official

What replaced 7-OH on the shelf, and how much of it is documented

by ch3ch3 · 19h ago · 0 comments

On August 26, 2026 the Drug Enforcement Administration placed three kratom derivatives in Schedule I. “This temporary order is effective August 26, 2026, until August 26, 2028.”[1] It did not place 7-hydroxymitragynine, the compound the whole fight had been about.

What moved into the gap is four different kinds of thing, and they are easy to mistake for one another. Some are compounds with a structure, a registry entry and published pharmacology. Some have been found in a product that somebody bought and a laboratory took apart. Some are names printed on packaging with no analysis behind them at all. And some are names that circulate with no source anywhere.

This page keeps those four apart, because the market does not. Every claim below is labelled:

In the literature. A described compound with published pharmacology. It says nothing about whether anyone is selling it.
Found in a product. A named laboratory or a regulator analysed something bought off a shelf and reported what was in it.
Marketing only. The name appears on a pack or a vendor page, and no analysis confirming it has been published.
Rumour. The name circulates and no source carries it.

Where this page says a thing was not found, it gives the search that was run and the database it was run against, so a reader can repeat it and get a different answer later if the record changes.

What was scheduled, and what was not

The August order covers mitragynine pseudoindoxyl, MGM-15 and MGM-16.[1] Each entry carries a catch-all for the naming problem these compounds have: “Since nomenclature of this substance is not internationally standardized, compounds of this structure, regardless of numerical designation of atomic positions are covered”.[1] MGM-16 is listed under two names that differ by one digit, “also known as 9-fluoro-dihydro-7-hydroxymitragynine; or 10-fluoro-dihydro-7-hydroxymitragynine (depending on numbering convention)”.[1] Same compound, two numbering conventions.

7-OH itself remains the subject of a notice of intent, not an order. The proposal is a concentration threshold rather than a ban on the compound: botanical material is covered when it “contains more than 0.050 percentage of 7-hydroxymitragynine on a dry weight basis”, and anything else when it carries “greater than 0.050 percentage by weight/weight, weight/volume, or volume/volume or greater than 1.00 milligram of 7-hydroxymitragynine in the article”.[2] As of October 5, 2026 the Federal Register holds five documents mentioning 7-hydroxymitragynine since the start of the year and none of them is a scheduling order.[3] Several trade sites report that 7-OH was scheduled in 2026. It was not.

The order explains the market in terms the rest of this page keeps using. Two of the three compounds arrived on shelves on a timetable: “the first confirmed appearance of mitragynine pseudoindoxyl in consumer products was reported in 2024”, and “the emergence of MGM-15 in commercially available products was in September 2025”.[1] DEA reads the packaging as deliberate, saying that “the introduction of these substances into the Mitragyna speciosa consumer market follows a classic pattern of new designer drugs where packaging appears like those of designer novel psychoactive substances” and is “sold strictly for laboratory, botanical and research purposes only”.[1] It notes the retail sites carry their own warnings, and that “the inclusion of warnings for lethal respiratory depression on retail sites confirms that the products possess a toxicity profile identical to scheduled opioids”.[1] On flavours and formats it says the choice “suggests an effort to appeal to a broader, potentially younger demographic, significantly increasing the scope of potential abuse”.[1]

The order's summary of the hazard is worth quoting in full, because it is an argument about missing evidence rather than about measured harm: “the lack of clinical data regarding their safety and efficacy, coupled with the risk of life-threatening respiratory depression and addiction, underscores the danger of marketing these unapproved highly potent opioids under the guise of therapeutic or wellness products”.[1]

The name on the pack is now DHM, and DHM already means something else

This is the most useful single fact on this page, and it is not about a new compound.

The Center for Forensic Science Research and Education runs a test-purchase programme that buys retail products and analyses them. In May 2026 it reported that the market had changed what it calls MGM-15. “market naming or labeling for dihydro-7-hydroxy mitragynine has switched to” DHM, and the report adds, about its own subject, “however, there are debates as to what true substance this acronym stands for”.[4]

DHM is already the standard abbreviation for dihydromyricetin, written in the literature as “dihydromyricetin (DHM)” and described there as “a flavonoid component of herbal medicines”.[5] It has been studied since at least 2012 under the title “dihydromyricetin as a novel anti alcohol intoxication medication”, and that is the use it is sold for.[5]

So two unrelated compounds now answer to the same three letters in the same retail aisle. One is a semi-synthetic opioid that a federal order describes as a highly potent opioid.[1] The other is a plant flavonoid taken with alcohol. Nothing in the name separates them. A clinician taking a history from somebody who says they took DHM has to know to ask which one is meant, and a consumer reading it on a pack has no way to know there is a question.

