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Tag: Halogenated ether volatile general anesthetic

Sevoflurane

Plain-language summaryIntrigue 65 / 100

Sevoflurane is the inhalational anesthetic of choice for pediatric mask induction, owing to its non-pungent character and pleasant odor that allow children to breathe down to anesthesia without IV access first. Synthesized by Ross Terrell at Travenol in 1968, brought to clinical use in Japan in 1990, FDA-approved in 1995 (Ultane). Blood-gas partition coefficient of 0.65 gives faster kinetics than isoflurane and a favorable cardiovascular profile with preserved cardiac output. Mechanism mirrors other halogenated ethers: GABA-A potentiation, K2P channel activation, glycine and NMDA modulation. The classical concern is Compound A, a degradation product formed when sevoflurane reacts with CO2 absorbents at very low fresh gas flows; nephrotoxic in rats but not demonstrated in humans within recommended flow limits. Workhorse modern volatile. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

49/100

Clinically dominant inhalational anesthetic with settled evidence but limited novelty as a research target

Look, sevoflurane is genuinely excellent at what it does. The clinical case is settled: low blood-gas partition coefficient (0.65), zero airway pungency, preserved cardiac output, and thirty-plus years of FDA-sanctioned use make it the dominant agent for pediatric mask induction and a reliable maintenance anesthetic for a reason. But “excellent clinical drug” and “compelling research target” are different things, and for a research library those distinctions matter a lot.

The mechanism story is familiar territory. GABA-A positive allosteric modulation, K2P channel activation, NMDA and glycine receptor involvement — this is the standard volatile anesthetic toolkit, shared with isoflurane, desflurane, and the rest of the halogenated ether class. There’s nothing mechanistically surprising here. The deeper question of why these compounds produce unconsciousness at a biological level remains genuinely open, and thats interesting, but sevoflurane isnt the primary probe you’d reach for to answer it. It’s achiral, well-characterized, and the CYP2E1 metabolism story (hexafluoroisopropanol, inorganic fluoride) is textbook at this point.

Where sevoflurane does generate real research traction is in anesthetic preconditioning biology. The compound confers cardiac and possibly neuroprotective preconditioning through mechanisms overlapping with ischemic preconditioning: reactive oxygen species signaling, mitochondrial K-ATP channels, PKC activation pathways. There’s a legitimate multi-center clinical literature here from cardiac surgery contexts. The Compound A nephrotoxicity story — CYP-mediated degradation in CO2 absorbents, definitively nephrotoxic in rats, not demonstrated in humans within clinical flow limits — remains a pharmacologically interesting species-specificity question that still doesnt have a clean mechanistic answer, and thats actually a genuine probe opportunity for researchers working on intrarenal CYP biology.

What we like: the evidence base is enormous by research library standards. Sevoflurane isnt guesswork. The cancer-outcomes literature — examining whether anesthetic choice during oncologic surgery affects tumor recurrence through immune modulation — is a live and contested area where sevoflurane appears in multiple ongoing trials, mostly contrasted against propofol-based TIVA. That’s a real open question with a real translational angle.

What we don’t like: for most bench programs, this is a procedural compound. It’s indispensable in animal surgery suites, but that’s utility, not novelty. Researchers aren’t designing studies to discover something new about sevoflurane — they’re using it so the animal stays still. That relationship is fundamentally different from what should sit at the top of a research library. Honest placement: strong reference compound, meaningful procedural tool, but not the kind of target that should be pulling investigator attention away from mechanisms that are actually unsettled.

Novelty

18

Mechanism promise

28

In-category differentiation

52

Evidence quality

82

Translational signal

80

Research bench value

55

Rationale Sevoflurane scores high on evidence quality and translational signal because it is a thirty-year FDA-approved clinical standard, but novelty and mechanism are both low: it shares the standard volatile anesthetic toolkit (GABA-A PAM, K2P, NMDA) with its class and brings no genuinely new biology. Differentiation credit is real but narrow, limited to its non-pungency and pediatric induction dominance within the inhalational class.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Halogenated ether volatile general anesthetic

A non-pungent fluorinated methyl isopropyl ether with a low blood-gas coefficient enabling fast induction and the dominant inhalational agent for pediatric mask induction.

