Opioids The Ultimate Opiate Potentiation Thread

[bodymore]

Smoke a newport trust me. The first time I did a line of dope I realy didnt feel anything till my friend told me to smoke a cigarette then I was like . The only time I smoke is when Im donig doing dope. It mgiht not work for everybody but it works for me

 

[rolls]

Smoking makes me feel sick and dizzy so I might give it a miss. Don't really want to end up a smoker either.

 

[bodymore]

Smoking makes me feel sick and dizzy so I might give it a miss. Don't really want to end up a smoker either.

Your smoking to much. Thats like saying I have no tolerance but I want to shoot a $20 of raw dope without throwing up. Take a few puffs from a cigarette when you are starting to feel your buzz I can gurantee you it will boost the effects

 

[mitragyna]

umm ok i know none of these
what that one u can buy from pharmacy that potentates i think only methadone. Like what plant extract can we get easy that can help and how much.

How much opiates related activity do these have

Maybe you are thinking of Cat's Claw? It's an NMDA antagonist like DXM and Nitrous.

In reference to your second question:

• Picralima nitida-

  Akuammine, an indole alkaloid, is the most abundant active alkaloid found in the seeds from the tree Picralima nitida, commonly known as Akuamma.
  
  The dried seeds from this plant are used in traditional medicine throughout West Africa, particularly in Ghana as well as in the Ivory Coast and Nigeria. The seeds are crushed or powdered and taken orally, and are mainly used for the treatment of malaria[1] and diarrhoea, and as a painkiller. An enterprising Ghanaian hospital started manufacturing standardised 250mg capsules of the powdered P. nitida seed, and sold them around the country where they became widely accepted as a safe and effective pain relief product. This then led researchers to try and discover the active component of the seeds.
  
  P. nitida seeds contain a mixture of alkaloids producing antipyretic and antiinflammatory effects along with analgesia.[2][3] Several of these were shown to bind to opioid receptors in vitro, and two compounds, akuammidine and ψ-akuammigine, were found to be potent μ-opioid agonists, although not particularly selective. Surprisingly the main alkaloid from the seeds, akuammine, was found to be an opioid antagonist when tested in vitro and canceled out the effects of the active agonist components.[4]
  
  Given the confirmed activity of the whole seed extract in humans, this makes it likely that akuammine is in fact being metabolised once inside the body to form an active metabolite, in a similar way to how the closely related compound mitragynine is metabolised to the more active 7-hydroxymitragynine.
  
  Akuammine is the main alkaloid found in the seeds, comprising 0.56% of the dried powder, indicating that the 250 mg "Picap Capsules" sold commercially should contain approximately 1.4 mg of akuammine, plus 0.085 mg akuammidine and 0.015 mg ψ-akuammigine. Akuammine is structurally related to both yohimbine and mitragynine, both of which are alkaloid plant products with uses in medicine.[*]

  Pericine is one of a number of indole alkaloids found in the tree Picralima nitida, commonly known as Akuamma. The dried seeds from this plant are used in traditional medicine throughout West Africa, particularly in Ghana as well as in the Ivory Coast and Nigeria. As with some other alkaloids from this plant such as akuammine, pericine has been shown to bind to mu opioid receptors, and has an IC50 of 0.6μmol, around 6x more potent than codeine when tested in the same assay.

  [*]
• Irvingia gabonensis stem bark-

  Irvingia gabonensis is used medicinally in most parts of tropical Africa for the treatment of a number of ailments. In West Africa the Mende tribe of Sierra Leone uses the stem bark to relieve pain. In order to establish a pharmacological rationale for the traditional use of this plant as a remedy for pain, the water and ethanol extracts of the powdered stem bark were screened for analgesic activity and compared with standard analgesic drugs. The water extract and morphine protected the mice from heat-induced pain. In contrast, the ethanol extract and metamizole sodium showed very low level of analgesic activity in this test. However, using tail pressure as a source of pain, the water and ethanol extracts, metamizole sodium and morphine offered protection to the mice against pain stimuli. Morphine and the water extract were more potent as analgesic agents in heat than non-heat pain test. The analgesic effects of the water extract and morphine were blocked by a non-selective opioid receptor antagonist, naloxone in both tests, whereas the analgesic effects of the ethanol extract and metamizole sodium were not antagonized by the same dose of the opioid antagonist. The data presented in this study suggest that the active principle(s) in the water extract has analgesic profile similar to that of the narcotic analgesic and the ethanol extract might contain compound(s) that behave like non-narcotic analgesic agent. These findings provide for the first time the pharmacological basis for the folkloric use of Irvingia gabonensis in the relief of pain.