The forensic laboratories have the same problem from the other side. The same report warns that “laboratories must be aware that kratom alkaloids, including dihydro-7-hydroxy mitragynine, present complex analytical challenges including isomers, interconversion and instability”.[4]

The Ole Miss deaths: what is established and what is not

Two students at the University of Mississippi died on September 21, 2026. Reporting on the investigation says that “what's in the packaged tablets that law enforcement discovered when investigating those deaths are mitragynine pseudoindoxyl, MGM-15 and 7-OH, which are semisynthetic, concentrated and potent derivatives of certain components of kratom”.[6]

Cause of death is not established. The same report states that “the compounds have not been confirmed to have caused or contributed to the deaths, as the autopsies and toxicology reports have not yet been released”.[6] Nothing further should be read into the presence of a pack near a person who died, and this page records the finding without an inference attached to it.

The attribution problem is general, and the outlet states it plainly: reports of harm are rising, “but reports of poisonings, mild to severe addictions or deaths from kratom or semisynthetic derivatives have been growing”, while “though data documentation limits mean it's not always clear how many of those reports are due to natural kratom versus semisynthetic derivatives”.[6] That sentence is the reason this site separates leaf from isolate on every page about either.

MGM-15: found in a product, and the record says exactly how

MGM-15 is the best documented of the successors, and the documentation is specific enough to check.

CFSRE's monograph describes it as “structurally similar to known kratom alkaloids and is the primary component in products being sold as” MGM-15, and records that it “was first identified by our laboratory in September 2025 and confirmed after acquiring standard reference material”.[7] The reference material matters: an identification confirmed against a purchased standard is a different class of claim from a name matched in a spectral library. The material it came from and the case it appeared in are both named. The “drug materials originated from New England and toxicology sample originated from New Jersey”, and in that sample it “was identified alongside mitragynine, 7-hydroxy mitragynine and trace ketamine”.[7] DEA's own reading of CFSRE's data records that “MGM-15 was detected as a tan solid drug that originated from New England”.[1]

Its pharmacology is in the literature. CFSRE reports that it “is reported to be a partial agonist of the mu opioid receptor and has increased opioid receptor affinity compared to 7-hydroxy mitragynine due to stereospecific saturation of the imine” double bond, which is the structural change the name dihydro records.[7] An independent analysis of commercially available MGM-labelled tablets found the same ordering, reporting that “MGM-15 shows greater hMOR and hDOR binding affinities than 7-HMG, indicating the potential for higher opioid effects and risks”.[8] That paper also found the tablets were what they claimed to be, “with no naturally occurring kratom alkaloids or illicit substances detected”.[8] A product can be accurately labelled and still be an unapproved opioid.

On potency against the leaf alkaloid, CFSRE is careful about its own confidence, saying only that “early data suggest dihydro-7-hydroxy mitragynine is approximately 30 times more potent than mitragynine”.[4] Its companion report on the two parent alkaloids, 7-OH and mitragynine pseudoindoxyl, says of both that “testing for these two alkaloids is extremely limited”.[9]

Forensic counts are small and worth reading as small. DEA reports that in the national forensic laboratory system “there have been 19 reports of mitragynine pseudoindoxyl in Arkansas (n=15), New York (n=1), Ohio (n=1), and Wyoming (n=2)”, and separately that a CFSRE “trend report identified mitragynine pseudoindoxyl in 103 toxicology specimens and 12 drug materials”.[1]

One line in the monograph is now out of date, and the date it carries is the reason it can be read safely. It says “dihydro-7-hydroxy mitragynine is not currently scheduled in the United States”, and the page stamps itself: “the following information was compiled in November 2025 and is subject to change”.[7] It was true in November 2025 and the August 2026 order changed it.[1]

Mitragynine pseudoindoxyl carries a complication that affects how any detection of it should be read. CFSRE describes it as “mitragynine pseudoindoxyl is categorized as a semi synthetic analogue of mitragynine”, and also as “mitragynine pseudoindoxyl is also a metabolite of mitragynine through 7-hydroxymitragynine and rearrangement of the hydroxyl imine to a spiropseudoindoxyl core”.[10] It is both a manufactured product and something the body makes from kratom leaf. DEA states the same difficulty about 7-OH: “Public health assessment is further complicated because 7-hydroxymitragynine is a known metabolite of mitragynine, making it difficult to distinguish between the ingestion of M. speciosa and other isolated 7-hydroxymitragynine products.”[2] CFSRE also notes that pseudoindoxyl “mitragynine pseudoindoxyl has emerged as a primary component in drug products often found alongside 7-hydroxy mitragynine and marketed as” kratom.[10]

MGM-16: two official documents disagree, and this page does not resolve it

MGM-16 was scheduled alongside the other two. Whether it has ever been in a product is contested by two government bodies, three weeks apart.