Abstract

Sevoflurane (fluoromethyl 2,2,2-trifluoro-1-(trifluoromethyl)ethyl ether; CAS 28523-86-6; molecular formula C4H3F7O; molecular weight 200.05) is a fluorinated methyl isopropyl ether volatile anesthetic synthesized by Ross Terrell at Travenol Laboratories in 1968, brought to clinical use in Japan in 1990, and approved by the FDA in 1995 (Ultane, Sojourn). The minimum alveolar concentration (MAC) at age 40 is 1.8 percent in oxygen; the blood-gas partition coefficient is 0.65, faster than isoflurane (1.4) but slower than desflurane (0.42). The non-pungent character and absence of airway irritation make sevoflurane the agent of choice for inhalational induction of anesthesia, particularly in pediatric patients where intravenous access is established after induction. Mechanism parallels other halogenated ethers (GABA-A positive allosteric modulation, K2P channel activation, glycine and NMDA effects); the agent is achiral. Hepatic metabolism via CYP2E1 produces hexafluoroisopropanol and inorganic fluoride; the fluoride concentrations approach the historical nephrotoxic threshold associated with methoxyflurane (50 micromolar plasma) during prolonged exposure but published clinical data have not demonstrated nephrotoxicity in humans even with extended cases, attributed to the absence of intrarenal defluorination. The principal residual concern is degradation of sevoflurane in carbon dioxide absorbents (soda lime, Baralyme) at low fresh gas flows producing Compound A, which is nephrotoxic in rats but lacks demonstrated human renal injury within recommended fresh gas flow limits (1 to 2 L/min). Cardiovascular profile is favorable with preserved cardiac output, modest reduction in systemic vascular resistance, and minimal coronary steal physiology.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-1302Open in new tab →

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 10, 2026
Desflurane

Plain-language summaryIntrigue 65 / 100

Desflurane is the fully fluorinated successor to isoflurane and produces the fastest induction and emergence of any clinical volatile anesthetic, courtesy of the lowest blood-gas partition coefficient in the class (0.42). Approved in 1992 (Suprane). The high vapor pressure (it boils near room temperature) requires a special heated, pressurized vaporizer rather than the standard variable-bypass design. Hepatic metabolism is essentially negligible (under 0.02 percent), eliminating the fluoride and trifluoroacetylation concerns of older agents. The downsides: it irritates airways too much for inhalational induction, it triggers transient sympathetic surges with rapid concentration changes, and it has the highest global warming potential of the class (GWP100 around 2540, versus 130 for sevoflurane). Several health systems have restricted its use on environmental grounds. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

40/100

Mature clinical volatile with unmatched emergence kinetics, actively being retired for environmental reasons

Honestly, desflurane occupies a strange spot in a research library. It’s a 1992 FDA approval with the lowest blood-gas partition coefficient in the clinical volatile class, at 0.42, and that single number is genuinely the compound’s most interesting fact. Emergence times are faster than sevoflurane by a meaningful margin in long procedures, and that pharmacokinetic property has real investigational value for anyone studying recovery, post-operative cognitive dysfunction, or the kinetics of consciousness return. Those are legitimate research questions. The problem is that desflurane itself isn’t the probe you’d reach for to answer them.

The mechanism of action is the standard halogenated ether playbook: positive allosteric modulation at GABA-A, K2P channel activation, glycine receptor enhancement, NMDA modulation. Ross Terrell synthesized it at Anaquest looking for a less metabolized successor to isoflurane, and he got exactly that. Hepatic metabolism is below 0.02 percent of the absorbed dose, the lowest in the class, which was the original pharmacological appeal. But thats not a novel mechanism story. Thats a pharmacokinetic engineering win from four decades ago, and the research community extracted most of what it can from that angle a long time ago. A MAC of 6.0 percent in oxygen, the highest in the class, tells you roughly where the potency sits: real but unremarkable relative to sevoflurane’s 2.05 at similar endpoints.