  [*]
• Buddliea cordata-

  Analgesic and antipyretic activities of an aqueous extract and of the flavone linarin of Buddleia cordata.
  
  The dried aqueous extract of leaves of Buddleia cordata (loganiaceae) and its main flavonoid glycoside, linarin, have been evaluated for analgesic and antipyretic effects in mice and rats, respectively. Both the extract and linarin exerted significant and dose-dependent analgesic and antipyretic activities, the first being obtained against a chemical stimulus (writhing a test in mice) and the second being obtained by a pyretogenic stimulus (yeast-induced hyperthermia test). Furthermore, the response of the animals in the hot plate test was modified by linarin and an aqueous extract. These activities were similar to that showed by morphine sulfate (MS) and they were inhibited by naxolone pretreatment, a specific morphinic antagonist compound. These findings lead to the conclusion that the aqueous extract and linarin exert central analgesic properties. On the other hand, linarin was shown to be responsible for the antipyretic activity of this species.

  [*]
• Sophora subprostrata-

  Antinociceptive effects of (+)-matrine in mice.
  Kamei J, Xiao P, Ohsawa M, Kubo H, Higashiyama K, Takahashi H, Li J, Nagase H, Ohmiya S.
  
  Department of Pathophysiology and Therapeutics, Faculty of Pharmaceutical Sciences, Hoshi University, Tokyo, Japan. [email protected]
  
  The antinociceptive potency of matridin-15-one ((+)-matrine) was examined using the acetic acid-induced abdominal contraction test and the tail-flick test in mice. (+)-Matrine, at doses of 1 to 10 mg/kg, s.c., produced a marked and dose-dependent inhibition of the number of acetic acid-induced abdominal contractions in mice. The antinociceptive effect of (+)-matrine in the acetic acid-induced abdominal contraction test in mice was identical to that of pentazocine. Indeed, there was no significant difference in the ED50 (mg/kg with 95% confidence limits) values for the inhibition of acetic acid-induced abdominal contractions between (+)-matrine (4.7 (4.1-5.3)) and pentazocine (3.3 (2.2-5.0)). Furthermore, in the tail-flick assay, (+)-matrine at doses of 10 and 30 mg/kg, s.c., again produced a dose-dependent antinociceptive effect. When nor-binaltorphimine (20 mg/kg, s.c.), a selective kappa-opioid receptor antagonist, was administered 3 h before treatment with (+)-matrine, the antinociceptive effect of (+)-matrine was markedly antagonized. Furthermore, the antinociceptive effect of (+)-matrine was partially antagonized by pretreatment with beta-funaltrexamine, a selective mu-opioid receptor antagonist. Naltrindole, a selective delta-opioid receptor antagonist, had no effect on the antinociceptive effect of (+)-matrine. In conclusion, (+)-matrine produced an antinociceptive effect mainly through the activation of kappa-opioid receptors and partially through mu-opioid receptors.

  [*]
• Nigella sativa seed oil-

  Antinociceptive effects of Nigella sativa oil and its major component, thymoquinone, in mice
  Abstract
  