The federal order says there is no evidence of it: “While no evidence supports the presence of MGM-16 on the Mitragyna speciosa consumer market, its profile as a highly potent opioid that is structurally related to 7-hydroxymitragynine lends itself as an attractive substitute that could emerge on the illicit drug market.”[1] The scheduling of MGM-16 is explicitly pre-emptive. DEA argues that “to schedule MGM-15 without MGM-16 would create a regulatory loophole that manufacturers are already poised to exploit” and that “its inclusion is necessary to prevent a market shift toward an even more potent derivative that poses a significant risk of respiratory depression”.[1]

The evidence DEA cites for anybody wanting MGM-16 is open-source signal detection, and the order labels it as such. It says “further open source signal detection demonstrates that users are seeking MGM-16 with the intent to abuse”, and its footnotes for that are a “market audit of online retailers” and a forum thread titled “Can anyone help with the MGM 16 rumors”.[1] A regulator reading a rumour thread and citing it as a rumour thread is the correct handling of that evidence, and it is worth noticing that the federal record on this compound contains one. In the labelling used on this page the retailer audit is marketing only and the thread is rumour. Neither is a laboratory result, and the order does not claim otherwise.[1]

Against that, the California Poison Control System warning, carried in August 2026, states that products marketed as kava and as cat's claw “were adulterated with kratom alkaloids, including 7-OH, MGM-15, and MGM-16”.[11] That is an assertion of laboratory detection, and it names the compound DEA says has never been found.

The conflict is not resolved here, and the reason is that the two statements are not equally specified. The poison-control text names no laboratory, gives no per-product result and identifies no analytical method, and this site could not locate a primary advisory carrying it. The federal order is a document with a docket. One of them is wrong about whether MGM-16 has reached a shelf, and on the published record there is no way to say which.

What the poison-control warning documents well is the labelling. It says the compounds found were not declared: “yet these substances are not listed on the product labels”, and worse, “in some cases the labels even claim the products contain no kratom or 7-OH”.[11] It warns that “these misleading labels can lead to life threatening opioid overdose, dependence or withdrawal”, and names the brands it knows about, saying “the products identified are from the buzzers and homiez brands but there may be others”.[11] Its medical director's framing of the general problem is the useful one: “neither kratom nor its derivatives are approved by the FDA and synthetic compounds like 7-OH carry a much greater risk of addiction, overdose and other serious health consequences”.[11] On volume, the same statement reports that “calls to CPCS about kratom have mirrored national trends, rising from 2 in 2015 to 233 in 2025” and that “harmful kratom related incidents are affecting every segment of the population, from infants to seniors”.[11]

Names with nothing behind them

Four names circulate as the next thing after MGM-15. None of them is documented anywhere, and the searches that establish that are given so a reader can run them again.

15-OH, or 15-hydroxymitragynine. Rumour. PubChem returns no compound record for the name 15-hydroxymitragynine, and its autocomplete for hydroxymitragynine returns exactly one term, 7-hydroxymitragynine. PubMed returns zero results for 15-hydroxymitragynine and zero for 15-hydroxy mitragynine. The CFSRE monograph index holds nothing of the kind.[12] No product sold under the name 15-OH could be located in any laboratory report, regulator notice or vendor listing, which means this page cannot tell a reader what such a product contains. Nobody has published what is in it.

The confusion may borrow from real chemistry. C15 is a genuine position in these molecules, and a 2026 structure-activity analysis “identified conserved pharmacophoric elements at C15 and C20 that govern receptor affinity and functional profile across both indole and oxindole scaffolds”.[13] A number that turns up in the pharmacology is an easy one to attach to a compound name.

MGM-15b and MGM-B. Rumour. PubMed returns zero results for MGM-15b and no compound record exists in PubChem under that name. MGM-B returns three PubMed records, none of them about kratom. MGM-17 returns zero. The full text of the August 2026 scheduling order does not mention any of them.[1]

The likeliest explanation is the naming change above. A pack reading MGM-15 (DHM), or a vendor spelling such as MG-M15, garbles easily into something that sounds like a successor compound. The successor is not a new molecule. It is the same molecule with a new abbreviation on the label, and that is the documented event.[4]

The borrowed botanical names

The clearest pattern in 2026 is not a new compound. It is an old, legal, familiar botanical name printed on a pack containing something else.

