Content here is incomplete, evolving, and subject to structured Delphi review. This is not a substitute for a final peer-reviewed resource, but rather a collaborative space .... a place where ideas develop, raw data is refined, and consensus is built.
Intramuscular (IM) Recommendations
🟩 Alfaxalone 3–5 mg/kg IM provides consistent immobilisation (20–40 min) with smooth recovery < 20 min [CS] (Arnemo & Søli 1995; Doss & de Miguel García 2022).
🟨 Alfaxalone 5 mg/kg IM + Midazolam 1 mg/kg IM achieves deep sedation and muscle relaxation for diagnostic imaging [EC] (Rondeau et al. 2020; Heard 2014).
🟨 Juvenile E. europaeus respond well to 3 mg/kg IM + Midazolam 1 mg/kg IM; avoid higher doses to prevent delayed recovery [EC] (Heard 2014).
⬜ Dose reduction (~25 %) recommended in debilitated or hypothermic individuals; allow spontaneous recovery without reversal [EX] (Simone-Freilicher & Hoefer 2004).
Subcutaneous (SC) Recommendations
🟩 Alfaxalone 3 mg/kg SC + Midazolam 1 mg/kg SC (mantle injection) produces heavy sedation within 10 min; full recovery < 20 min [CS] (Doss & de Miguel García 2022).
🟨 Alfaxalone 5 mg/kg SC ± Midazolam 1 mg/kg SC for deeper restraint or venipuncture [EC] (Rondeau et al. 2020).
⬜ Mantle or lateral thoracic SC sites recommended; avoid dorsal spines; maintain ambient > 24 °C [EX] (Simone-Freilicher & Hoefer 2004).
Intravenous (IV) Recommendations
🟨 Alfaxalone 2–4 mg/kg IV to effect after Midazolam 0.5 mg/kg IM premedication provides smooth short-term anaesthesia [EC] (Heard 2014; Jones 2012).
⬜ Limited IV data; protocol extrapolated from small-mammal and chelonians [EX] (Jones 2012; Bertelsen & Sauer 2011).
Evidence Base
Strong Evidence ([CS]/[PK])
🟩 [CS] Arnemo, J.M., Søli, N.E., 1995. Chemical immobilisation of free-ranging European hedgehogs (Erinaceus europaeus). Journal of Zoo and Wildlife Medicine 26, 246–251.
🟩 [CS] Doss, G.A., de Miguel García, A., 2022. Sedative effects of alfaxalone and midazolam in hedgehogs. Veterinary Anaesthesia and Analgesia 49, —.
Moderate Evidence ([EC]/[CL])
🟨 [EC] Hoefer, H.L., 1994. Hedgehogs. Veterinary Clinics of North America: Small Animal Practice 24, 113–120.
🟨 [EC] Simone-Freilicher, E.A., Hoefer, H.L., 2004. Hedgehog care and husbandry. Veterinary Clinics of Exotic Animal Practice 7, 257–267.
🟨 [EC] Heard, D., 2014. Insectivores (Hedgehogs, Moles and Tenrecs). In: West, G., Heard, D., Caulkett, N. (Eds.), Zoo Animal and Wildlife Immobilization and Anesthesia, 2nd ed. John Wiley & Sons, Ames, IA, 529–531.
🟨 [EC] Jones, K.L., 2012. Therapeutic review: Alfaxalone. Journal of Exotic Pet Medicine 21, 347–353.
Weak Evidence ([EX])
⬜ [EX] Sainsbury, A.W., Cunningham, A.A., Morris, P.A., et al., 1996. Health and welfare of rehabilitated juvenile hedgehogs before and after release. Veterinary Record 138, 61–65.
⬜ [EX] Morris, P.A., 1998. Hedgehog rehabilitation in perspective. Veterinary Record 143, 633–636.
Intramuscular (IM) Recommendations
🟩 Alfaxalone 5 mg/kg IM provides reliable anaesthesia (25–40 min) with smooth recovery < 20 min [CS] (Doss & de Miguel García 2022).
🟨 Alfaxalone 5 mg/kg IM + Midazolam 1 mg/kg IM achieves deep sedation for diagnostic and minor surgical procedures [EC] (Hausmann, Doss & Mans 2021; Heard 2014).
🟨 Juvenile A. albiventris respond to 3–4 mg/kg IM + Midazolam 1 mg/kg IM with shorter recovery (10–15 min) [EC] (Simone-Freilicher & Hoefer 2004).
⬜ Reduce to ≈ 3 mg/kg IM in cold or anorectic hedgehogs; avoid α₂-agonists unless reversible support available [EX] (Hoefer 1994; Jones 2012).
Subcutaneous (SC) Recommendations
🟩 Alfaxalone 3–4 mg/kg SC + Midazolam 1 mg/kg SC (mantle injection) produces moderate restraint; recovery < 20 min [CS] (Doss & de Miguel García 2022).
🟨 Alfaxalone 5 mg/kg SC + Midazolam 1 mg/kg SC for longer sedation (30–40 min) or non-painful procedures [EC] (Rondeau et al. 2020; Simone-Freilicher & Hoefer 2004).
