Acetylfentanyl

# Research Output: Acetylfentanyl

## Chemical Identity

**PubChem CID:** 527015 (api_verified via PubChem lookup)

**IUPAC name:** N-phenyl-N-[1-(2-phenylethyl)piperidin-4-yl]acetamide — confirmed by PubChem, matches the systematic name in the seed brief.

**Molecular formula:** C₂₁H₂₆N₂O — NOT in seed brief; confirmed via PubChem [Ref 1 is implicit PubChem, see registry].

**Molecular weight:** 322.4 g/mol — NOT in seed brief; confirmed via PubChem.

**InChIKey:** FYIUUQUPOKIKNI-UHFFFAOYSA-N — NOT in seed brief; confirmed via PubChem.

**CAS number:** 3258-84-2 (from Cayman Chemical reference; not directly API-verified — FLAG for confirmation).

**SMILES:** PubChem API did not return SMILES in the summary response. Should be retrieved separately from PubChem CID 527015 for the database record. Known structure: N-acetyl, N-phenyl, 1-(2-phenylethyl)piperidine-4-amine backbone — acetyl group replaces propionyl group from fentanyl.

**Stereochemistry:** No chiral centers in the acetylfentanyl molecule; no enantiomers or diastereomers to distinguish. The compound is achiral.

**Physical properties:** No published data found for melting point, aqueous solubility, or log P specific to acetylfentanyl from peer-reviewed sources. The DEA drug chemistry information sheet (PDF, not extractable) is the primary DEA source for these parameters.

**Discrepancies with seed data:** The seed brief had SMILES, molecular formula, molecular weight, InChIKey, and PubChem CID all as empty fields. PubChem lookup confirms CID 527015 and populates formula (C₂₁H₂₆N₂O), weight (322.4), and InChIKey. These should be added to the database record.

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## Pharmacology

### Mechanism of Action

Acetylfentanyl is a full agonist at the mu-opioid receptor (MOR), the primary molecular target responsible for its analgesic, euphoric, and respiratory depressant effects (Zawilska 2017 [Ref 20]; Prekupec et al. 2017 [Ref 23]). There is no published evidence of clinically significant activity at kappa or delta opioid receptors, though the class structurally permits weak activity at both.

### Receptor Binding / Agonist Activity

Published cell-based assay data (Kanamori et al. 2021 [Ref 4]) establishes the following rank order of MOR agonistic activity among fentanyl analogs: **fentanyl > isobutyrylfentanyl ≈ butyrylfentanyl ≈ methoxyacetylfentanyl > acetylfentanyl**. A follow-up study (Kanamori et al. 2022 [Ref 3]) confirmed this ranking extended to metabolites. No published Ki values (binding affinity constants) for acetylfentanyl at MOR, KOR, or DOR could be identified through PubMed or OpenAlex searches.

**⚠️ FLAG:** No confirmed Ki or EC50 values for acetylfentanyl at MOR are available in peer-reviewed literature. The potency data below derives from in vivo animal studies.

### In Vivo Potency (Animal Data)

From DEA drug chemistry documentation and regulatory summary data (web-retrieved, not directly extracted):
- **ED50:** 0.021 mg/kg (mice, analgesic assay)
- **LD50:** 9.3 mg/kg (mice)
- **Potency relative to morphine:** ~15–16× more potent (analgesic assay, mice)
- **Potency relative to fentanyl:** ~30% of fentanyl's potency (~1/3)
- **Therapeutic index:** The LD50/ED50 ratio is approximately 443 (mice), but this ratio is **23× narrower than that of fentanyl**, and **10× narrower than morphine**, making acetylfentanyl exceptionally dangerous (Takase et al. 2016 [Ref 14]; Schueler 2017 [Ref 13])

A structure-activity relationship study in mice (Varshneya et al. 2023 [Ref 2]) demonstrated that across the N-acyl chain length series (acetylfentanyl → fentanyl → butyrylfentanyl → valerylfentanyl), the rank order of potencies for **respiratory depression (hypoventilation)** differs from the rank order for antinociception. Acetylfentanyl is among the lower-potency members for hypoventilation in this series compared to fentanyl, but is still sufficiently potent to cause fatal respiratory depression at low doses.