Cat's claw

Utah's agriculture department and poison control centre issued a joint warning in July 2026. They “are issuing a warning regarding illegally sold kratom products mislabeled as cat's claw products in Utah retailers”, and reported that “investigations are ongoing regarding a recent death and several severe health incidents associated with” a branded cat's claw tablet.[14] The analysis is stated: “The tested products contained both mitragynine pseudoindoxyl and MGM-15, which are opioid-acting compounds derived from the kratom plant and Schedule I drugs in Utah under Title 58-37-2”.[14]

The release is careful to clear the plant whose name was used. “kratom is a leafy plant that contains psychoactive compounds”, whereas cat's claw “is a woody vine and herbal supplement that is not expected to cause adverse effects”, and cat's claw “products do not contain the psychoactive compounds found in and derived from kratom”.[14] The genuine herb did nothing. Its name was the vehicle.

It also carries the clinical advice, which belongs on this page rather than in a footnote: “UPCC recommends administering naloxone in suspected overdoses involving these products”, and “patients experiencing opioid withdrawal from these products may be treated in usual fashion by providers experienced in addiction management”.[14]

Tennessee reported the same substitution two months later. Its bureau of investigation warned that “TBI said it is seeing an increase in products marketed as cat's claw that actually contain MGM-15, which is a compound made from kratom”.[15] The legal logic is explicit in the coverage: “cat's claw is legal in Tennessee, but kratom is illegal in any form”, and “cat's claw, a South American vine, is legal to buy and consume in Tennessee”.[15] The bureau's own summary of the consumer problem was that “mislabeled products can make it difficult for buyers and retailers to know what they are purchasing or selling”, and its advice was “don't assume a product is safe or legal simply because of the name on the package”.[15]

Utah's warning records the same precondition. “Utah banned kratom products other than pure leaf products during the 2026 legislative session”.[14] Both states prohibited kratom, and in both states an opioid then appeared under the name of a legal vine.

The borrowed name is a good choice for the purpose, which is worth stating precisely because it sounds like a chemical coincidence and is not. Cat's claw genuinely is an alkaloid-bearing botanical. The standard 2025 review of Uncaria tomentosa describes “the discovery of two chemotypes of UT with a different pattern of tetracyclic (TOA) and pentacyclic oxindole alkaloids”, and its account of what those alkaloids do is cardiovascular: “the tetracyclic uncaria alkaloids rhynchophylline (7) and isorhynchophylline (8) mainly act on the cardiovascular system”.[16] Two searches of that review are worth reporting as searches. The word opioid does not occur in it. Neither does mitragynine.[16]

One qualification, so this page is not read as saying more than the evidence does. The alkaloids of genuine cat's claw have now been measured at human opioid receptors, and one of them did something. Speciophylline “demonstrated positive allosteric modulation at hMOR without direct orthosteric binding, a mechanism not previously demonstrated experimentally for kratom alkaloids at human opioid receptors”, and “speciophylline failed to enhance β-arrestin 2 recruitment”.[13] That is a single 2026 finding, it is modulation rather than agonism, and it is not a reason to treat the herb as an opioid.

Kava

The same substitution has been run with kava, and that case has a peer-reviewed analysis behind it rather than a press release.

“in October 2025 the Alabama Poison Information Center and local addiction medicine providers identified a cluster of cases involving liquid products marketed as containing kava associated with opioid like withdrawal symptoms”.[17] The reason that was a signal rather than a coincidence is stated in the paper: “kava is not typically associated with physical dependence, raising concern for opioid active substances”.[17] Five retail products were analysed. “qualitative GC-MS detected both mitragynine and kavalactones in one product, while another contained mitragynine with no detectable kavalactones”.[17] A product sold as kava that contains no measurable kava is the clearest form this pattern takes.

The authors' reading is the conservative one: “detection of kratom alkaloids and related semisynthetic derivatives in products labeled as kava may explain the observed opioid like withdrawal”, and their conclusion is that “unrecognized exposure to opioid active kratom compounds may occur through products marketed as kava, highlighting the need for improved surveillance and increased awareness”.[17]

Corynoxine: a real kratom alkaloid that is not a product

Corynoxine comes up in discussion of cat's claw products, on the theory that a concentrated botanical extract could account for the effects people report. The compound is real and the theory is not supported.