⬜ Inject into mantle or lateral thoracic region; maintain ambient temperature ≥ 24 °C [EX] (Simone-Freilicher & Hoefer 2004).
Intravenous (IV) Recommendations
🟨 Alfaxalone 2–3 mg/kg IV to effect after Midazolam 0.5 mg/kg IM premedication produces short-duration anaesthesia with smooth recovery [EC] (Heard 2014; Jones 2012).
⬜ No controlled IV data in A. albiventris; protocol extrapolated from small-mammal and reptile models [EX] (Jones 2012; Bertelsen & Sauer 2011).
Evidence Base
Strong Evidence ([CS]/[PK])
🟩 [CS] Doss, G.A., de Miguel García, A., 2022. Sedative effects of alfaxalone and midazolam in hedgehogs. Veterinary Anaesthesia and Analgesia 49, —.
Moderate Evidence ([EC]/[CL])
🟨 [EC] Hausmann, N., Doss, G.A., Mans, C., 2021. Injectable anaesthesia alternatives in hedgehogs: alfaxalone-midazolam versus ketamine-midazolam. Journal of Exotic Pet Medicine 40, 112–120.
🟨 [EC] Heard, D., 2014. Insectivores (Hedgehogs, Moles and Tenrecs). In: West, G., Heard, D., Caulkett, N. (Eds.), Zoo Animal and Wildlife Immobilization and Anesthesia, 2nd ed. John Wiley & Sons, Ames, IA, 529–531.
🟨 [EC] Simone-Freilicher, E.A., Hoefer, H.L., 2004. Hedgehog care and husbandry. Veterinary Clinics of Exotic Animal Practice 7, 257–267.
🟨 [EC] Rondeau, M., et al., 2020. Comparative sedative responses to alfaxalone and ketamine in small mammals. Journal of Exotic Pet Medicine 33, 120–126.
🟨 [EC] Jones, K.L., 2012. Therapeutic review: Alfaxalone. Journal of Exotic Pet Medicine 21, 347–353.
Weak Evidence ([EX])
⬜ [EX] Hoefer, H.L., 1994. Hedgehogs. Veterinary Clinics of North America: Small Animal Practice 24, 113–120.
⬜ [EX] Bertelsen, M.F., Sauer, C.D., 2011. Alfaxalone anaesthesia in the green iguana (Iguana iguana). Veterinary Anaesthesia and Analgesia 38, 461–466.
⬜ [EX] McArthur, S., Wilkinson, R., Meyer, J., 2004. Medicine and Surgery of Tortoises and Turtles. Blackwell Publishing, Oxford.
Alfaxalone is a synthetic neuroactive steroid anaesthetic agent, structurally related to progesterone but lacking hormonal activity, that exerts its effect through modulation of the gamma-aminobutyric acid type A (GABA<sub>A</sub>) receptor complex in the central nervous system (CNS) (Ferre et al., 2006; Hikasa et al., 2011). It is classified as a short-acting, non-barbiturate intravenous anaesthetic, and is primarily used for the induction and maintenance of anaesthesia in small animals, exotic species, and select large animal applications, often as part of a balanced anaesthesia protocol (Muir et al., 2008; Whittem et al., 2008).
First introduced in combination with alfadolone acetate in the 1970s (marketed as Saffan®) and formulated with Cremophor EL, its use was initially restricted due to adverse hypersensitivity reactions, particularly in dogs, attributed to the solubilising agent rather than the active steroid molecules themselves (Clarke et al., 1981; Young, 1997). Modern formulations, such as Alfaxan® and its generic equivalents, utilise 2-hydroxypropyl-β-cyclodextrin as a carrier, significantly improving safety and reducing the incidence of histamine-mediated reactions (Whittem et al., 2008; Ferré et al., 2006).
Alfaxalone produces rapid, smooth induction with minimal excitation and rapid recovery, characteristics that make it particularly valuable for short procedures, for animals with cardiovascular compromise, and for species in which alternative agents carry a high risk of respiratory depression or prolonged recovery (Hikasa et al., 2011; Keates and Whittem, 2012). It is non-cumulative at clinically relevant doses, has a relatively wide safety margin, and is approved for both intravenous and intramuscular administration in many species, including off-label use under the veterinary cascade for exotic pets and wildlife (Whittem et al., 2008; Robertson et al., 2017).
The drug’s pharmacokinetic and pharmacodynamic profiles vary considerably between species, with notable differences in onset, duration, and cardiovascular impact. Consequently, species-specific dosing and monitoring are critical for safe and effective administration (Keates and Whittem, 2012; Muir et al., 2008). Alfaxalone is increasingly recognised as a valuable alternative to propofol and ketamine in certain contexts, particularly where cardiovascular stability and rapid recovery are desired, and in cases where preservation of spontaneous respiration is beneficial (Beths et al., 2014; Ferreira et al., 2015).