  The antinociceptive effects of Nigella sativa oil and its major component, thymoquinone, were examined in mice. The p.o. administration of N. sativa oil (50–400 mg/kg) dose-dependently suppressed the nociceptive response in the hot-plate test, tail-pinch test, acetic acid-induced writhing test and in the early phase of the formalin test. The systemic administration (2.5–10 mg/kg, p.o. and 1–6 mg/kg, i.p.) and the i.c.v. injection (1–4 μg/mouse) of thymoquinone attenuated the nociceptive response in not only the early phase but also the late phase of the formalin test. Naloxone injected s.c. (1 mg/kg) significantly blocked N. sativa oil- and thymoquinone-induced antinociception in the early phase of the formalin test. Moreover, the i.c.v. injection of naloxone (10 μg/mouse), the μ1-opioid receptor antagonist, naloxonazine (1–5 μg/mouse), or the κ-opioid receptor antagonist, nor-binaltorphimine (1–5 μg/mouse), significantly reversed thymoquinone-induced antinociception in the early phase but not the late phase of the formalin test, whereas the δ-opioid receptor antagonist, naltrindole (1–5 ng/mouse, i.c.v.), had no effect on either phase. The antinociceptive effect of morphine was significantly reduced in thymoquinone- and N. sativa oil-tolerant mice, but not vice versa. These results suggest that N. sativa oil and thymoquinone produce antinociceptive effects through indirect activation of the supraspinal μ1- and κ-opioid receptor subtypes.

  [*] N. sativa is also a calcium channel blocker.
• Tabernaemontana pachysiphon-

  Titre du document / Document title
  Isolation of opioid-active compounds from Tabernaemontana pachysiphon leaves
  
  Résumé / Abstract
  A procedure for prefractionation of crude plant extracts by centrifugal partition chromatography (CPC) has been developed to enable rapid identification of known-positive compounds or false-positive compounds and to increase the chance of identifying minor unknown-active compounds. The study explored the use of CPC as a tool in the prefractionation step before investigation of bioactivity. Fractions obtained by CPC from an ethanolic extract of Tabernaemontana pachysiphon Stapf (Apocynaceae) were screened by means of an opiate-receptor-binding assay and an adenosine A1-receptor-binding assay. Fractions containing fatty acids, which had false-positive effects on the assay, were identified, as were unknown-positive fractions from which two opioid-active compounds, tubotaiwine and apparicine, were subsequently isolated. The affinities (Ki) of tubotaiwine and apparicine at the opiate receptor were 1.65±0.81 and 2.65± 1.56 μmol, respectively. Both alkaloids had analgesic activity in the abdominal constriction test in mice. CPC prefractionation led to the rapid isolation of two opioid-active compounds, tubotaiwine and apparicine, from the unknown-positive fraction; false-positive fractions were rapidly identified. Both tubotaiwine and apparicine had affinity for adenosine receptors in the micromolar range and also had in-vivo analgesic activity in mice.

  [*]

Hope that answers your question.

EDIT: Spinach Rubisco is another one.

Rubiscolin-6, a δ opioid peptide derived from spinach Rubisco, has anxiolytic effect via activating σ1 and dopamine D1 receptors

Abstract

Rubiscolin-6 (Tyr-Pro-Leu-Asp-Leu-Phe) is a δ opioid peptide derived from the large subunit of spinach d-ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco). We previously reported that rubiscolin-6 had an analgesic effect and stimulated memory consolidation. Here we show that intraperitoneally (i.p.) or orally administered rubiscolin-6 has an anxiolytic effect at a dose of 10 mg/kg or 100 mg/kg, respectively, in the elevated plus-maze test in mice. The anxiolytic effects of rubscolin-6 after i.p. (10 mg/kg) and oral (100 mg/kg) administration were blocked by a δ opioid receptor antagonist, naltrindole (1 mg/kg, s.c.), suggesting that the anxiolytic activity of rubiscolin-6 is mediated by δ opioid receptor. The anxiolytic effect of rubiscolin-6 (10 mg/kg, i.p.) was also blocked by a dopamine D1 antagonist, SCH23390 (30 μg/kg, i.p.), but not by a dopamine D2 antagonist, raclopride (15 μg/kg, i.p.). The anxiolytic effect of rubiscolin-6 (10 mg/kg, i.p.) was blocked by σ1 receptor antagonist, BMY14802 (0.5 mg/kg, i.p.) or BD1047 (10 mg/kg, i.p.). Taken together, the anxiolytic effect of rubiscolin-6 is mediated by σ1 and dopamine D1 receptors downstream of δ opioid receptor.

[*]

 

[tadfish]

ah cats claw does that work with codeine or any other opiates and to what extent? whats everyones experiences and thoughts with using it? eg. phenergan and grapefruit juice convert ~10% more morphine.