The differentiation case rests almost entirely on emergence speed, and that case is eroding. Environmental restrictions are real and accelerating. The global warming potential of desflurane (GWP100 approximately 2540) is roughly 20 times that of sevoflurane and five times that of isoflurane. NHS England banned it in 2021. Major US academic health systems, including UCSF and Massachusetts General, have moved to sevoflurane-dominant protocols. When the compound is being actively removed from operating rooms, its utility as a clinical research tool contracts in parallel. You cant easily run a trial on a molecule your institution is phasing out.

Where desflurane retains genuine bench value is in controlled preclinical inhalational pharmacology work where rapid wash-in and wash-out are the specific variable under study. Rodent EEG work measuring anesthetic state signatures, or precise concentration-response experiments requiring fast kinetics, genuinely benefit from the 0.42 partition coefficient in ways sevoflurane can’t exactly replicate. The Tec 6-style heated pressurized vaporizer setup is a barrier, but for labs already equipped for inhalational work, theres a real niche here. Its just narrow.

We think the honest picture is a compound with a strong clinical track record, genuinely excellent pharmacokinetic properties for its original purpose, and almost no frontier research interest remaining. Evidence quality is high because thirty years of clinical use generates a lot of data. Novelty is essentially zero. For a bench scientist looking for compounds that illuminate new biology or address a question that cant be answered another way, desflurane isn’t where the signal is right now.

Novelty

18

Mechanism promise

20

In-category differentiation

42

Evidence quality

72

Translational signal

68

Research bench value

30

Rationale Desflurane’s pharmacokinetic edge is real and clinically documented, but the mechanism is entirely standard halogenated ether pharmacology with no novel angle, and institutional restrictions driven by a GWP100 of ~2540 are contracting its research footprint fast. High evidence quality and translational confirmation lift the score; near-zero novelty and shrinking bench utility hold it to the low forties.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Halogenated ether volatile general anesthetic

The fully fluorinated successor to isoflurane with the lowest blood-gas coefficient of any clinical volatile, enabling the fastest induction and emergence in the class.

Abstract

Desflurane (1,2,2,2-tetrafluoroethyl difluoromethyl ether; CAS 57041-67-5; molecular formula C3H2F6O; molecular weight 168.04) is a fully fluorinated methyl ethyl ether developed by Ross Terrell at Anaquest in the 1980s and approved by the FDA in 1992 (Suprane). The minimum alveolar concentration (MAC) at age 40 is 6.0 percent in oxygen, the highest of the clinical volatile anesthetics; the blood-gas partition coefficient is 0.42, the lowest in the class, producing the fastest induction and emergence kinetics among approved inhalational agents. The high vapor pressure (664 mmHg at 20 degrees Celsius, near the boiling point of 23 degrees Celsius) requires a heated, pressurized vaporizer (Tec 6 or equivalent) rather than the variable-bypass design used for isoflurane and sevoflurane. Mechanism is the standard halogenated ether profile: GABA-A positive allosteric modulation, K2P channel activation, glycine and NMDA modulation. Hepatic metabolism is minimal (less than 0.02 percent of an absorbed dose), the lowest among inhalational anesthetics, virtually eliminating fluoride-related nephrotoxicity and trifluoroacetylated hepatotoxicity. The principal clinical limitations are airway irritation that precludes inhalational induction (coughing, breath-holding, laryngospasm at concentrations above 6 percent in non-anesthetized patients) and sympathetic stimulation with rapid concentration increases producing transient tachycardia and hypertension. The high MAC and high vapor pressure make desflurane the most expensive volatile per case at typical fresh gas flows, though low-flow techniques mitigate cost. Environmental concerns about high global warming potential (GWP100 approximately 2540 versus 130 for sevoflurane and 510 for isoflurane) have driven institutional restrictions on desflurane use in several health systems.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-1303Open in new tab →