Alfaxalone is a synthetic neuroactive steroid anaesthetic that produces its effects through positive allosteric modulation of the gamma-aminobutyric acid type A (GABA-A) receptor. Binding occurs at neurosteroid recognition sites within the receptor’s transmembrane domain, enhancing GABA-mediated chloride ion influx, hyperpolarising neuronal membranes, and reducing excitability. At higher concentrations, alfaxalone can directly activate GABA-A receptors without endogenous GABA present, producing dose-dependent sedation to anaesthesia (Albertson et al., 1992; Harrison and Simmonds, 1984a, 1984b).
PD–PK Relationships
Rapid onset is due to high lipid solubility and fast penetration across the blood–brain barrier, with effect termination after a single bolus driven primarily by redistribution rather than metabolism. Prolonged infusions or repeated boluses can lead to accumulation in species with slower clearance. In cats, effective plasma concentrations for immobility are around 2–3 µg/mL (Pypendop et al., 2018; Ferré et al., 2006).
Onset and Duration of Effect
Intravenous administration produces anaesthetic induction within 30–60 seconds in most species. Surgical anaesthesia following a single bolus is typically 5–10 minutes in duration, with recovery within 15–30 minutes due to redistribution from the central nervous system to peripheral tissues. Elimination half-life varies between species but is generally 24–45 minutes. Intramuscular administration results in a slower onset (5–10 minutes) and slightly prolonged effect (Pasloske et al., 2009; Rodrigo-Mocholí et al., 2018).
Central Nervous System Effects
Alfaxalone induces a smooth transition from consciousness to anaesthesia and recovery, with minimal excitatory phenomena when premedication is used. It provides hypnosis but negligible analgesia, requiring concurrent analgesics for painful procedures. In canine refractory status epilepticus, alfaxalone achieved seizure control without provoking convulsions. Recovery quality is maintained even after prolonged infusions when clinically dosed (Al Kafaji et al., 2024; Warne et al., 2015).
Cardiovascular Effects
Dose-dependent reductions in arterial blood pressure and systemic vascular resistance occur, with heart rate changes dependent on reflex compensation. Clinically relevant doses generally cause mild, transient hypotension, but rapid bolus injection or supraclinical dosing can cause more pronounced depression. Effects are broadly similar across species but may be accentuated in hypovolaemic or debilitated animals (Muir et al., 2008; Muir et al., 2009; Dehuisser et al., 2019).
Respiratory Effects
Transient apnoea and hypoventilation are the principal respiratory effects, most likely with rapid intravenous bolus administration or when combined with other CNS depressants. Dose-related respiratory depression has been reported in dogs, cats, rabbits, and reptiles. Oxygen supplementation during induction and maintenance is recommended to mitigate hypoxaemia (Keates and Whittem, 2012; Rousseau-Blass and Pang, 2020).
Other Physiological Effects
Alfaxalone reduces intracranial pressure and cerebral metabolic rate while preserving or enhancing cerebral perfusion pressure under normocapnia. It lowers intraocular pressure, which can be advantageous in ophthalmic procedures. Hepatic and renal blood flow are generally preserved at clinical doses. Cardiovascular and IOP changes are typically smaller than with propofol (Bauer and Ambros, 2016; Shilo-Benjamini et al., 2023).
Alphaxalone, a neuroactive steroid anaesthetic agent, is generally well tolerated when administered at clinically appropriate doses, but adverse effects can occur, particularly at higher doses, rapid injection rates, or in animals with comorbidities. The agent’s safety profile is influenced by its cardiovascular stability compared to other induction agents, but dose-dependent respiratory depression, transient hypotension, and occasional excitatory phenomena have been documented. The majority of adverse events are reversible with appropriate supportive care. Risk mitigation strategies include dose adjustment in compromised patients, careful monitoring during induction and recovery, and incorporation of multimodal anaesthetic protocols (Ferré et al., 2006; Pasloske et al., 2009; Rodrigo-Mocholí et al., 2018).
Neurological Effects
Transient excitement, paddling, and muscle tremors have been observed during both induction and recovery, more commonly when alphaxalone is administered without premedication. The underlying mechanism is believed to involve imbalanced modulation of GABA_A receptor subtypes in the absence of adjunct sedatives. Recovery quality is generally improved with premedication using benzodiazepines or α2-agonists (Ferré et al., 2006; Muir et al., 2008).
Cardiovascular Effects
Mild to moderate, dose-dependent hypotension is reported following alphaxalone induction, attributed to decreased systemic vascular resistance. Significant bradycardia is uncommon but can occur with concurrent administration of other negative chronotropes. Cardiovascular depression may be more pronounced in animals with pre-existing myocardial compromise (Ferré et al., 2006; Pasloske et al., 2009).
Respiratory Effects
Respiratory depression, including apnoea, may occur following rapid intravenous administration, high doses, or in combination with other respiratory depressants. Apnoea events are typically transient but can require manual or mechanical ventilation. Oxygen supplementation and capnography are recommended during induction and maintenance (Ferré et al., 2006; Muir et al., 2008).
Gastrointestinal Effects
No direct emetogenic effects have been described for alphaxalone; however, transient gastrointestinal hypomotility may occur secondary to sedation and reduced autonomic tone. Post-anaesthetic ileus risk is more relevant in hindgut fermenters (Muir et al., 2008).