So whats everyones fav combo.
i think catapres, soma, phenergan, and a few different opiates really my fav.
Not going to put dose's and some of my combos cause i think alot of people might try that and well OD. But still i would like to know everyones fav combos to potentate there opiate be it heroin or codeine

 

['medicine cabinet']

yea a little clonidine mixed into a shot of dope is pretty nice. I dont know too many other ppl that have tried it, least in real life. There are probably some ppl on here who dig it tho.

I think once you start shooting dope its pretty pointless to try and potentiate it. If you want to get higher you just do another shot. This is my opinion tho and im not advocating shooting dope or anything, but it just seems like a waste any other way. especailly when its good dope.

 

[Unknown]

^^^the best potentiater of opiates is, more opiates....lol... i love it!

 

[lenses]

Have any of you tried DLPA?

I have been using it on and off (3-6 times weekly) and I do notice some opiate potentiation. I learned about the combo through reading some research papers about DLPA.
From:

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WN2-45C0PT8-K&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=10&md5=46f698c54fbdbb3a360543efc5b015cb

DL-phenylalanine markedly potentiates opiate analgesia – an example of nutrient/pharmaceutical up-regulation of the endogenous analgesia system

A. L. Russella and M. F. McCartyb
a Brampton Pain Clinic, Bramalea, Ontario, Canada b Pantox Laboratories, San Diego, CA, USA

Abstract

In the author’s clinical experience, concurrent treatment with DL-phenylalanine (DLPA) often appears to potentiate pain relief and also ease depression in patients receiving opiates for chronic non-malignant pain. An analysis of this phenomenon suggests that it may be mediated, at least in part, by up-regulation of the ‘endogenous analgesia system’ (EAS), a neural pathway that projects caudally from medullary nuclei to the dorsal horn of the spinal column; when stimulated by chronic pain or therapeutic measures such as opiates or acupuncture, the EAS suppresses activation of second-order pain-receptive neurons in the dorsal horn, and thereby alleviates pain. Since serotonin and enkephalins are key neurotransmitters in the EAS, it is reasonable to predict that measures which promote serotonin activity (such as 5-hydroxytryptophan and serotonin-reuptake inhibitors) as well as enkephalin activity (such as D-phenylalanine, an enkephalinase inhibitor) should potentiate EAS-mediated analgesia – a view consistent with much previous medical research. Comprehensive support of the EAS with well-tolerated nutrients and pharmaceuticals may amplify the analgesic efficacy of chronic opiate therapy, while enabling dosage reductions that minimize opiate side-effects. Analogously, this approach may complement the efficacy of acupuncture and other analgesic measures that activate the EA

Regardless, DLPA is a pretty good supplement. I prefer it over l-tyrosine or similar things . It's the best IMO for amphetamine recovery, I notice my recovery times are DRASTICALLY reduced since i've been taking it, but i've also been doing and craving less amphetamines.

Benadryl works well. I remember being in florida with no drugs except one 60 mg morphine pill and some benadryl. Made a needle-less syringe with a turkey baster and plugged it. I nodded out REAL hard. It just kinda puts your head into the "nodspace" a lot easier I think...

 

[Lushlife]

You're looking for Kanna

Tried this once and was shocked at the result. 15 mg of morphine (swallowed half a pill) and smoked a pinch of kanna. The result was euphoric, and I've never been a big fan of opiates. I've done bigger doses--OC, dilauded, Vics, but never had an opiate response like this. The only caution with Kanna is not to take it with Prozac-type (MOAI?) medications.

 

[tadfish]

interesting not sure how that l-trosine and LDPA would do anything
ah benadry thats just dimenhydrinate or alike?

 

[Mr Blonde]

The only caution with Kanna is not to take it with Prozac-type (MOAI?) medications.

Prozac isn't an MAOI, it's an SSRI but so is Kanna so yeah they should not be combined. I wouldn't take it with any MAOI's either.

Interesting you said it potentiated the opioid high... I wonder how it did that.

 

[tadfish]

doesn't kanna make your ears ringing kinda buz funny taste stuff
i thought he meant kratom that would make more sense?

