a striatal dopamine burst.

fluvoxamine locks in top-down serotonergic behavioral inhibition and physically rewires the addicted brain's synaptic architecture. by inhibiting sert in the orbitofrontal cortex (ofc) and anterior cingulate cortex (acc), it elevates prefrontal 5-ht tone and activates 5-ht2c and postsynaptic 5-ht1a receptors. this directly suppresses amygdala-driven urgency and obsessive-compulsive intrusive loops while restoring the prefrontal "veto power" over limbic impulses.

at the intracellular level, fluvoxamine is the most potent sigma-1 receptor (sig-1r) agonist in pharmacology (ki = 36 nm) and a powerful allosteric activator of 3α-hydroxysteroid dehydrogenase (3α-hsd). sig-1r activation drives endogenous bdnf/trkb synaptogenesis and dendritic spine remodeling to physically overwrite deltafosb-wired addiction pathways, while 3α-hsd upregulation floods the brain with allopregnanolone to silence the high-cortisol stress and boredom states that normally trigger relapse.

[Dr. Nocopes @drnocopes]

@lavender_hazes @vereskheath every dopamine antagonist is like that, stay away.

[Dr. Nocopes @drnocopes]

how to nuke porn addiction permanently stack

• cariprazine
• bupropion
• fluvoxamine

here's how they work

porn addiction is not a moral failing, it is a structural hijacking of the mesolimbic reward circuitry. chronic supraphysiological visual novelty triggers massive ventral striatal dopamine spikes that accumulate deltafosb, downregulate postsynaptic d2/d3 receptors, and uncouple prefrontal executive control (hypofrontality).

quitting with "willpower" fails because you are left with a hypodopaminergic baseline where only extreme digital novelty can register a signal, while conditioned cues instantly fire d3-mediated craving loops.

cariprazine is a third-generation dopamine receptor partial agonist with a sub-nanomolar affinity for the d3 receptor (ki = 0.085 nm) that is nearly 10x higher than its affinity for d2, and actually exceeds the binding affinity of endogenous dopamine itself. in the nucleus accumbens and islands of calleja, d3 receptors are the exact molecular switches that govern cue-induced craving and conditioned incentive salience ("wanting").

because cariprazine acts as a partial agonist (~30-40% intrinsic activity) with an ultra-long half-life via its active metabolite didesmethyl-cariprazine (ddcpa, 1-3 weeks), it acts as a permanent molecular clamp on d3 receptors. during baseline hypodopaminergic states, it provides enough intrinsic tonic stimulation to erase anhedonia and withdrawal apathy.

the moment a porn cue or intrusive thought attempts to fire a massive phasic dopamine spike, cariprazine physically blocks endogenous dopamine from binding d3, completely flatlining the cue-induced craving spike before it can escalate into compulsion.

bupropion provides the tonic catecholaminergic drive and cholinergic circuit-breaker required to redirect focus into productive work. it inhibits the dopamine transporter (dat) and norepinephrine transporter (net), restoring baseline tonic dopamine and norepinephrine levels in the dorsolateral prefrontal cortex (dlpfc) to reverse hypofrontality and restore top-down executive impulse control.

bupropion and its primary metabolite hydroxybupropion act as potent non-competitive antagonists at neuronal α3β4 and α4β2 nicotinic acetylcholine receptors (nachrs) located on ventral tegmental area (vta) dopaminergic terminals. conditioned visual triggers rely on mesopontine cholinergic inputs firing these exact nicotinic receptors to trigger burst-firing dopamine release in the striatum. blocking α3β4 and α4β2 severs the Pavlovian link between an environmental trigger and a striatal dopamine burst.

fluvoxamine locks in top-down serotonergic behavioral inhibition and physically rewires the addicted brain's synaptic architecture. by inhibiting sert in the orbitofrontal cortex (ofc) and anterior cingulate cortex (acc), it elevates prefrontal 5-ht tone and activates 5-ht2c and postsynaptic 5-ht1a receptors. this directly suppresses amygdala-driven urgency and obsessive-compulsive intrusive loops while restoring the prefrontal "veto power" over limbic impulses.