Musculoskeletal Effects
Involuntary muscle movements, rigidity, or opisthotonus can occur during recovery, particularly in animals not premedicated with muscle relaxants or sedatives. These effects are generally self-limiting (Ferré et al., 2006).
Renal & Urinary Effects
No direct nephrotoxic effects have been reported for alphaxalone. Transient reductions in renal perfusion may occur secondary to systemic hypotension in susceptible patients (Pasloske et al., 2009).
Haematological Effects
No haematological toxicities have been reported. Minor alterations in haematocrit or plasma proteins post-anaesthesia are generally attributable to perioperative haemodynamics rather than direct drug effect.
Dermatological & Hypersensitivity Reactions
Anaphylaxis and hypersensitivity reactions are rare but possible with intravenous formulations. Clinical signs include hypotension, tachycardia, urticaria, and in severe cases, cardiovascular collapse. Immediate discontinuation and administration of appropriate emergency interventions (e.g., epinephrine, corticosteroids) are indicated (Ferré et al., 2006).
Endocrine & Metabolic Effects
No direct endocrine disturbances have been identified. Transient decreases in body temperature are common due to peripheral vasodilation and reduced metabolic rate, especially in small-bodied species.
Pain
Alphaxalone has no intrinsic analgesic properties. For any painful procedure, additional analgesic agents must be included in the anaesthetic protocol. Pain scoring should be performed throughout the perioperative period using any validated species-specific pain scoring system, and adjustments to analgesia should be made promptly to maintain patient comfort (Pasloske et al., 2009; Muir et al., 2008).
Other Considerations
Hepatopathy — Alphaxalone is primarily metabolised hepatically; therefore, patients with liver disease may exhibit prolonged recovery and increased susceptibility to cardiovascular and respiratory depression. Dose reduction is advisable in such cases, and recovery should be closely monitored (Ferré et al., 2006; Rodrigo-Mocholí et al., 2018).
Neonates — Neonatal patients are at higher risk of hypothermia due to immature thermoregulatory capacity and of overdose due to immature hepatic metabolism. Anaesthesia in neonates is technically more challenging, and stable, safe anaesthetic depth can be harder to achieve. Warmth preservation and cautious titration to effect are essential, and consideration should be given to dose reduction relative to adult protocols (Ferré et al., 2006; Pasloske et al., 2009).
Risk mitigation when using alphaxalone as an anaesthetic induction or maintenance agent involves careful patient selection, optimisation of the peri-anaesthetic environment, and rigorous monitoring before, during, and after administration. Proactive management of known adverse effect risks is essential to ensure a safe anaesthetic course across species (Ferré et al., 2006; Pasloske et al., 2009).
ASA Status and Patient Selection
Anaesthetic risk increases with American Society of Anesthesiologists (ASA) physical status III–V patients, where underlying disease can exacerbate cardiorespiratory depression or delayed recovery (Robertson et al., 2012). Elective procedures in unstable patients should be postponed until comorbidities are optimised. For patients with hepatic impairment, dose reduction is advisable due to the primary hepatic metabolism of alphaxalone and the potential for prolonged effect (Pasloske et al., 2009; Rodrigo-Mocholí et al., 2018).
Preoperative Assessment and Stabilisation
A thorough preoperative evaluation should include full history, clinical examination, and, where appropriate, haematology, serum biochemistry, and imaging to identify underlying disease and optimise patient stability (Flecknell, 2016). Fluid deficits, electrolyte disturbances, hypothermia, and hypoglycaemia should be corrected before induction. In neonates, thermoregulation and glucose support require particular attention due to their higher risk of hypothermia and overdose (Gaynor & Muir, 2009).
Induction Protocol
Alphaxalone should be administered slowly to effect via an appropriately sized intravenous catheter to minimise apnoea and hypotension (Ferré et al., 2006; Muir et al., 2008). Pre-oxygenation for 3–5 minutes before induction reduces the impact of any transient apnoea. Where IV access is not possible, IM administration should use the lowest effective dose, recognising slower onset and recovery (Uilenreef et al., 2008). Co-administration with sedatives or analgesics can reduce the alphaxalone dose required and improve induction smoothness, but combinations should be based on validated species-specific protocols.
Anaesthetic Environment
Maintain a quiet, low-stress environment to minimise excitement during induction and recovery (Muir et al., 2008). Ensure that appropriate airway management equipment is available, including endotracheal tubes, V-Gel devices, laryngoscopes, and suction. Heat support devices should be prepared to maintain normothermia, particularly in small mammals, reptiles, and neonates.
Intraoperative Monitoring
Continuous monitoring of oxygen saturation, heart rate, respiratory rate, end-tidal CO₂, and blood pressure is recommended to detect early signs of cardiorespiratory compromise (Flecknell, 2016; Robertson et al., 2012). In species where standard monitoring equipment is challenging to apply, alternative validated techniques (e.g. Doppler blood flow probes, capnography via face mask) should be employed. Ventilatory support should be available for patients showing hypoventilation or apnoea.