Download PDF →

FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 10, 2026
Enflurane

Plain-language summaryIntrigue 45 / 100

Enflurane is the immediate predecessor to isoflurane in Ross Terrell’s halogenated ether series, with both molecules emerging within two years of each other (1963 and 1965). It reached clinical use in 1972 as Ethrane and was widely used through the 1980s. The mechanism mirrors other volatiles, but enflurane has a peculiar quirk: at end-tidal concentrations above 2.5 percent and especially during low CO2 levels, it produces high-amplitude epileptiform activity on EEG and occasional clinical seizures during deep anesthesia. The mechanism appears to involve thalamocortical disinhibition. This contraindicates the agent in epilepsy patients and was the principal reason isoflurane (the structural isomer with similar profile but no seizure signal) displaced it. Clinical use has nearly disappeared in developed economies. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

25/100

Historically displaced volatile anesthetic with narrow SAR utility as an isoflurane comparator

Look, enflurane is a compound that exists primarily as a cautionary chapter in volatile anesthetic history. Ross Terrell synthesized it in 1963 as part of the halogenated ether SAR series at Ohio Medical Products, and it reached clinical use as Ethrane in 1972. The problem is that Terrell’s very next entry in that series, isoflurane (1965), is a structural isomer that performs essentially the same anesthetic job without the main thing that makes enflurane pharmacologically interesting in the first place.

That main thing is the epileptiform activity. At end-tidal concentrations above 2.5 percent in oxygen, particularly during hypocapnia, enflurane generates high-amplitude EEG spikes and, occasionally, clinical seizures. The proposed mechanism involves thalamocortical disinhibition at concentrations where cortical inhibition outpaces excitatory tone. Thats a genuinely interesting mechanistic question. But as a research target it’s also a decades-old question that the anesthesia community set aside when isoflurane proved equally potent and absent that signal.

The base mechanism isnt novel. GABA-A potentiation, K2P channel opening, glycine receptor modulation, NMDA inhibition. That’s the same pharmacological fingerprint as halothane, isoflurane, sevoflurane, and desflurane. Enflurane doesn’t add a new target or an interesting new pharmacological angle; it adds a liability profile that was considered serious enough to justify switching agents at scale. MAC is well-established at 1.68 percent (age 40, oxygen), blood-gas partition coefficient sits at 1.9, hepatic metabolism runs 2 to 5 percent with fluoride generation that raised nephrotoxicity concerns during prolonged exposures. All of this is characterized. None of it is under active investigation because there’s no clinical reason to keep studying it.

Evidence quality gets modest credit because the 1970s and 1980s clinical literature is real, multi-center, and well-documented. But there’s no ongoing phase program, no novel indication with signal, and the translational arrow points firmly at a product that developed economies have already phased out.

What bench utility enflurane retains is narrow and specific: if you’re investigating why thalamocortical circuits go epileptiform under volatile anesthetic exposure, enflurane is the comparator that produces the effect isoflurane avoids. That’s legitimate probe value for a small group of investigators. We wouldn’t prioritize it for a library meant to surface interesting research targets. It’s best understood as isoflurane’s foil, useful precisely for what it does wrong, and with no independent research trajectory worth following in 2025.

Novelty

12

Mechanism promise

22

In-category differentiation

15

Evidence quality

55

Translational signal

25

Research bench value

35

Rationale Enflurane scores low on novelty and differentiation because it was superseded by its own structural isomer for the same clinical application, and its base mechanism (GABA-A, K2P, NMDA, glycine) is shared across the entire halogenated ether class. Evidence quality lifts the raw score slightly given real clinical data from the 1970s-80s, but there is no active development and the translational signal is essentially frozen in a discontinued product.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Halogenated ether volatile general anesthetic

The immediate predecessor to isoflurane in the Terrell ether series, marketed as Ethrane, displaced by isoflurane owing to electroencephalographic seizure activity at high concentrations.