at the intracellular level, fluvoxamine is the most potent sigma-1 receptor (sig-1r) agonist in pharmacology (ki = 36 nm) and a powerful allosteric activator of 3α-hydroxysteroid dehydrogenase (3α-hsd). sig-1r activation drives endogenous bdnf/trkb synaptogenesis and dendritic spine remodeling to physically overwrite deltafosb-wired addiction pathways, while 3α-hsd upregulation floods the brain with allopregnanolone to silence the high-cortisol stress and boredom states that normally trigger relapse.

[Dr. Nocopes @drnocopes]

@nonprofitistic stfu fag and fuck your shitty website

[Dr. Nocopes @drnocopes]

safinamide mogs selegiline and its not even close, it is one of the most potent sigma-1 agonists with mao-b inhibition that makes it 10x more powerful than selegiline for cognitive enhancement

safinamide is an α-aminoamide derivative that completely redefines monoaminergic and glutamatergic optimization. it is a highly selective, reversible non-covalent mao-b inhibitor with a selectivity ratio over 1000:1 against mao-a and zero amphetamine or methamphetamine metabolites.

by binding non-covalently to the mao-b enzyme niche, safinamide blocks the oxidative deamination of striatal and prefrontal dopamine and multiplies endogenous beta-phenylethylamine (β-pea) to fire intracellular trace amine-associated receptor 1 (taar1).

what makes safinamide 10x more powerful than selegiline for raw cognitive output is that mao-b inhibition is only one-third of its mechanism.

first, safinamide is one of the highest-affinity sigma-1 receptor (sig-1r) ligands in clinical pharmacology (ki ≈ 19 nm even tighter binding affinity than fluvoxamine at 36 nm).

anchored directly on the mitochondria-associated endoplasmic reticulum membrane (mam), safinamide's sig-1r activation dissociates the inhibitory bip chaperone and stabilizes ip3r3 calcium channels.

this forces precision calcium transfer straight into the mitochondrial matrix to activate pyruvate dehydrogenase (pdh) and the tricarboxylic acid (tca) cycle while driving endogenous bdnf/trkb synaptogenesis, dendritic spine remodeling, and endoplasmic reticulum stress protection.

second, high-focus cognitive marathons and elevated dopaminergic tone frequently trigger excessive extrasynaptic glutamate release in the prefrontal cortex and striatum leading to nmda receptor calcium overload, excitotoxicity, mental fatigue, and "stimulant brain fog."

safinamide acts as a state- and frequency-dependent blocker of voltage-gated sodium channels (nav1.1–nav1.7) and neuronal n-type calcium channels.

it selectively binds to the inactivated state of sodium channels only on hyper-excitable, rapidly depolarizing glutamatergic terminals. it leaves normal baseline physiological glutamate neurotransmission (memory formation and synaptic plasticity) 100% untouched, while clamping down on pathological, high-frequency glutamate storms.

this creates a triple-pathway nootropic triad in a single molecule:

1. reversible mao-b blockade elevates tonic prefrontal and striatal dopamine + endogenous β-pea with zero levo-amphetamine peripheral dirty stress.

2. sub-20 nm sigma-1 agonism supercharges mam mitochondrial atp production and bdnf neuroplasticity.

3. state-dependent sodium/calcium channel modulation filters out glutamatergic excitotoxicity and synaptic noise, turning high dopamine into crystal-clear, hyper-calm signal-to-noise execution.

[Dr. Nocopes @drnocopes]

@nonprofitistic cognitive behavioral therapy is useless and doesn't work. btw stop putting ">" in front of every sentence, it makes it obvious you used an LLM.

[Dr. Nocopes @drnocopes]

@CBTenjoyer2 stattera is useful for adhd not for nuking addictions.

[Dr. Nocopes @drnocopes]

@CBTenjoyer2 it reduces dextroamphetamine effectiveness slightly because sigma-1 creates heterodimers with dat and dopamine receptors.