⚠️ **FLAG:** All potency data above are from **animal studies (mice)**. No published controlled human pharmacological studies on acetylfentanyl potency exist.

### Pharmacokinetics

No published human pharmacokinetic studies for acetylfentanyl were identified. The following is inferred from the fentanyl class and available forensic/metabolism data:

- **Lipophilicity:** High (class property of anilidopiperidines); enables rapid CNS penetration
- **Distribution:** Significant brain accumulation — postmortem studies show brain concentrations higher than blood or vitreous humor (Chesser et al. 2019 [Ref 10])
- **Onset by insufflation:** 7–10 minutes (seed data; no published verification found — FLAG for editorial review)
- **Onset by sublingual:** 20–40 minutes (seed data; no published verification found — FLAG for editorial review)
- **Duration:** 1–4 hours (seed data; no published verification found)
- **Protein binding:** No published data specific to acetylfentanyl

### Metabolism

A liver-humanized mouse study (Kanamori et al. 2018 [Ref 24]) directly characterized acetylfentanyl metabolism using PXB-cells (hepatocytes from humanized mouse), providing the most species-relevant in vitro data available. The general metabolic pathway reviewed by Wilde et al. (2019 [Ref 19]) for new fentanyl analogs applies:

- **Phase I reactions:**
  - Hydrolysis of the acetamide bond → 4-ANPP (4-anilino-N-phenethylpiperidine), a major metabolite and scheduled precursor
  - N-dealkylation → nor-acetylfentanyl (desalkyl metabolite)
  - Hydroxylation at the piperidine ring and phenyl rings
  - Further oxidation of hydroxylated metabolites
- **Phase II reactions:**
  - Glucuronide conjugation
  - Sulfate conjugation

The metabolite **4-ANPP** is itself a DEA-controlled substance and a known precursor to illicit fentanyl synthesis. Its presence in urine can confirm acetylfentanyl exposure (Concheiro et al. 2018 [Ref 22]).

**CYP enzymes:** No acetylfentanyl-specific CYP enzyme involvement data found in published literature. Fentanyl is primarily metabolized by CYP3A4; by structural analogy and class inference, acetylfentanyl is expected to undergo CYP3A4-mediated N-dealkylation. ⚠️ **FLAG:** This is structural analogy — not acetylfentanyl-specific data.

### Stability in Biological Specimens

Acetylfentanyl is stable in blood for up to 9 months under refrigerated (4°C) and room-temperature conditions (Palmquist & Swortwood 2021 [Ref 7]). Unlike acryloylfentanyl (which degrades rapidly), acetylfentanyl is analytically stable for forensic purposes. Frozen samples with limited freeze-thaw cycles are preferred for long-term storage.

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## History

### Original Synthesis

Acetylfentanyl was first synthesized in the late 1960s by **Janssen and Gardocki**, as part of structure-activity investigations into fentanyl analogs. The compound represents the simplest N-acyl homolog of fentanyl, replacing the propionyl group of fentanyl with an acetyl group (Jannetto et al. 2019 [Ref 21]; Schueler 2017 [Ref 13]). It was never developed for clinical use, has no approved medical indication, and was not commercially available until it appeared on clandestine markets approximately four decades after its synthesis.

### Illicit Market Emergence

Acetylfentanyl first appeared on the illicit drug market approximately in **2012–2013**, initially sold online as a "research chemical." It was manufactured predominantly in China and distributed via darknet and internet vendors (Schueler 2017 [Ref 13]; Jannetto et al. 2019 [Ref 21]).

**First documented US outbreak:** March–May 2013, Rhode Island, USA — **14 overdose deaths** attributable to acetylfentanyl (Lozier et al. 2015 [Ref 17]). This was the first major public health report on acetylfentanyl in the United States and precipitated the DEA emergency scheduling response. By 2014, acetylfentanyl was being detected in heroin supplies across multiple US states (O'Donnell et al. 2017 [Ref 11]).

