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Nifoxipam Facts

Depressant; Anxiolytic; Benzodiazepine; GABA-A receptor positive allosteric modulator

Description

Nifoxipam is a synthetic depressant of the benzodiazepine class. It amplifies the brain's main inhibitory system — GABA — producing the heavy, prolonged sedation characteristic of benzodiazepines.[1]

Subjective effects include anxiety suppression, sedation, muscle relaxation, amnesia, and disinhibition. The experience is a flat, prolonged numbness — notably lacking the euphoria characteristic of more potent designer benzodiazepines.[2]

Nifoxipam carries high physical and psychological dependence liability, and abrupt cessation can trigger life-threatening withdrawal.[3] Combining it with opioids or alcohol dramatically amplifies the risk of breathing failure; its duration of up to 75 hours makes dose accumulation a distinct hazard.[4][5]

Dose and durationby route · individual sensitivity varies

Oral(mg)
Threshold< 0.1 mgLight0.25 – 0.5 mgCommon0.5 – 1 mgStrong1 – 2 mgHeavy2+ mg

Starts in 45 – 120 minLasts 10 – 75 hoursAfter-effects 6 – 24 hours

Body and dependence

Acute toxicity
Moderate
Chronic toxicity
Low
Physical dependence
High
Psychological dependence
High
Withdrawal
Life-threatening · fatal · medical supervision
Compulsive redosing
Moderate

Tolerance

Builds
Rapid
Fully resets after
10.5 days
Carries over to
benzodiazepines; alcohol; barbiturates; GABA-A positive allosteric modulators

Effectslikely at a common dose

Perception
none likely · 7 possible, including Visual acuity suppression, Spatial disorientation, Vestibular distortion
Body
Motor control impairment; Muscle relaxation; Sedation; Physical fatigue; +6 possible, including Dizziness, Nystagmus (eye wobbles), Insomnia
Thinking
Analysis suppression; Thought deceleration; Memory suppression; Cognitive impairment; Cognitive fatigue; +14 possible, including Decision impairment, Information processing suppression, Delusions of sobriety
Feeling
Emotional suppression; Anxiety suppression; +3 possible, including Emotional lability
Self
Disinhibition; +5 possible, including Craving
Time
none likely · 2 possible, including Temporal disorientation

Who shouldn't take it

Absolute
Respiratory insufficiency; Myasthenia gravis; Pregnancy and lactation; Concurrent CNS depressant use
Relative
History of paradoxical benzodiazepine reactions; Severe hepatic impairment; Acute narrow-angle glaucoma

Combinations60 recorded

Lethal (1)
Opioids
Dangerous (21)
Alpha-2 adrenergic receptor antagonist; Antipsychotics; Atypical antipsychotics; Benzodiazepines; Buprenorphine, Kratom; Cannabis, THC; Clonidine, Guanfacine; Gabapentin, Pregabalin; GHB, Baclofen; GHB, GBL; Local anesthetics; Naltrexone; SNRIs; Stimulants; Synthetic cannabinoids; Ibogaine; Ketamine, DXM, PCP; MAOIs; NSAIDs; Poppers (Alkyl nitrites); Poppers, Nitrates
Caution (26)
See full page: psychedex.org/substances/nifoxipam
Not graded (12)
Not listed never means safe.

Seek help immediately if

  • Extreme drowsiness — can't stay awake or be roused
  • Confusion, slurred speech, severe loss of coordination
  • Slow, shallow, or irregular breathing
  • Unconsciousness / unresponsive; limp, floppy body
  • Blue lips or fingertips
  • Vomiting while sedated (choking / aspiration risk)
  • Cold, clammy skin; weak pulse

What to do

  1. Try to wake them — shout, firm sternal rub
  2. If unresponsive or breathing is impaired, call emergency services
  3. Place them in the recovery position — critical, they can choke on vomit
  4. Monitor breathing continuously; be ready to give rescue breaths / CPR
  5. Never leave them alone to "sleep it off"
  6. Do not give other drugs, stimulants, or more depressants

Most depressant overdoses resolve with airway protection, breathing support, and monitoring. The danger is respiratory depression and choking on vomit — sharply worse when combined with opioids or alcohol. GHB/GBL overdoses often involve sudden deep unconsciousness and may self-resolve, but airway protection is essential.

988 Suicide & Crisis LifelineFireside Project: 62-FIRESIDE

Version r1 · Not medical advice

References

  1. [1]
    ^Doyno CR, White CM (2021) Sedative-Hypnotic Agents That Impact Gamma-Aminobutyric Acid Receptors: Focus on Flunitrazepam, Gamma-Hydroxybutyric Acid, Phenibut, and Selank — Journal of Clinical Pharmacology doi:10.1002/jcph.1922
  2. [2]
    ^El Balkhi S, Monchaud C, Herault F, Geniaux H, Saint-Marcoux F (2020) Designer benzodiazepines' pharmacological effects and potencies: How to find the information — Journal of Psychopharmacology doi:10.1177/0269881119901096
  3. [3]
    ^Saini S, Tahlan S, Minocha N (2024) Current Therapeutic Strategies for the Management of Benzodiazepine (BZD) Withdrawal Syndrome: A Review. — Current topics in medicinal chemistry doi:10.2174/0115680266296096240408032738
  4. [4]
    ^Manchester KR, Lomas EC, Waters L, Dempsey FC, Maskell PD (2018) The emergence of new psychoactive substance (NPS) benzodiazepines: A review. — Drug testing and analysis doi:10.1002/dta.2211
  5. [5]
    ^Katselou M, Papoutsis I, Nikolaou P, Spiliopoulou C, Athanaselis S (2017) Metabolites replace the parent drug in the drug arena. The cases of fonazepam and nifoxipam. — Forensic toxicology doi:10.1007/s11419-016-0338-5
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