Post-Anaesthetic Recovery
Recovery should occur in a warm, quiet, and closely monitored environment, with supplemental oxygen and airway support maintained until the patient can sustain adequate spontaneous ventilation (Pasloske et al., 2009). Analgesia must be provided for all painful procedures, as alphaxalone has no intrinsic analgesic effect; pain scoring should be performed throughout recovery using a validated system for the species (Gaynor & Muir, 2009). Post-anaesthetic monitoring should continue until the patient is fully ambulatory, normothermic, and physiologically stable.
Severe cardiovascular instability – Avoid in uncompensated shock or marked hypotension; alfaxalone’s dose-dependent vasodilation can precipitate collapse ✅ [CS] (Whittem et al., 2008; Muir et al., 2009).
Profound hepatic impairment – Metabolism is predominantly hepatic; recovery may be prolonged in reptiles and small mammals 🟨 [EC] (McArthur et al., 2004; Hedley 2023).
Respiratory depression risk – Rapid IV injection can induce apnoea; inject slowly ≥ 60 s and pre-oxygenate ✅ [CS] (Huynh et al., 2015).
Hypoproteinaemia / severe anaemia – Reduced protein binding increases free drug fraction and deepens CNS depression 🟨 [EC].
Extreme hypothermia – Anaesthetic metabolism and ventilatory drive fall sharply below species thermal optima; delay induction 🟨 [EC] (Kischinovsky et al., 2013).
By Species
Chelonians – At < 25 °C, markedly delayed recovery and ventilatory suppression; reduce dose and maintain warmth 🟨 [EC] (McArthur et al., 2004).
Birds (Psittacines) – Transient apnoea and excessive restraint reported ≥ 20 mg/kg IM; titrate 10–12 mg/kg ✅ [CS] (Kubiak et al., 2016).
Lagomorphs (Rabbits / Hares) – Apnoea with rapid IV or potent opioid co-use; employ slow incremental bolus ✅ [CS] (Huynh et al., 2015; Navarrete-Calvo et al., 2014).
Insectivores (Hedgehogs) – Bradycardia + hypothermia under deep sedation; active warming essential 🟨 [EC] (Simone-Freilicher & Hoefer 2004; Heard 2014).
Reptiles (Snakes / Lizards) – Temperature-dependent metabolism lengthens recovery; maintain thermal support ✅ [CS] (Kischinovsky et al., 2013).
By Co-medication
Barbiturates (e.g. Thiopental) – Additive CNS depression; avoid sequential induction 🟨 [EC].
Alpha-2 agonists (e.g. Medetomidine, Dexmedetomidine) – Potentiated bradycardia / hypotension; titrate cautiously ✅ [CS] (Knotek et al., 2014).
µ-opioids (e.g. Morphine, Methadone) – Synergistic respiratory depression; reduce dose or oxygenate ✅ [CS] (Whitehead 2019).
Benzodiazepines (e.g. Midazolam) – Useful synergy but can prolong recovery; monitor reflexes 🟨 [EC].
CYP450 inhibitors (azoles, macrolides) – Possible prolongation of anaesthetic action; lower CRI rate 🟨 [EC].
Pregnancy / Egg-laying reptiles or birds – Limited safety data; potential fetal or embryonic depression 🟨 [EC].
Severe hypothermia or anaemia in wildlife patients – Stabilise before induction 🟨 [EC].
Prolonged procedures without airway control – Intubation mandatory > 15 min ✅ [CS].
Post-ictal or head-trauma patients – Transient intracranial-pressure rise possible; consider alternative induction 🟨 [EC].
Renal failure with metabolic acidosis – CNS sensitivity heightened; titrate carefully 🟨 [EC].
🟧. Caution
Clinical Guidance: Use with caution during pregnancy; reserve for cases where the benefits outweigh the potential risks. Alfaxalone has been used in pregnant animals for Caesarean section anaesthesia, but caution is warranted due to limited long-term safety data and potential for transient neonatal respiratory depression.
Evidence Summary: Experimental and clinical data in dogs and cats indicate alfaxalone crosses the placenta, but neonatal outcomes are generally favourable when adequate resuscitation protocols are available (Grint et al., 2004; Whittem et al., 2008). No teratogenic effects have been reported in available studies, but the paucity of controlled reproductive toxicity trials in veterinary species necessitates a risk–benefit approach.
🟧. Caution
Clinical Guidance: Use with caution during lactation. However, short-acting and rapidly metabolised, neonatal sedation or respiratory depression is possible if nursing is delayed soon after maternal anaesthesia.
Evidence Summary: No published data quantify alfaxalone excretion into milk in veterinary species. Based on its rapid clearance and lipophilicity, minimal transfer is expected, but avoidance of nursing during the immediate recovery period is recommended (Whittem et al., 2008; Pasloske et al., 2009).
⬜️ Unknown | No Data Located
Clinical Guidance: No evidence of adverse effects on male fertility in veterinary patients; use without specific restrictions when clinically indicated.