Corynoxine is an alkaloid of the kratom leaf itself, isolated from Malaysian material. The study that measured it reports that “this study reports in vitro opioid receptor binding affinity for the following low abundance Malaysian M. speciosa oxindole alkaloids”, naming corynoxine among them, and found that “corynoxine (1) showed high binding affinity to opioid receptors”.[18] In animals it was active systemically: “corynoxine (1) was 1.8-fold more potent than morphine in rats subjected to a nociceptive hot plate assay”.[18]

Its epimer behaves differently, which is a useful warning about reasoning from a name. In an independent screen, “screening of corynoxine B showed poor binding affinity at all opioid subtypes”, and consequently “this molecule was not screened in BRET assays for either G protein or arrestin 2 recruitment, nor is it tested in mice”.[19] Corynoxine and corynoxine B differ only at one carbon. One binds tightly and the other, in that paper, barely binds at all.

No laboratory or regulator has reported corynoxine in a marketed product. It is absent from the CFSRE monograph index[12] and is named in no federal or state notice found for this page. The tested cat's claw products contained MGM-15 and mitragynine pseudoindoxyl, not concentrated corynoxine.[14]

The real point about corynoxine is the one that follows from it being in the leaf. It is a mu-opioid receptor binder present at low abundance in kratom,[18] so any process that concentrates kratom alkaloids concentrates it as well. That is a fact about extracts in general and not about any product sold under its name.

Herkinorin: a real compound with no market

Herkinorin appears in the same conversations and does not belong in them, for a reason that is easy to check.

It is semi-synthetic rather than a plant product, which several reagent vendors get wrong in their own catalogue copy. The paper that introduced it describes “a novel selective agonist derived from the naturally occurring plant product salvinorin A”, which is a derivative and not an extract.[20] It became well known because of one property: “it is interesting that this compound, termed herkinorin, does not promote the recruitment of β-arrestin 2 to the μOR and does not lead to receptor internalization”.[20]

The limitation that keeps it out of products is in the medicinal-chemistry literature, stated by the group working on the series. “the utility of 2 is also limited by the fact that it is peripherally restricted” and it “thus cannot be used to probe centrally mediated processes”.[21] A compound that does not usefully reach the brain is a poor candidate for a recreational market.

Herkinorin has never been reported in a marketed, seized or test-purchased product anywhere. It is absent from the CFSRE monograph index, which carries entries for dihydro-7-hydroxy mitragynine and mitragynine pseudoindoxyl and nothing for herkinorin, corynoxine or 7-acetoxymitragynine.[12] It is absent from the UNODC early-warning substance records.

There is exactly one detection in a human sample, and it is worth stating precisely because it is the only one. A 2016 study screened agitated emergency-department patients: “this is a prospective observational case series that was conducted in the ED of an urban level I trauma center”, and “six patient samples yielded seven different NPS”, herkinorin among them.[22] That is one sample, from a non-targeted method whose own stated purpose was to demonstrate feasibility: “this study demonstrates that prospective non targeted NPS screening in a selected ED patient population is feasible and effective in identifying NPS”.[22] It has not been replicated in the decade since.

Every vendor listing located for herkinorin sells an analytical standard or research reagent. There is no grey-market seller and no consumer scene. In the labelling used on this page it is in the literature and it is nowhere else.

Two checks relevant to this compound did not complete and are not reported as absences: the European drug agency's database and DEA's own site search both refused scripted requests.

What the label says, and what is in the bottle

The labelling failure is now measured rather than alleged. A 2026 analysis of semi-synthetic kratom products across formats found that “results demonstrated substantial variability in alkaloid composition across tablets, films and liquid shots, with frequent inconsistencies between labeled and actual contents”.[23] The direction of error ran both ways: “products often contained additional unreported alkaloids or lacked those listed on the label”.[23] The authors conclude that “these findings indicate inconsistent manufacturing practices, labeling inaccuracies and potential adulteration”.[23]

The retail naming has moved to defeat label reading altogether. CFSRE reports that “similar to the trajectory of other smoke shop products, kratom alkaloids now appear under the guise of” proprietary blend wording, and that products use scientific-sounding terms such as nano technology claims in place of a compound name.[4] One product in that report advertised a proprietary blend labelled DHM and contained dihydro-7-hydroxymitragynine together with mitragynine. Another advertised itself as a nano technology mitragynine product and contained both as well.[4]

CFSRE also states the market mechanism directly, and it is the sentence this whole page is about: “due to changes in legal status of kratom and the rise in popularity of other related alkaloids, novel synthetic kratom alkaloids have begun appearing among products sold in smoke shops and similar retail marketplaces”.[4] On how much is known about any of them, the same report says “limited data exist regarding these novel psychoactive substances”.[4]

Breathing, and the safety story that does not survive this family

The claim most often made for kratom alkaloids is that they are safer than conventional opioids because they do not recruit beta-arrestin-2, the signalling partner once thought to carry opioid respiratory depression. Within this exact family, that link has now been tested and it fails. This is the part of the page where the evidence goes somewhere other than where either side wants it.