**European emergence:** The EMCDDA-Europol Joint Report (2016 [Ref 31]) documented 32 acetylfentanyl fatalities in four EU member states between 2013 and August 2015: Sweden (27), Germany (2), Poland (1), and the United Kingdom (2). Sweden bore the largest burden, likely due to its established market for research chemicals and fentanyl analogs.

**Canada:** A 3 kg law enforcement seizure of acetylfentanyl occurred in Canada in 2013, one of the earliest recorded seizures globally (Zawilska 2017 [Ref 20]).

**Japan and Australia:** Acetylfentanyl was also identified on illicit markets in Japan and Australia, with cases appearing from approximately 2014–2015 onward (Wilde et al. 2019 [Ref 19]).

### Market Evolution

By 2016–2017, acetylfentanyl's role in the US drug supply had shifted. While earlier cases (2015–2016 Detroit cohort) showed acetylfentanyl as the primary or co-primary drug with mean blood concentration of 8.9 ng/mL, later cases (2016–2017) showed it predominantly as a minor component alongside fentanyl, with mean concentration of only 0.9 ng/mL (Avedschmidt et al. 2019 [Ref 15]). This shift suggests acetylfentanyl increasingly appeared as a manufacturing artifact or contaminant of illicit fentanyl production rather than as an intentionally distributed standalone product. The compound "can be readily converted into fentanyl and is frequently detected as an impurity from illicit manufacturing of fentanyl" (Schueler 2017 [Ref 13]).

By 2017, Prekupec et al. (2017 [Ref 23]) documented **52 confirmed acetylfentanyl deaths** in the United States since 2013.

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## Subjective Effects

**No controlled human studies on the subjective effects of acetylfentanyl have been published.** The DEA explicitly noted that "clinical studies evaluating pharmacological effects of acetylfentanyl in humans have not been reported in the scientific literature."

Subjective effects described below are inferred from:
1. Animal pharmacology (MOR full agonism)
2. Forensic case descriptions
3. Class-level effects of fentanyl-type opioids
4. User reports cited in pharmacology literature (indirect)

### Opioid Toxidrome / Clinical Presentation

The classic opioid toxidrome, consistent across all case reports involving acetylfentanyl, includes (Müller et al. 2019 [Ref 33]; Prekupec et al. 2017 [Ref 23]):
- Loss of consciousness / deep sedation
- Bradypnea (slow breathing) / hypoventilation
- Hypercapnia (elevated CO₂)
- Arterial hypotension
- **Miosis** (pupil constriction) — hallmark opioid sign
- Respiratory arrest in fatal cases

### Expected Subjective Effects by Effect Class

Based on MOR full agonism and fentanyl class analogy (all labeled as class inference, not acetylfentanyl-specific data):

**Body:** Sedation (prominent), pain suppression/analgesia, respiratory depression, pupil constriction, constipation, dry mouth, nausea/vomiting, muscle relaxation, tactile euphoria, spontaneous body sensations, appetite suppression, dehydration sensation, increased urination (diuretic effect of some opioids)

**Feeling:** Euphoria (prominent with sufficient dose), anxiety suppression, emotional suppression

**Thinking:** Cognitive euphoria, cognitive impairment at higher doses, compulsive redosing urge

**Perception:** Double vision at high doses, dreaming enhancement during sedation

**Self:** Disinhibition, compulsive redosing urge, craving with repeated use, depersonalization at high doses

**Awareness:** Reality testing impairment, sexual arousal suppression

The Takase et al. (2016 [Ref 14]) autopsy case described the user as "snoring loudly for at least 12 hours prior to death," indicating profound sedation consistent with the opioid class.

### Dose Data (Seed Data — Unverified)

The seed database contains dose data for two ROAs:
- **Sublingual:** Threshold 2 mg; Light 5–10 mg; Common 10–15 mg; Strong 15–20 mg
- **Insufflated:** Threshold 2 mg; Light 5–10 mg; Common 10–15 mg; Strong 15–20 mg

⚠️ **FLAG:** These dose values could not be confirmed against published pharmacological studies. No peer-reviewed dose-finding or clinical studies exist. The values are consistent with acetylfentanyl's approximately 15–16× potency vs. morphine and 1/3 potency vs. fentanyl, and are broadly plausible relative to reported fatal blood concentrations. However, they remain based on community consensus rather than controlled research data. Given the extremely narrow therapeutic index (LD50/ED50 ratio 23× narrower than fentanyl), these dose values carry significant safety implications and should be treated with caution.

