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What Drug Class Is Kratom In? A Detailed Pharmacological Review

4 min read

According to the Substance Abuse and Mental Health Services Administration, an estimated 1.7 million Americans aged 12 and older used kratom in 2021 [1.7.1]. This widespread use raises a critical question for both users and regulators: what drug class is kratom in?

Quick Summary

Kratom defies simple classification. It functions as a stimulant in low doses and produces opioid-like effects at higher doses, placing it in a unique category often described as an 'atypical opioid' [1.8.5].

Key Points

  • Dual Action: Kratom functions as a stimulant at low doses, increasing energy, while acting as a sedative and analgesic at high doses [1.4.1].

  • Atypical Opioid: Its alkaloids are G-protein biased agonists at opioid receptors, which may lead to a lower risk of respiratory depression compared to classical opioids [1.9.2].

  • No Single Class: Kratom does not fit into a single drug class due to its complex, dose-dependent effects and is best described as an atypical opioid with stimulant properties [1.8.5].

  • Variable Legal Status: Kratom is not federally scheduled in the U.S., but as of 2025, it is banned in six states and regulated in many others [1.5.5].

  • Active Compounds: Mitragynine and the more potent 7-hydroxymitragynine are the primary alkaloids responsible for kratom's effects by interacting with opioid, serotonin, and dopamine receptors [1.2.3].

  • Addiction Risk: Regular use can lead to dependence and a withdrawal syndrome similar to that of opioids, featuring symptoms like body aches, hostility, and insomnia [1.4.1].

  • Regulatory Scrutiny: While the kratom plant is not federally scheduled, the FDA and DEA are considering placing its concentrated alkaloid, 7-OH, on the controlled substance list as of 2025 [1.5.3].

In This Article

The Unconventional Nature of Kratom

Kratom, derived from the leaves of the Mitragyna speciosa tree native to Southeast Asia, presents a significant challenge to traditional drug classification [1.6.2]. Unlike substances that produce consistent effects, kratom's impact on the user is highly dose-dependent. At low doses (1–5 grams of raw leaves), it acts as a stimulant, producing increased energy, alertness, and sociability [1.4.1, 1.4.5]. Conversely, at high doses (5–15 grams), its effects become sedative and analgesic, mimicking those of opioids [1.4.3, 1.4.5]. This dual nature is central to the confusion and debate surrounding its pharmacological identity.

A Deep Dive into Kratom's Pharmacology

The key to understanding kratom lies in its active alkaloids, primarily mitragynine and 7-hydroxymitragynine (7-HMG) [1.3.1]. While mitragynine is the most abundant alkaloid in kratom leaves, 7-HMG is significantly more potent, with some research suggesting it has 13 times the potency of morphine [1.2.1, 1.6.5].

Interaction with Opioid Receptors

Both mitragynine and 7-HMG are partial agonists at the mu-opioid receptor, the same primary target for classical opioids like morphine and codeine [1.2.5, 1.3.1]. This interaction is responsible for the analgesic (pain-relieving) and euphoric effects experienced at higher doses. The alkaloids also interact with other receptor systems, including delta and kappa-opioid receptors, as well as serotonin and dopamine receptors, contributing to their complex effects [1.2.3, 1.8.4].

The 'Atypical Opioid' Distinction

Despite its action on opioid receptors, kratom is frequently labeled an 'atypical opioid' [1.8.5]. The crucial difference lies in the downstream signaling pathway. When classical opioids bind to the mu-opioid receptor, they activate two main pathways: the G-protein pathway (responsible for analgesia) and the β-arrestin (beta-arrestin) pathway [1.9.1]. The β-arrestin pathway is heavily implicated in the most dangerous side effects of opioids, such as respiratory depression, severe sedation, and constipation [1.8.1, 1.9.1].

Kratom's alkaloids are G-protein biased agonists, meaning they preferentially activate the G-protein pathway without significantly recruiting the β-arrestin pathway [1.9.2, 1.9.4]. This unique mechanism is believed to be why kratom exhibits a lower risk of respiratory depression compared to traditional opioids, making it a subject of intense scientific research for pain management [1.9.2, 1.9.3].

So, What Is the Official Classification?

Pharmacologically, kratom does not fit neatly into one category. It possesses both stimulant and opioid-like properties [1.4.4]. Due to its primary mechanism of action, the most accurate scientific description is an atypical opioid with stimulant properties.

From a legal standpoint, the situation is equally complex. In the United States, kratom is not a federally controlled substance under the Controlled Substances Act [1.4.3, 1.5.2]. The Drug Enforcement Administration (DEA) has listed it as a "Drug and Chemical of Concern" but withdrew its intent to place it in Schedule I after public pushback in 2016 [1.5.2, 1.4.3]. The Food and Drug Administration (FDA) has not approved kratom for any medical use and warns against its consumption due to risks of liver toxicity, seizures, and addiction [1.5.1, 1.6.3]. However, recent developments in 2025 show the FDA and DEA are considering classifying 7-OH, the concentrated byproduct, as a Schedule I substance, separate from the whole kratom leaf [1.5.3, 1.5.4].