Start with what has actually been measured, with species and route attached.

Mitragynine, the leaf alkaloid, is a respiratory stimulant in rats. “respiratory parameters were measured in awake freely moving female and male Sprague-Dawley rats using whole body plethysmography” and “drugs were administered intravenously”.[24] In that preparation, “in contrast, MG administration unexpectedly increased respiratory frequency”, and the increase was not an opioid effect: “naloxone fully reversed the respiratory depression induced by both morphine and 7-HMG but did not alter the respiratory stimulant effects produced by MG”.[24] The authors conclude that “MG exerts respiratory stimulant effects through mechanisms independent of opioid receptor pathways”.[24]

7-OH, in the same study and the same animals, did the opposite. “morphine and 7-HMG induced significant respiratory depression, evidenced by reductions in breathing frequency, tidal volume and minute volume”.[24] It was more potent than morphine on that measure: “The potency of 7-HMG to decrease minute volume by 50% was 4.5-fold greater than that of morphine”.[24] Naloxone reversed it.[24] The paper's own framing is that this is a reason for concern about concentrates, “underscoring the risk associated with high 7-HMG containing kratom products”.[24]

Now the part that settles the biased-agonism argument inside this family. 7-OH does not recruit beta-arrestin-2, and it depresses respiration anyway. A 2026 commentary on that study, by a group that works on these compounds, states both halves. On the signalling, “it shows strong affinity and moderate partial agonism and does not recruit β-arrestin2 up to 10 μM”, and “unlike MG, 7-OH shows μOR activity as its primary target both in vitro and in vivo”.[25] On the consequences, “despite being a partial agonist and a ligand that does not recruit β-arrestin2, 7-OH shows typical adverse effects such as tolerance, dependence”.[25] The commentary describes the respiratory question as the gap that had been left open: “a missing piece in the pharmacology of MG and 7-OH is respiratory depression, which is linked to the lethality of μOR agonists”.[25]

That commentary's authors disclose a commercial interest in this chemistry, and it is recorded here rather than left for a reader to find. “Susruta Majumdar is a co-founder of Sparian Biosciences”, and “Susruta Majumdar and Barnali Paul have filed patents related to the mitragynine class of compounds”.[25]

The kratom pharmacology field has now said the same thing about its own hypothesis. A 2026 characterisation of lesser-known kratom alkaloids notes that “reports of reduced respiratory depression and lower abuse liability associated with kratom use” “have prompted interest in whether such outcomes might relate to biased signaling profiles”, and then states the finding: “current evidence does not support a direct or uniform causal relationship between reduced β-arrestin 2 recruitment and improved safety”.[13]

The same conclusion was reached outside this family first. One 2020 study is titled “morphine induced respiratory depression is independent of β-arrestin2 signalling”.[26] A 2025 study using beta-arrestin-2 knockout mice and two salvinorin-derived agonists found that “these results largely suggest that βArr2 signaling does not drive MOR mediated antinociceptive tolerance, respiratory depression, constipation, or reward”, and that the results “do not support the development of G protein biased compounds as a broadly effective strategy to reduce side effects”.[27]

One kratom-family compound does stimulate breathing in the way the optimistic account predicts, and the paper reporting it says the mechanism is unknown. Given a single dose directly into the cerebral ventricles of mice, “this dose of corynoxine showed no depression of breath rate” and instead “it showed statistically significant respiratory stimulation”.[19] The authors saw it in two compounds, noting that “an unexpected increase in breathing rate was observed with both corynoxine as well as mitraciliatine”, and they decline to explain it: “the exact mechanism of this respiratory stimulation remains unknown and requires more detailed examination”.[19] One dose, one route, one laboratory, mice.

For the three compounds this page is mostly about, the honest statement is that nobody has measured the thing that kills people. There is no published respiratory measurement for MGM-15, for MGM-16 or for herkinorin, in any species. DEA's statement that these compounds “pose similar health risks as other mu-opioid agonists”, “including physical and psychological dependence and respiratory depression”, is an inference from receptor pharmacology, and the order presents it as one.[1] It is a reasonable inference. It is not a measurement, and a page that reported it as one would be doing what this page is about.