---

## Safety & Toxicity

### Acute Toxicity

**Overall:** High acute toxicity. Acetylfentanyl has a **narrow therapeutic index** and a small margin between effective and lethal doses, described as critical in the first insufflation fatality case (Takase et al. 2016 [Ref 14]).

**Animal LD50:** 9.3 mg/kg (mice, i.p.) — web-retrieved from DEA source; not directly API-verified.

**Fatal human blood concentrations** (from case reports):
- **Single-agent fatalities:** ~250–270 ng/mL peripheral blood (McIntyre et al. 2015 [Ref 16]; Takase et al. 2016 [Ref 14])
- **Polysubstance fatalities:** Wide range — 0.13 to 2100 ng/mL (Dwyer et al. 2017 [Ref 12]; Fagiola et al. 2019 [Ref 9])
- **Pennsylvania series (n=41):** Median 11 ng/mL; mean 169.3 ng/mL; 96% involved multiple drugs (Dwyer et al. 2017 [Ref 12])
- **Detroit series (2016-2017):** Mean 0.9 ng/mL (lower due to co-present fentanyl as primary agent)
- **Impaired driving (alive):** 1.0–9.2 ng/mL (Kiely & Juhascik 2021 [Ref 6])

The extreme variability in fatal concentrations (0.13 to 2100 ng/mL) reflects the dominant role of co-intoxicants, individual opioid tolerance, and postmortem redistribution (Concheiro et al. 2018 [Ref 22]).

### Cause of Death

Primary mechanism of death in all documented fatalities: **respiratory depression leading to respiratory arrest and hypoxic death**. Multiple case series confirmed that acetylfentanyl, like all fentanyl analogs, causes fatal respiratory failure as the endpoint (Lozier et al. 2015 [Ref 17]; O'Donnell et al. 2017 [Ref 11]; Dwyer et al. 2017 [Ref 12]).

### Postmortem Distribution

Brain exhibits highest concentrations among postmortem matrices, followed by blood and vitreous humor (Chesser et al. 2019 [Ref 10]). This is consistent with high lipophilicity and preferential CNS accumulation. Postmortem redistribution from central to peripheral blood compartments is documented (Concheiro et al. 2018 [Ref 22]).

### Skin Exposure Risk

The seed brief notes: "unintentionally spilling a very small amount of acetylfentanyl on one's skin could result in a fatal overdose." This claim is consistent with fentanyl class properties and DEA statements, but no peer-reviewed case reports of fatal or near-fatal dermal acetylfentanyl absorption were identified. ⚠️ **FLAG:** Safety-critical claim based on class inference and DEA regulatory statements, not peer-reviewed acetylfentanyl-specific evidence.

### Chronic Toxicity

No published data on chronic organ toxicity specific to acetylfentanyl. Based on opioid class: chronic use expected to produce opioid-associated effects including immune suppression, hormonal dysregulation (HPA axis), and constipation-related gastrointestinal complications.

---

## Harm Reduction

### Naloxone Reversal

Acetylfentanyl overdose responds to naloxone (opioid antagonist) reversal, as documented in case reports and confirmed by its MOR-mediated mechanism (Takase et al. 2016 [Ref 14]; Prekupec et al. 2017 [Ref 23]).

**Dosing consideration:** Due to the high potency of synthetic opioids, Prekupec et al. (2017 [Ref 23]) recommend **starting with 2 mg naloxone** rather than the standard 0.4 mg initial dose. Multiple doses may be required. In the Takase insufflation fatality, the treating physicians noted that "transport to a hospital during this time and treatment with naloxone may have saved his life" — the patient had been "snoring loudly for at least 12 hours" prior to death.

### Fentanyl Test Strips

Commercial fentanyl immunoassay test strips (BTNX Rapid Response and others) show **high cross-reactivity with acetylfentanyl**, making them suitable for harm reduction screening of drug supplies for acetylfentanyl contamination (Rodriguez-Cruz 2023 [Ref 27]). However, these strips may not detect carfentanil at dangerous concentrations — users should be aware that a negative test does not guarantee absence of all dangerous opioids.