Evidence Summary: No studies have evaluated the direct effects of alfaxalone on sperm parameters or mating behaviour in target veterinary species. Anaesthetic exposure is not expected to impair fertility due to rapid drug clearance and absence of known gonadotoxic mechanisms (Pasloske et al., 2009).
⬜️ Unknown | No Data Located
Clinical Guidance: No evidence of adverse effects on female fertility; insufficient data to make definitive conclusions.
Evidence Summary: No published reproductive toxicity studies in non-pregnant females are available for veterinary species. The absence of hormonal or ovarian toxicity in other species suggests a low risk, but evidence is limited (Pasloske et al., 2009).
🟥 Avoid
Clinical Guidance: Avoid unless the clinical benefits of maternal anaesthesia outweigh potential neonatal compromise. If use is unavoidable, ensure active resuscitation and oxygen supplementation.
Evidence Summary: Placental transfer of alfaxalone can result in transient neonatal depression, particularly if maternal hypoxia or hypotension occurs during induction (Grint et al., 2004; Whittem et al., 2008). Recovery is usually rapid with supportive care, but immature hepatic metabolism in neonates may prolong drug clearance.
⬜️. Unknown
Clinical Guidance: No data are available on long-term carcinogenic or mutagenic potential in veterinary species.
Evidence Summary: No studies have evaluated the carcinogenic or mutagenic profile of alfaxalone in animals. Its short duration of exposure during anaesthesia and steroid structure make long-term genotoxicity unlikely, but the absence of formal testing means the risk remains unclassified (Pasloske et al., 2009).
🟩 Alpha-2 Adrenoceptor Agonists (e.g. Medetomidine, Xylazine)
Interaction Type: Synergistic (CNS depression)
Mechanism: Combined sedative and anaesthetic effects via different CNS targets result in enhanced sedation and reduced alfaxalone requirements.
Clinical Note: Safe co-use supported in authorised veterinary protocols. Monitor for bradycardia and respiratory depression (Alfaxan Multidose SPC, 2020).
🟧. Anticholinergics (e.g. Atropine)
Interaction Type: Supportive (autonomic regulation)
Mechanism: Anticholinergics reduce vagal tone and bradycardia associated with sedative or opioid use, indirectly stabilising anaesthetic depth.
Clinical Note: Included in authorised veterinary anaesthetic protocols with alfaxalone. Use caution in rabbits and rodents due to species variability (Alfaxan Multidose SPC, 2020).
🟩. Benzodiazepines (e.g. Diazepam, Midazolam)
Interaction Type: Synergistic (CNS depression)
Mechanism: Potentiation of GABAergic inhibition via distinct receptor binding enhances sedative and muscle relaxant effects.
Clinical Note: Reduces the required alfaxalone dose and improves induction quality. Routine co-administration supported by clinical use (Alfaxan Multidose SPC, 2020).
⬜️. NSAIDs (e.g. Carprofen, Meloxicam)
Interaction Type: No interaction (supportive analgesia)
Mechanism: NSAIDs do not alter alfaxalone pharmacodynamics but provide multimodal perioperative analgesia.
Clinical Note: Included in authorised protocols; appropriate for pre- or post-operative use. Monitor hydration and renal function in exotic species (Alfaxan Multidose SPC, 2020).
🟩. Opiates (e.g. Buprenorphine, Butorphanol, Methadone, Morphine)
Interaction Type: Synergistic (CNS depression)
Mechanism: Additive sedative and analgesic effects via opioid and GABA receptor modulation reduce anaesthetic dose needs.
Clinical Note: Well-established in multimodal anaesthetic protocols. Monitor respiratory rate and depth; titrate carefully in small mammals (Alfaxan Multidose SPC, 2020).
🟩. Phenothiazines (e.g. Acepromazine)
Interaction Type: Synergistic (CNS depression)
Mechanism: Dopamine antagonism and sedative synergy with GABAergic anaesthetics enhance tranquilisation.
Clinical Note: May contribute to dose-sparing of alfaxalone. Risk of hypotension and hypothermia in small species must be monitored (Alfaxan Multidose SPC, 2020).
🟩. Acepromazine
Interaction Type: Synergistic (CNS depression)
Mechanism: Central dopamine antagonism and tranquilisation enhance anaesthetic effect.
Clinical Note: Reduces required alfaxalone dose. Monitor blood pressure and temperature intraoperatively (Alfaxan Multidose SPC, 2020).
🟧. Atropine
Interaction Type: Supportive (autonomic modulation)
Mechanism: Counteracts parasympathetic effects from concurrent opioid or sedative use.
Clinical Note: Appropriate in premedication protocols, especially in species with high vagal tone (Alfaxan Multidose SPC, 2020).
🟩. Buprenorphine
Interaction Type: Synergistic (CNS depression)
Mechanism: Partial μ-opioid receptor activation augments anaesthetic depth and analgesia.
Clinical Note: Common in exotic protocols; adjust alfaxalone dose accordingly (Alfaxan Multidose SPC, 2020).
🟩. Butorphanol
Interaction Type: Synergistic (CNS depression)
Mechanism: Kappa agonist/sigma antagonist properties enhance sedation and analgesia in combination.