The one human data set that compares them

The strongest human evidence that the concentrates behave differently from leaf comes from paediatric poisonings, which have the advantage of being unintentional and therefore unselected. A 2026 analysis of national poison centre data covered single-substance ingestions in children under twelve. “of 169 cases that met inclusion, 60% were male with a median age of 2 years”, and “most ingestions (97%) were unintentional”.[28]

Comparing 7-OH or mitragynine pseudoindoxyl against mitragynine, “7-OH or MP exposures had higher odds of serious respiratory and neurologic effects”, and “naloxone use was nearly twice as likely among children exposed to 7-OH or MP”.[28] The authors conclude that “high potency kratom alkaloids may pose significant respiratory and neurologic risks to pediatric patients when unintentionally exposed”, and state their policy reading: “this data supports the recent scheduling of 7-OH and MP products”.[28]

It is observational, it is small, and it is children rather than adult users. It is also the only comparison of leaf alkaloid against isolate in humans that this page could find, and it points the same way as the rat plethysmography.

A clinician quoted on the Ole Miss case gives the mechanism in plain terms: “they are more potent since they're isolated, which can amplify the opioid like abilities and effects that can lead to dependency and overdose via slowed breathing and stimulant toxicity”, and notes these “products have been available in the United States consumer market, though not regulated or verified, for about three years”.[6]

Why a laboratory result here is weaker than it sounds

Several claims on this page rest on a laboratory naming a compound, so the limits of that naming belong on the page too.

These molecules turn into each other during sample preparation. The public health laboratories' 2026 bulletin states that “due to the chemical instability of these analytes it is recommended to avoid the addition of acid and base during sample preparation”, because “adding acid to MG may result in the formation of 7-OH” and “adding base to 7-OH may result in the formation of MP”.[29] A laboratory can create the compound it then reports finding.

They are also hard to tell apart even when nothing converts. “7-OH and MP are isomers requiring testing to differentiate”.[29] A 2026 method paper found that “multiple overlapping chromatographic peaks were observed” at the relevant mass, and that relying on mass alone “can lead to false positive identification of 7-OH in complex botanical matrices”.[30]

And one of the compounds destroys itself in a common instrument. CFSRE reports that “analysis of dihydro-7-hydroxy mitragynine is challenging due to the analytical conversion of dihydro-7-hydroxy mitragynine to mitragynine during GC-MS analysis”.[7] A laboratory using that technique on a DHM product can report ordinary mitragynine and be wrong without any error in its procedure.

None of this makes the findings on this page unreliable. The MGM-15 identification was confirmed against purchased reference material,[7] and the kava work used tandem mass spectrometry.[17] It does mean that a bare claim that a laboratory found 7-OH in a sample is a weaker statement than it appears, and that the method matters more here than it does for most compounds.

The next name is already in a state rule

Florida did not wait for a product. Its June 2026 emergency rule “labels these 7-OH related compounds as Schedule 1 drugs”, listing “7-hydroxymitragynine, mitragynine pseudoindoxyl, 7-acetoxymitragynine, 9-hydroxycorynantheidine, 10-hydroxycorynantheidine, MGM-15 or MGM-16”.[31]

Three of those names are worth marking, and the marking is a set of searches a reader can repeat. All were run on October 5, 2026.

Name	PubChem record	PubMed	Europe PMC full text
7-acetoxymitragynine	CID 11015924	0	0
9-hydroxycorynantheidine	none under this name	6	25
10-hydroxycorynantheidine	none under this name	0	1

So the three are not alike. 9-hydroxycorynantheidine is a well studied kratom constituent. 7-acetoxymitragynine has a structure record and no literature at all under its own name. 10-hydroxycorynantheidine has neither. None of the three has been reported in a marketed product by any laboratory or regulator found for this page. Florida prohibited all three anyway, on the same reasoning DEA gave for MGM-16: that the obvious substitute should be covered before it arrives.[1]

That is the shape of this market, and it is the reason the four labels at the top of this page are worth keeping separate. A compound can be scheduled before anyone has sold it, sold before anyone has analysed it, analysed before anyone has measured what it does to breathing, and named three different things in the course of all of that.

