βk-2C-B
β-keto-4-bromo-2,5-dimethoxyphenethylamine
Lethal interactions
| Combination | Type | Severity | Mechanisms | Confidence |
|---|---|---|---|---|
| MAOIs | Drug class | lethal | 2 | high |
Dangerous interactions
29 dangerous interactions recorded for this substance.
See the full interactions tableContraindications
| Condition | Severity | Note |
|---|---|---|
| Cardiovascular | ||
| Cardiovascular disease | absolute | hypertension, arrhythmias, coronary artery disease, heart failure The dual cathinone-type sympathomimetic (NDRI) and serotonergic cardiovascular stimulation from βk-2C-B represents a theoretical additive cardiovascular burden. Substituted cathinones produce tachycardia and hypertension; the parent compound 2C-B raises blood pressure and heart rate in controlled human studies. One unverified Erowid report describes sudden cardiac arrest following use. Individuals with any pre-existing cardiovascular condition face unquantified but theoretically significant risk. |
| Neurological | ||
| Seizure disorders | relative | epilepsy, history of seizures, conditions lowering seizure threshold Both substituted cathinones and serotonergic psychedelics have been independently associated with seizure threshold reduction. The dual mechanism of βk-2C-B may present additive risk for individuals with seizure disorders or other conditions that lower seizure threshold. |
| Psychiatric | ||
| Personal or family history of psychotic disorders | absolute | schizophrenia, schizoaffective disorder, bipolar disorder with psychotic features, family history of psychotic disorders Phenethylamine psychedelics can precipitate transient or sustained psychotic episodes, particularly at higher doses or in individuals with personal or family history of psychotic disorders. The cathinone component may add further risk of paranoia and agitation beyond typical serotonergic psychedelic class risk. |
| Hepatic | ||
| Hepatic impairment | relative | hepatic insufficiency, liver disease, cirrhosis The structurally related compound 2C-B-FLY is metabolized by CYP2D6 in human liver microsomes. If CYP2D6 or other hepatic enzymes mediate βk-2C-B metabolism, individuals with hepatic impairment could experience prolonged or intensified effects due to reduced clearance. This is entirely speculative — no metabolic data exist for βk-2C-B. |
| Metabolic | ||
| CYP2D6 poor metabolizer phenotype | relative | CYP2D6 poor metabolizers may have altered pharmacokinetics for βk-2C-B if this enzyme is involved in its metabolism, as it is for the structurally related 2C-B-FLY. This could result in prolonged duration, higher peak plasma concentrations, or intensified effects. This contraindication is entirely speculative. |
| Pregnancy & Breastfeeding | ||
| Pregnancy and lactation | relative | No reproductive toxicity, teratogenicity, or lactation transfer data exist for βk-2C-B. Both stimulant cathinones and serotonergic psychedelics are contraindicated during pregnancy and breastfeeding by precautionary principle due to unknown fetal and neonatal effects. |
| Other | ||
| Concurrent MAOI use | absolute | phenelzine, tranylcypromine, moclobemide, selegiline, linezolid βk-2C-B's predicted serotonergic activity (5-HT2A agonism and possible serotonin transporter effects from the cathinone scaffold) creates high risk of serotonin syndrome when combined with monoamine oxidase inhibitors. Both receptor agonism and potential transporter inhibition may contribute to serotonin excess under MAO inhibition. |
| Concurrent serotonergic medication | relative | SSRIs, SNRIs, triptans, tramadol Concurrent use of serotonergic medications (SSRIs, SNRIs, triptans, tramadol) with βk-2C-B creates risk of serotonin syndrome and unpredictable pharmacodynamic interactions. SSRIs may blunt psychedelic effects via chronic 5-HT2A downregulation while potentially contributing to serotonin excess. |