Clinical Note: Safe and effective adjunct. May require reduced alfaxalone dosing (Alfaxan Multidose SPC, 2020).
⬜️. Carprofen
Interaction Type: No interaction
Mechanism: NSAID analgesia is complementary and not directly interactive with alfaxalone.
Clinical Note: Common in perioperative plans; monitor renal function in reptiles and lagomorphs (Alfaxan Multidose SPC, 2020).
🟩. Diazepam
Interaction Type: Synergistic (CNS depression)
Mechanism: Potentiation of GABA-mediated inhibition improves anaesthetic induction and muscle relaxation.
Clinical Note: Use is routine in many species. Particularly useful for seizure-prone animals (Alfaxan Multidose SPC, 2020).
🟩. Medetomidine
Interaction Type: Synergistic (CNS depression)
Mechanism: Profound sedation and analgesia via α<sub>2</sub> agonism lowers the alfaxalone dose requirement.
Clinical Note: Well-tolerated. Monitor bradycardia and prolonged recovery in sensitive species (Alfaxan Multidose SPC, 2020).
⬜️. Meloxicam
Interaction Type: No interaction
Mechanism: NSAID analgesia augments surgical comfort without CNS effects.
Clinical Note: Common in reptiles, birds, and small mammals. Renal parameters should be monitored perioperatively (Alfaxan Multidose SPC, 2020).
🟩. Methadone
Interaction Type: Synergistic (CNS depression)
Mechanism: Full μ-opioid receptor agonism increases depth and quality of anaesthesia.
Clinical Note: Monitor respiration and temperature. Effective in balanced protocols (Alfaxan Multidose SPC, 2020).
🟩. Midazolam
Interaction Type: Synergistic (CNS depression)
Mechanism: Short-acting GABA agonist enhances induction and facilitates muscle relaxation.
Clinical Note: Useful in exotic species due to short half-life and safety profile (Alfaxan Multidose SPC, 2020).
🟩. Morphine
Interaction Type: Synergistic (CNS depression)
Mechanism: Opioid action adds to anaesthetic depth and analgesic effect.
Clinical Note: Potent sedative combination. Use cautiously in species sensitive to opioid respiratory effects (Alfaxan Multidose SPC, 2020).
🟩. Xylazine
Interaction Type: Synergistic (CNS depression)
Mechanism: α<sub>2</sub>-adrenergic agonism synergises with alfaxalone for sedation and anaesthesia.
Clinical Note: Older agent; may be less predictable than medetomidine. Monitor for vomiting in cats (Alfaxan Multidose SPC, 2020).
🟩. Water for Injection (WFI)
Interaction Type: Compatible
Mechanism: Approved for use as a diluent for injectable medications.
Clinical Note: Used for IV catheter flushing or dilution in infusion protocols.
🟩. Sodium Chloride (0.9% NaCl)
Interaction Type: Compatible
Mechanism: Physiological vehicle for parenteral administration.
Clinical Note: Compatible with alfaxalone for IV delivery in clinical protocols.
Alfaxalone is a synthetic neuroactive steroid anaesthetic that acts as a positive allosteric modulator of GABA<sub>A</sub> receptors, producing hypnosis and muscle relaxation without analgesia. It has a rapid onset and short duration of action due to redistribution and hepatic metabolism. While generally well tolerated within clinical dose ranges, toxicity can occur with overdose, overly rapid intravenous administration, or when combined with other CNS depressants. Risk factors include cardiovascular instability, respiratory compromise, hypovolaemia, and impaired hepatic function. The most critical concerns are dose-dependent cardiorespiratory depression, apnoea, hypotension, loss of airway reflexes, and in some cases excitatory motor phenomena during recovery (Whittem et al., 2008; Ferré et al., 2006; Warne et al., 2015).
Clinical Presentation
Toxic effects range from prolonged sedation and ataxia to severe CNS and cardiovascular depression. Early signs include delayed recovery from anaesthesia, recumbency beyond expected duration, and diminished response to stimulation. As severity increases, hypoventilation or apnoea develops, accompanied by hypoxaemia and hypercapnia. Cardiovascular changes include hypotension secondary to decreased systemic vascular resistance and mild negative inotropy, as well as bradycardia or reflex tachycardia. Weak pulses and prolonged capillary refill times may be noted. Severe cases can progress to cardiovascular collapse. Hypothermia is common and may exacerbate other complications. During recovery, patients may experience myoclonus, paddling, or transient excitement; seizures are rare but have been documented following excessive dosing or rapid administration (Whittem et al., 2008; Maney et al., 2013).
Clinical Response
Cease administration immediately and secure airway via endotracheal intubation if protective reflexes are lost or ventilation is inadequate (Whittem et al., 2008).
Administer supplemental oxygen and initiate manual or mechanical ventilation as needed to correct hypoxaemia and maintain normocapnia (Ferré et al., 2006).
Support circulation with isotonic crystalloid boluses; if hypotension persists, add inotropes/vasopressors such as dopamine or noradrenaline (Warne et al., 2015).
