25H-NBOMe, also known as NBOMe-2C-H, is a derivative of the phenethylamine hallucinogen 2C-H, which acts as a highly potent full agonist for the human 5-HT_2A receptor.

The active dose range of 25H-NBOMe in humans has not been reported and hence is unknown. This is in notable contrast to many other NBOMe drugs.

NBOMe compounds are often associated with life-threatening toxicity and death. Studies on NBOMe family of compounds demonstrated that the substance exhibit neurotoxic and cardiotoxic activity. Reports of autonomic dysfunction remains prevalent with NBOMe compounds, with most individuals experiencing sympathomimetic toxicity such as vasoconstriction, hypertension and tachycardia in addition to hallucinations. Other symptoms of toxidrome include agitation or aggression, seizure, hyperthermia, diaphoresis, hypertonia, rhabdomyolysis, and death. Researchers report that NBOMe intoxication frequently display signs of serotonin syndrome. The likelihood of seizure is higher in NBOMes compared to other psychedelics.

NBOMe and NBOHs are regularly sold as LSD in blotter papers, which have a bitter taste and different safety profiles. Despite high potency, recreational doses of LSD have only produced low incidents of acute toxicity. Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD, and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently". While most fatalities are due to the physical effects of the drug, there have also been reports of death due to self-harm and suicide under the influence of the substance.

Many of the NBOMe compounds have high potency agonist activity at additional 5-HT receptors and prolonged activation of 5-HT_2B can cause cardiac valvulopathy in high doses and chronic use. 5-HT_2B receptors have been strongly implicated in causing drug-induced valvular heart disease. The high affinity of NBOMe compounds for adrenergic α₁ receptor has been reported to contribute to the stimulant-type cardiovascular effects.

In vitro studies, 25C-NBOMe has been shown to exhibit cytotoxicity on neuronal cell lines SH-SY5Y, PC12, and SN471, and the compound was more potent than methamphetamine at reducing the visibility of the respective cells; the neurotoxicity of the compound involves activation of MAPK/ERK cascade and inhibition of Akt/PKB signaling pathway. 25C-NBOMe, including the other derivative 25D-NBOMe, reduced the visibility of cardiomyocytes H9c2 cells, and both substances downregulated expression level of p21 (CDC24/RAC)-activated kinase 1 (PAK1), an enzyme with documented cardiac protective effects.

25H-NBOMe acts as an agonist of the serotonin 5-HT₂ receptors.

Its affinity for the serotonin 5-HT_2A receptor (K_i = 2.83 nM) was 133-fold higher than that of 2C-H and 24-fold higher than that of 25H-NB (N-benzyl-2C-H), whereas it was 4-fold lower than that of 2C-I and 64-fold lower than that of 25I-NBOMe. In terms of activational potency at the receptor, the drug's potency (EC₅₀Tooltip half-maximal effective concentration = 15.3 nM) was 67-fold higher than that of 2C-H, whereas it was 6-fold lower than that of 2C-I and 35-fold lower than that of 25I-NBOMe. Hence, unlike other NBOMe drugs, 25H-NBOMe appears to have affinity and activational potency at the serotonin 5-HT_2A receptor more in line with the 2C psychedelics like 2C-I and much lower than NBOMe drugs like 25I-NBOMe.