 

[Mr Blonde]

^ What?

 

[LillyF40]

GREAT THREAD
ill throw a few i know all too well out there... that most dont know


METHADONE - Cats Claw. 25%+ incease in duration using cats claw.

OPIUM and various others opiods - Propoxyphene. Ya, darvocet, its shit alone. HUGE potentiator of opium... stumbled on it years ago w/ huge supply of what i thought was useles darvies. check out its unique p450 properties along with many other pubmed discoveries.... be careful tho.... dangerous and ez drug to OD on. im talking like 1 or 2 darvies with a seriously reduced dose.

OPIUM - Cimetedine. seems to fuck with and kill other opoids (stops vicodin from metabolizing into hydromorph, etc) but it adds one hell of a kick to opium and increases duration.

ummm... magnesium is a must. always have high levels of magnesium obviously... take it with any opiate/oid. helps with absorbtion also.

SOooooooooOoOOOOOoo many prescription drugs will potientiate opiates.... mostly due to unique and strong p450 enzyme inhibition but its tricky stuff and specific to the opiate/oid your fucking around with. Then there are some that potentiate it simply due to synergy of pleasurable effects (or more generally unknown "magic" in da brain
Phenergan even tho it should only potentiate because of its antihistimine properties goes beyond that. many will back me up. there is something more to antihistamines, ESPECIALLY w phenergan, than the sedation effect adding to the nod.

there are a ton of potentiators.... ill post more later. so many unknown ones too... alot of herbal shit people dont know about ta boot

if you want a REAL Ultimate Opiate Potentiation thread then somebody (ill do it eventually needs to post a nice bigass conclusive list of p450 enzyme inhibitors and inducers and a list of opiates/opoids and how they metabolize/how they can be modified for potentiation. its all out there on the net but nobody has ever gotten more than 50% of the real data on one page, etc etc.

Thank you so much for your post I thought I was the only person in the world who knows that promethazine is an opiate enhancer. I was on another
forum several years back and people said I didnt know what I was talking about. I will start at the beginning. I went to my GYN when I was 14 years old because I had severe menstrual cramps, He gave me a capsule called Synalgos DC The DC stands for dihydrocodeine. It is not popular anymore in the US. and I susspect it had to do with the Powers that be decided to take the promethazine out of this capsule. This capsule had dihydrocodeine, aspirin, caffeine, and promethazine. Well one day just for the Hell of it my friend and I did an experiment. We each took codeine # 4 with aspirin, remember I am old All the codeine did was make me itch, and I threw up. We waited, and about 6 hours later we each took 2 Synalgos DC Capsules. That was it. That is why those pills crept up on me and had me hooked in just a few months. I think they changed the formula in 1987, and ever since then, no one asked for them anymore. They are now being markerted as Panlor DC, but still no promethazine. If I am not mistaken it is no longer being made in the US. However with the rumor that hydrocodone may be rescheduled to a class 2 narcotic, this country will see an inflex of the new and "Improved" dihydrcodeine.

LillyF40

 

[Mr Blonde]

^ Promethazine is very well known here in OD and across BL I believe you'll find. I've only recentley started using it with codeine, and so far I love it.

 

[mikebobjohn]

So many have been mentioned that I am lost.

I am currently taking 300mg's of morphine per day. I feel no buzz or warmth or anything when I take my 50-100mg doses at once. All it does is help a bit with my pain, but I want much more.

So, for morphine specifically, what are the best, absolutely safe, non-prescription (in the US) potentiators I should take, and how much of them should I take, and when?

Please advise.

Thank you very much.

 

[mikebobjohn]

MITRAGYNA!

Don't forget the beloved Kratom with Mitragynine and 7-Hydroxymitragynine!

What is this?

I'm so lost.

 

[Mr Blonde]

^ Do a search.

 

[dynamo]

i mustve searched about 5 pages befoe i gave up (sorry) , but i have in my possesion oxycontin and i was wondering exactly how many mg of doxylamine would be sufficient to potentiate the effects and at what time to take it

 

[dread]

I will still stick to my opinion, midazolam or triazolam is the way to go.