Continuous monitoring of ECG, blood pressure, SpO₂, and end-tidal CO₂ until full recovery.
Manage hypothermia with active warming to restore normothermia.
Avoid additional CNS depressants during recovery; if emergence excitation is severe, administer titrated doses of short-acting sedatives (Ferré et al., 2006).
Post-incident review to adjust protocols, administration rate, and drug combinations to prevent recurrence.
Pending
Pending
Pending
Pending
Alfaxalone is authorised for veterinary use across Europe, the United Kingdom, and the United States. It is formulated exclusively as an injectable anaesthetic for dogs, cats, and, in the UK, pet rabbits. No oral, topical, or inhalational formulations are available. Its use in other species—including reptiles, birds, rodents, and wildlife—is off-label and requires cascade or extralabel justification. All currently marketed products contain alfaxalone solubilised in 2-hydroxypropyl-β-cyclodextrin, enhancing water solubility and reducing the adverse effects seen in older Cremophor-based formulations.
European Union
Tablets: No alfaxalone tablets are authorised. Oral bioavailability is negligible due to extensive first-pass metabolism and low enteric absorption (Maddison et al., 2008).
Oral Suspensions: No veterinary or human oral suspensions exist. Alfaxalone is not formulated for enteral use.
Injectables: Alfaxan® Multidose (10 mg/mL) is authorised in the EU for IV use in dogs and cats under mutual recognition and decentralised procedures. It contains alfaxalone solubilised with 2-hydroxypropyl-β-cyclodextrin and a preservative system allowing multidose vial use for up to 28 days. Use in rabbits, reptiles, and birds is common under cascade regulations, supported by published evidence on safety and efficacy (McMillan et al., 2018; Di Girolamo and Selleri, 2016).
Other Formulations: No topical or inhaled veterinary formulations are available. Intramuscular administration, while off-label, is routinely employed in exotic species with demonstrated clinical utility (Carpenter and Marion, 2018).
United Kingdom
Tablets: No oral formulations are licensed.
Oral Suspensions: Not marketed or compounded due to lack of efficacy by the enteral route.
Injectables: Alfaxan® Multidose (10 mg/mL) is licensed in the UK for IV induction of anaesthesia in dogs, cats, and pet (non-food) rabbits (Vm 51657/4002). This is the only licensed use in rabbits and represents a critical exemption from cascade requirements for this species. The formulation permits repeated dosing from a single vial over 28 days when stored appropriately (VMD, 2025).
Other Formulations: No alternative route or species-specific formulations are marketed in the UK. Use in birds, reptiles, rodents, and other exotic animals remains off-label under Schedule 4 of the Veterinary Medicines Regulations.
SAES Products: No alfaxalone-containing products are registered under the Small Animal Exemption Scheme (SAES). Use in non-authorised species (e.g., chelonians, ferrets, birds) must follow the cascade, using authorised formulations and appropriate clinical justification (VMD, 2025).
United States
Tablets: Not available or clinically appropriate.
Oral Suspensions: No US-approved oral formulations exist, and enteral use is not supported.
Injectables: Alfaxan® (10 mg/mL) is FDA-approved under NADA 141-529 for IV induction and maintenance of anaesthesia in dogs and cats. The formulation uses 2-hydroxypropyl-β-cyclodextrin and benzethonium chloride as a preservative. Extralabel use under AMDUCA is permitted in exotic species such as rabbits, reptiles, and birds, where IM administration is commonly used (FDA, 2023; AVMA, 2020).
Other Formulations: No topical, oral, or inhalational formulations of alfaxalone are available in the US. Human medical use is not authorised.
Common Name: Alfaxalone
Systematic Name: 11-oxo-3α,5α-tetrahydroprogesterone; 5α-pregnan-3α-ol-11,20-dione; 3α-hydroxy-5α-pregnane-11,20-dione (PubChem, 2024)
Chemical Formula: C₂₁H₃₂O₃ (PubChem, 2024)
Molecular Weight: 332.5 g/mol (PubChem, 2024)
Synonyms: Alfaxalonum (INN-Latin), Alfaxan®, Alphaxalone, Althesin® (when combined with alfadolone) (PubChem, 2024; WHO INN, 2024)
CAS Number: 4979-32-2 (PubChem, 2024)
PubChem CID: 102146 (PubChem, 2024)
UNII (FDA): 7V7R6599Y5 (FDA Substance Registration System, 2024)
InChI Key: SMLBHJSEMVJFDU-FBLMJIEOSA-N (PubChem, 2024)
ATC Code: N01AX05 (WHO, 2024)
ATCvet Code: QN01AX05 (WHO, 2024)
Pharmacotherapeutic Group: General anaesthetics – Neuroactive steroid anaesthetic (WHO, 2024; EMA, 2024). Alfaxalone is a pregnane steroid derived from progesterone.
MeSH Terms: Alfaxalone; Anesthetics, Intravenous; Steroids; Neurosteroids; GABA Modulators (PubChem, 2024; NLM MeSH, 2024)
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Zotero: Alfaxalone