Abstract

Enflurane (2-chloro-1,1,2-trifluoroethyl difluoromethyl ether; CAS 13838-16-9; molecular formula C3H2ClF5O; molecular weight 184.49) is a halogenated methyl ethyl ether developed by Ross Terrell at Ohio Medical Products in the structure-activity series that produced both enflurane (1963) and its structural isomer isoflurane (1965). Enflurane reached clinical use in 1972 (Ethrane) and was widely used through the 1980s before isoflurane displaced it. The minimum alveolar concentration (MAC) at age 40 is 1.68 percent in oxygen; the blood-gas partition coefficient is 1.9, intermediate between halothane and isoflurane. Mechanism parallels other volatile anesthetics (GABA-A, K2P, glycine, NMDA modulation). The principal clinical limitation is dose-dependent generation of high-amplitude epileptiform activity on electroencephalography, particularly at end-tidal concentrations above 2.5 percent and during hypocapnia, with occasional clinical seizures during deep anesthesia. The mechanism of enflurane epileptogenesis is incompletely characterized but appears to involve thalamocortical disinhibition at concentrations where cortical inhibition exceeds cortical excitatory tone. This electrophysiological profile contraindicates enflurane in patients with seizure disorders and contributed substantially to its displacement by isoflurane, the structural isomer with similar clinical profile but absent the epileptiform signal. Hepatic metabolism is approximately 2 to 5 percent (intermediate between halothane and isoflurane); fluoride generation is sufficient to raise plasma concentrations into the historically nephrotoxic range during very prolonged exposures. Cardiovascular effects include modest myocardial depression and dose-dependent vasodilation. Clinical use of enflurane has nearly disappeared in developed economies; it remains available as a research tool for halogenated ether structure-activity studies.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-1305Open in new tab →

Download PDF →

FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 10, 2026
Isoflurane

Plain-language summaryIntrigue 60 / 100

Isoflurane is a halogenated ether volatile anesthetic introduced in 1981 and the dominant inhalational agent of the 1990s before sevoflurane and desflurane displaced it. Its blood-gas partition coefficient sits in the middle of the class, giving moderately fast induction and emergence, slower than the modern agents but much faster than the old halothane. Mechanism is multifactorial and incompletely worked out: positive modulation of GABA-A receptors at sites distinct from benzodiazepine and barbiturate sites, activation of two-pore potassium channels, glycine receptor potentiation, and NMDA inhibition. Cardiovascular effects include dose-dependent vasodilation with preserved cardiac output. Hepatic metabolism is only 0.2 percent (versus 20 percent for halothane), so immune-mediated hepatitis is rare. Still widely used in veterinary anesthesia and lower-resource clinical settings where cost favors it over the newer agents. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundResearch workhorse

43/100

Clinically displaced 1981 volatile anesthetic still earning its keep as a rodent research tool

Look, isoflurane had its moment. Introduced in 1981, it was the workhorse of the operating room through the 1990s, and for good reason. The blood-gas partition coefficient of 1.4 put it meaningfully ahead of halothane for emergence speed, the cardiovascular profile was clinically manageable, and the hepatotoxicity story was dramatically cleaner than halothane (0.2% trifluoroacetylated metabolism versus 20%). In its day, this was genuinely important pharmacology, and the clinical literature reflects that. Decades of use, large patient populations, well-characterized physiology. You’re not going to find better evidence for anything in this library.

The mechanism is still partly unresolved, which is actually the most interesting thing about it from a research standpoint. Isoflurane hits GABA-A at allosteric sites distinct from the benzo and barbiturate pockets, activates TREK-1 and TASK two-pore domain potassium channels, potentiates glycine receptors, and suppresses NMDA glutamate currents at clinically relevant partial pressures. That’s a four-target pharmacology profile that took decades to work out. The problem is that sevoflurane and desflurane share most of this mechanistic territory, so isoflurane doesn’t serve as a clean dissection tool. You cant use it to isolate the TREK-1 contribution in a way that’s specific to isoflurane alone.