Kratom vs. Classical Opioids: A Comparison Table

Feature Kratom Classical Opioids (e.g., Morphine)
Primary Mechanism Partial agonist at mu-opioid receptors; also affects serotonin & dopamine receptors [1.2.3]. Full agonist at mu-opioid receptors [1.2.5].
β-Arrestin Recruitment Low to no recruitment [1.9.1, 1.9.2]. Strong recruitment [1.8.1].
Respiratory Depression Risk Considered significantly lower [1.9.2]. High; a primary cause of overdose death [1.8.1].
Dose-Dependent Effects Stimulant at low doses, sedative at high doses [1.4.1]. Primarily sedative and analgesic across effective doses.
Addiction Potential Dependence and withdrawal symptoms can occur [1.2.5, 1.4.1]. High potential for addiction and dependence.
Federal Legal Status (USA) Not a controlled substance; legality varies by state and municipality [1.5.2, 1.5.5]. Schedule II or III controlled substances.

The Patchwork of Legality in 2025

While federally legal, kratom's status is inconsistent across the U.S. As of mid-2025, six states have completely banned kratom: Alabama, Arkansas, Indiana, Rhode Island, Vermont, and Wisconsin [1.5.5]. In contrast, at least 22 states have enacted regulations, often called a Kratom Consumer Protection Act (KCPA), which set standards for product purity and restrict sales to minors [1.5.5, 1.5.6]. This legal landscape is constantly evolving, with states like North Carolina considering a full ban and Texas implementing strict limits on 7-HMG content in 2025 [1.5.5].

Risks and Reported Uses

Users commonly report taking kratom for pain relief, mood enhancement, and to self-manage symptoms of opioid withdrawal [1.4.4, 1.6.6]. However, these uses are not FDA-approved. The primary risks associated with kratom include the potential for dependence, addiction, and withdrawal symptoms such as hostility, body aches, and insomnia [1.4.1, 1.6.4, 1.6.5]. Other serious concerns include liver toxicity, seizures, and the risk of products being contaminated with heavy metals or salmonella [1.6.1, 1.6.3, 1.6.6].

Conclusion: A Complex Plant Demanding Caution and Further Study

To answer the question, "What drug class is kratom in?" is to say it defies simple categorization. It is best understood as a unique substance with a dual identity: a stimulant at low doses and an atypical opioid at higher doses. Its distinct pharmacological profile, particularly its G-protein bias, separates it from classical opioids and reduces the risk of certain severe side effects like respiratory depression [1.9.1]. Nonetheless, it carries significant risks, including addiction and contamination, and its legal status remains fragmented and uncertain. As research continues, users and regulators alike must approach this complex botanical with caution.

For more information from a government health perspective, you can visit the National Institute on Drug Abuse (NIDA) page on Kratom [1.4.4].

Frequently Asked Questions

Not officially. While its main compounds act on opioid receptors, kratom is pharmacologically distinct from classical opioids and is often called an 'atypical opioid' because it activates different signaling pathways in the brain [1.8.1, 1.8.5].

It means that unlike classical opioids such as morphine, kratom's alkaloids activate the mu-opioid receptor without strongly recruiting the β-arrestin pathway. This pathway is linked to severe side effects like respiratory depression, so kratom may have a lower risk for this specific effect [1.9.1, 1.9.2].

The effects are dose-dependent. Low doses typically produce stimulant effects like increased energy and alertness. High doses result in opioid-like effects, including pain relief, sedation, and euphoria [1.4.3].

Kratom is not federally illegal. However, its legality varies by state and even city. As of 2025, it is banned in six states (Alabama, Arkansas, Indiana, Rhode Island, Vermont, and Wisconsin), while many others have regulations on its sale [1.5.5].

Yes, regular use of kratom can lead to psychological and physiological dependence. Users can experience withdrawal symptoms if they stop taking it, which may include anxiety, muscle pain, and insomnia [1.4.1, 1.2.5].

The two primary active alkaloids are mitragynine and 7-hydroxymitragynine (7-HMG). Both bind to mu-opioid receptors, but 7-HMG is significantly more potent [1.2.3, 1.3.2].

The FDA has issued warnings about serious health risks including liver toxicity, seizures, and substance use disorder. There is also a risk of kratom products being contaminated with heavy metals and harmful bacteria like Salmonella [1.5.1, 1.6.3].

Its dual effects come from its complex alkaloids. Mitragynine and 7-hydroxymitragynine interact with multiple brain receptors, including opioid, serotonin, and dopamine receptors, producing different effects at different concentrations [1.2.3, 1.4.4].

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.