[Dr. Nocopes @drnocopes]

fluvoxamine is the best longevity medicine in the world if combined with high dose melatonin

here's why

exogenous oral melatonin normally suffers from a brutal 85% hepatic first-pass destruction via cytochrome p450 1a2 (cyp1a2) 6-hydroxylation and a short 45-minute elimination half-life. fluvoxamine is the most potent cyp1a2 and cyp2c19 inhibitor in pharmacology. combining them blocks hepatic melatonin breakdown, multiplying serum and tissue melatonin area-under-the-curve (auc) by 15x to 30x and turning a transient spike into a sustained, supraphysiological saturation wave.

this massive concentration gradient forces melatonin straight into the mitochondrial matrix via high-affinity pept1 and pept2 oligopeptide transporters on the inner mitochondrial membrane. once inside, melatonin acts as the apex terminal antioxidant: it directly scavenges hydroxyl radicals and peroxynitrite without undergoing redox cycling, stabilizes cardiolipin to lock respiratory supercomplexes together, and blocks mitochondrial permeability transition pore (mptp) opening to prevent age-related cellular senescence and apoptosis.

simultaneously, fluvoxamine binds intracellular sigma-1 receptors (sig-1r, ki = 36 nm) anchored on the mitochondria-associated endoplasmic reticulum membrane (mam). aging cells lose mam structural integrity, starving mitochondria of calcium and stalling bioenergetics. sig-1r activation dissociates the inhibitory bip chaperone and stabilizes ip3r3 channels, restoring precision er-to-mitochondria calcium flux to activate pyruvate dehydrogenase and tricarboxylic acid (tca) cycle enzymes for youthful atp and nad+ regeneration.

together, this stack completely silences sterile systemic inflammation. fluvoxamine suppresses the er stress sensor ire1α to halt nf-κb cytokine storms and acts as a functional inhibitor of acid sphingomyelinase (fiasma) to stop pro-aging ceramide accumulation on cell membranes. at the same time, high-dose mitochondrial melatonin activates sirtuin-1 (sirt1) and sirtuin-3 (sirt3) to deacetylate foxo3a and pgc-1α, shutting down the nlrp3 inflammasome and driving pink1/parkin mitophagy to clear out mutated mitochondrial dna (mtdna).

in the brain, fluvoxamine allosterically upregulates 3α-hydroxysteroid dehydrogenase (3α-hsd) to flood neural tissue with allopregnanolone and endogenous bdnf/trkb signaling, while cyp1a2-amplified melatonin polarizes astrocytic aquaporin-4 (aqp4) water channels. this maximizes slow-wave nocturnal glymphatic convection, physically flushing beta-amyloid, hyperphosphorylated tau, and lipofuscin out of the central nervous system every single night.

outside the brain, fluvoxamine blocks platelet sert to deplete >80-90% of peripheral platelet serotonin. stripping peripheral vascular serotonin prevents age-related 5-ht2a/5-ht2b endothelial vasoconstriction, microthrombi, and tgf-β1 organ fibrosis across the heart, kidneys, and vasculature.

[Dr. Nocopes @drnocopes]

@CBTenjoyer2 good for many things but not for nuking addictions alone.

[Dr. Nocopes @drnocopes]

@NoID2312 bupropion + fluvoxamine would be the best for you if you want to nuke addictions and distractions + learn new things at the same time.

[Dr. Nocopes @drnocopes]

@vereskheath if you want to be retarded and depressed sure.

[Dr. Nocopes @drnocopes]

@2stoned2trench then target ACh for LTP by donepezil.

[Dr. Nocopes @drnocopes]

@2stoned2trench super short half-life, you need something like fluvoxamine for 24/7 bdnf/ngf/plasticity.

[Dr. Nocopes @drnocopes]

@Crocostiago based

[Dr. Nocopes @drnocopes]

@2stoned2trench lots of practice + fluvoxamine for bdnf/ngf/plasticity