References

Schedules of Controlled Substances: Temporary Placement of Mitragynine Pseudoindoxyl, MGM-15, and MGM-16 in Schedule I (temporary order, Docket DEA-1644) — Drug Enforcement Administration, Federal Register, 2026-08-26
Schedules of Controlled Substance: Temporary Placement of 7-Hydroxymitragynine Above a Specified Threshold in Schedule I (notice of intent, Docket DEA-1570) — Drug Enforcement Administration, Federal Register, 2026-07-06
Federal Register full-text search for 7-hydroxymitragynine — Office of the Federal Register
Test Purchase: Dihydro-7-Hydroxy Mitragynine (MGM-15), May 2026 — Krotulski AJ, Denn MT, Walton SE, Logan BK, Center for Forensic Science Research and Education, NPS Discovery
Dihydromyricetin as a novel anti-alcohol intoxication medication — Shen Y and colleagues, Journal of Neuroscience, 2012 (PMID 22219299)
What to know about the kratom-related drugs found near the late Ole Miss students — ABC 17 News, carrying CNN's report, 2026-10-03
NPS Discovery monograph: dihydro-7-hydroxy mitragynine — Center for Forensic Science Research and Education, compiled November 2025
Analysis of commercially available MGM-labelled tablets and the binding affinities of purified MGM-15 — Gour A and colleagues, Drug Testing and Analysis, 2025 (PMID 40936282)
Test Purchase: Mitragynine & 7-Hydroxy Mitragynine, May 2026 — Krotulski AJ, Denn MT, Eccarius LK, Logan BK, Center for Forensic Science Research and Education
NPS Discovery monograph: mitragynine pseudoindoxyl — Center for Forensic Science Research and Education
California Poison Control issues warning as dangerous kratom derivatives appear in popular herbal products — The Union, carrying the California Poison Control System warning, August 2026
NPS Discovery monograph index — Center for Forensic Science Research and Education
Pharmacological characterization of lesser known kratom alkaloids at human opioid receptors — Hemby SE and colleagues, 2026
Illegal kratom product sold in Utah County linked to death in Utah — Utah Department of Agriculture and Food with the Utah Poison Control Center, 2026-07-30
What is cat's claw and why is Tennessee law enforcement warning public about it containing illegal compound — WSMV, reporting the Tennessee Bureau of Investigation, 2026-09-14
Uncaria tomentosa as a promising natural source of molecules with multiple activities: review of its ethnomedicinal uses, phytochemistry and pharmacology — Marques O and colleagues, International Journal of Molecular Sciences, 2025 (PMID 40725012)
Unlabeled kratom alkaloids detected in products marketed as kava — Marshall S and colleagues, Clinical Toxicology, 2026 (PMID 42374886)
Exploring the chemistry and opioid receptor activity of the minor oxindole alkaloids of Malaysian Mitragyna speciosa — Chear NJ and colleagues, Journal of Natural Products, 2021 (PMID 33635670)
Kratom alkaloids as probes for opioid receptor function — Chakraborty S and colleagues, ACS Chemical Neuroscience, 2021 (PMID 34213886)
An opioid agonist that does not induce mu-opioid receptor arrestin interactions or receptor internalization — Groer CE and colleagues, Molecular Pharmacology, 2007 (PMID 17090705)
Synthetic studies of neoclerodane diterpenes from Salvia divinorum — Crowley RS and colleagues, Journal of Medicinal Chemistry, 2016 (PMID 27958743)
Non-targeted screening for novel psychoactive substances among agitated emergency department patients — Lung D and colleagues, Clinical Toxicology, 2016 (PMID 26846684)
Mislabeling and status of semisynthetic kratom-derived products in the US market — Gour A and colleagues, Drug Testing and Analysis, 2026 (PMID 42448619)
Mitragynine and 7-hydroxymitragynine: bidirectional effects on breathing in rats — Zuarth Gonzalez JD and colleagues, Journal of Pharmacology and Experimental Therapeutics, 2025 (PMID 41106041)
Atypical respiration patterns of kratom alkaloids — Wells E, Paul B, Ramos-Gonzalez N, Majumdar S, Journal of Pharmacology and Experimental Therapeutics, 2026 (PMID 42054852)
Morphine-induced respiratory depression is independent of beta-arrestin2 signalling — Kliewer A and colleagues, British Journal of Pharmacology, 2020 (PMID 32052419)
Kurkinorin and kurkinol in beta-arrestin2 knockout mice — van de Wetering R and colleagues, Neuropsychopharmacology, 2025 (PMID 40897856)
Risk of respiratory and neurologic effects in children ingesting kratom and related alkaloids — Hoffmann NA and colleagues, American Journal of Emergency Medicine, 2026 (PMID 42715782)
Substance Awareness Bulletin: kratom alkaloids, mitragynine, 7-hydroxy mitragynine and mitragynine pseudoindoxyl — Association of Public Health Laboratories, June 2026
Avoiding false identification of 7-hydroxymitragynine in kratom products using a multicriteria LC-MS confirmation — Sheehan D and colleagues, Journal of the American Society for Mass Spectrometry, 2026 (PMID 41989479)
More 7-OH related products made illegal in Florida by a new emergency rule — Florida Phoenix, 2026-06-22