### Adulteration Risk

The major harm-reduction challenge with acetylfentanyl is that users frequently receive it **without knowledge** — it is mixed into heroin or sold as heroin (Stevens et al. 2021 [Ref 8]; Dwyer et al. 2017 [Ref 12]). The compound can be a byproduct of illicit fentanyl manufacture, appearing as a contaminant even when fentanyl is the intended product.

### Emergency Response

Standard opioid overdose response applies: call emergency services immediately, administer naloxone (2 mg recommended for synthetic opioid suspected), rescue breathing if not breathing, place in recovery position if unconscious but breathing, do not leave alone.

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## Tolerance & Dependence

### Tolerance

Develops with repeated use, consistent with mu-opioid receptor mechanisms (downregulation, desensitization). Seed data states: buildup with prolonged and repeated use; tolerance half-life approximately 5 days; full reset ~1.5 weeks. Cross-tolerance occurs with all opioids acting via MOR. ⚠️ **FLAG:** These specific tolerance timeline values (5-day half-life, 1.5-week reset) are not verified against published acetylfentanyl-specific data — they appear to be class-level estimates based on opioid pharmacology.

### Dependence

Classified as **extremely addictive with high potential for abuse** (seed data). The reinforcing effects study (Maitland et al. 2024 [Ref 1]) specifically investigated fentanyl analogs including acetylfentanyl in the context of illicit drug market substances, examining reinforcing properties. No animal or human self-administration studies specific to acetylfentanyl were identified via PubMed searches.

Physical dependence expected to develop with repeated use, with an opioid withdrawal syndrome upon cessation. Withdrawal characteristics would mirror opioid withdrawal class effects.

### Abuse Liability

Acetylfentanyl was placed in DEA Schedule I partly because of its **high potential for abuse** with no accepted medical use (Federal Register 2017 [Ref 29]).

---

## Interactions

The following drug interactions are documented or highly probable based on mechanism (CNS/respiratory depression synergy):

### Life-Threatening (Seed Data: Lethal)

- **Alcohol:** Synergistic CNS and respiratory depression. Documented in multiple polysubstance overdose deaths (Dwyer et al. 2017 [Ref 12]).
- **GHB/GBL:** Synergistic CNS depression. High-risk combination; both cause respiratory depression via different mechanisms (GABA_B for GHB/GBL, MOR for acetylfentanyl).
- **Ketamine:** Co-administration in overdose cases reported (Müller et al. 2019 [Ref 33]). Synergistic respiratory depression and loss of protective airway reflexes.
- **Tramadol:** Synergistic MOR agonism (tramadol is also a weak MOR agonist) plus serotonin reuptake inhibition. High-risk combination.

### Case-Documented Interactions

- **Benzodiazepines (alprazolam):** Alprazolam co-present in the Fagiola et al. (2019 [Ref 9]) case at toxic concentration (64.9 μg/L) alongside acetylfentanyl (32.9 μg/L) and fentanyl — combined CNS and respiratory depression. The combination was attributed as the cause of death.

### Interaction Severity Notes

⚠️ **FLAG:** The seed brief lists the following as **"unknown"** severity: Nitrous oxide, PCP. These carry mechanistic risk (nitrous: CNS depressant; PCP: dissociative/NMDA antagonist with CNS depressant potential at high doses) but no acetylfentanyl-specific combination data were identified in the literature.

### CYP Interactions

No published acetylfentanyl-specific CYP inhibition or induction data found. Structural analogy to fentanyl suggests potential interaction with CYP3A4 inhibitors (e.g., ketoconazole, erythromycin, grapefruit) which could increase acetylfentanyl plasma levels and respiratory depression risk. ⚠️ **FLAG:** Class analogy inference only.

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## Legal Status

### United States
- **Current status:** Schedule I, Controlled Substances Act (DEA)
- **Temporary placement:** Effective July 17, 2015 (Federal Register 2015 [Ref 30])
- **Permanent placement:** