General risks

• Despite the “safer opioid” academic framing, MP is still a potent MOR agonist with full opioid-class dependence, withdrawal, and overdose risk in real-world unregulated use.
• The reduced-respiratory-depression findings come from controlled animal studies — they don’t mean MP is safe to mix with depressants. Combining with benzos, alcohol, gabapentinoids, or other opioids significantly raises overdose risk.
• Naloxone reverses overdose. Higher or repeated doses may be needed because of MP’s tight MOR binding.
• Withdrawal looks like classical opioid withdrawal.
• Products labeled MP, 7-OH, or “pseudoindoxyl kratom” frequently contain a mix of compounds. What’s on the label is not necessarily what’s in the bottle.

Legal status

MP is named in state-level scheduling actions targeting mitragynine-derived semi-synthetics. The FDA’s July 2025 recommendation to schedule 7-OH would likely sweep MP under analog enforcement at the federal level.

7-Pseudoindoxyl / MP (Mitragynine Pseudoindoxyl)

What it is

MP is a skeletal rearrangement product of 7-OH. The indolenine core of 7-OH gets restructured into a spiro-pseudoindoxyl scaffold, making it chemically and pharmacologically distinct from its parent compound. Also called VM1502 or “Compound 3” in research literature, and sometimes “7-pseudo,” “pseudoindoxyl,” or “mit-pseudo” in community discussion.

Where it came from

MP was originally identified as a research target because of its unusual receptor profile — it’s been studied as a template for developing opioids with reduced side effects. It started showing up in U.S. consumer products in 2024–2025, sold as its own thing or as part of “enhanced” products.

Important: lab analyses of products marketed as “7-OH” have repeatedly found MP present alongside the labeled 7-OH, mitragynine in varying concentrations. There’s also evidence that 7-OH converts to MP metabolically in human plasma.

Pharmacology

• Mu-opioid receptor agonist + delta-opioid receptor antagonist. This dual profile is what makes MP pharmacologically unusual — most opioids don’t have this combination.
• Extremely high MOR affinity: 0.087 nM, compared to mitragynine at 7.24 nM and 7-OH at 13.5 nM. Lower number = tighter binding. MP binds MOR tighter than most clinical opioids do — including buprenorphine.
• In animal studies, the mu-agonist + delta-antagonist combination has been associated with reduced tolerance, reduced respiratory depression, and reduced reward compared to morphine. These findings are rodent data and don’t reliably translate to humans taking unregulated isolates at unknown doses.

Half-life

Direct half-life data for MP itself is thin — most published pharmacology focuses on receptor activity rather than human pharmacokinetics. Reports indicate it’s similar to 7oh (a few hours).

Suboxone considerations

MP binds MOR tighter than buprenorphine does. MP’s MOR affinity (~0.087 nM) is stronger than buprenorphine’s (~1.5 nM). In fentanyl-to-bupe transitions, this kind of affinity mismatch is part of why those inductions are notoriously difficult — the higher-affinity drug doesn’t budge easily, and bupe struggles to fully take over. The same logic applies here:

• Standard 12–24 hour washout windows may not be enough — receptor occupancy can outlast plasma levels when affinity is this high.
• Precipitated withdrawal during induction is a real risk if MP is still bound when bupe arrives.
• Even after stabilization, some people report bupe doesn’t feel like a clean replacement.

The delta picture is actually favorable here: buprenorphine is essentially a delta antagonist, and MP is too — so there’s no significant delta-receptor activation gap when switching. The main complication is the affinity at MOR.

What people have found helps: a longer washout when feasible, prescribers familiar with high-affinity opioid transitions (the fentanyl-induction playbook is more relevant here than the standard kratom-recovery playbook), and being patient with stabilization — it can take 2–3 weeks.