Clinically, its been almost fully displaced in modern ORs. Sevoflurane is less pungent, non-irritating for mask induction, and offers faster emergence. Desflurane is faster still. Isoflurane survives in veterinary practice and lower-resource settings where cost per mL matters, and those arent trivial niches. But in serious human clinical research, its no longer a competitive agent. Thats not a knock on the chemistry; its just where the class went over thirty years.

Where isoflurane does show up in the current literature is in rodent basic science as a standard anesthetic, and in the ischemic preconditioning space. Multiple groups have replicated preclinical data showing that brief repeated exposures activate protective pathways ahead of a subsequent ischemic insult, in both cardiac and neural models. The human translational picture is murkier. There’s also an active, contested debate about neonatal neurotoxicity in animal models and what it means for human infants. Both are real research questions, but neither defines isoflurane as an exciting frontier compound.

For bench investigators, its core value is as a practical rodent anesthetic with well-established animal dosing and wide availability. It’s a means to an end, not the object of study itself. We score it 43. The evidence base is strong, the bench utility is real, but the novelty and differentiation just aren’t there. If you’re studying volatile anesthetic mechanisms specifically, sevoflurane’s cleaner pharmacokinetic profile probably makes it the better probe in 2024.

Novelty

18

Mechanism promise

35

In-category differentiation

22

Evidence quality

75

Translational signal

68

Research bench value

62

Rationale Isoflurane’s multi-target mechanism (GABA-A, TREK-1/TASK, glycine, NMDA) is genuinely interesting but shared with sevoflurane and desflurane, removing its value as a specific probe; massive clinical evidence and real bench utility for rodent anesthesia pull the score up, but near-zero novelty and weak differentiation keep it squarely in workhorse territory at 43.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Halogenated ether volatile general anesthetic

A halogenated methyl ethyl ether introduced in 1981 that remained the dominant inhalational anesthetic of the 1990s before sevoflurane and desflurane displaced it.

Abstract

Isoflurane (1-chloro-2,2,2-trifluoroethyl difluoromethyl ether; CAS 26675-46-7; molecular formula C3H2ClF5O; molecular weight 184.49) is a halogenated methyl ethyl ether volatile anesthetic introduced clinically by Ohio Medical Products in 1981. The minimum alveolar concentration (MAC) at 40 years of age is 1.15 percent in oxygen and 0.5 percent in 70 percent nitrous oxide. The blood-gas partition coefficient is 1.4, intermediate between halothane (2.4) and the modern agents desflurane (0.42) and sevoflurane (0.65); this corresponds to moderately fast induction and emergence relative to halothane but substantially slower than desflurane. Mechanism is multifactorial and incompletely characterized: principal targets include positive allosteric modulation of GABA-A receptors at sites distinct from benzodiazepine and barbiturate sites, two-pore domain potassium channel (TREK-1, TASK) activation, glycine receptor potentiation, and inhibition of NMDA glutamate currents at clinically relevant partial pressures. Cardiovascular effects include dose-dependent reduction in systemic vascular resistance and modest negative inotropy with preserved cardiac output through reflex tachycardia; coronary vasodilation has been studied for steal physiology but the clinical significance is limited. Respiratory effects include dose-dependent depression of tidal volume with compensatory tachypnea. Hepatotoxicity through trifluoroacetylated protein adduct formation occurs in 0.2 percent of metabolism (versus 20 percent for halothane) and the clinical incidence of immune-mediated hepatitis is correspondingly low. Used widely in veterinary anesthesia and in lower-resource settings where acquisition cost favors isoflurane over the newer agents.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-1301Open in new tab →

Download PDF →

FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 10, 2026

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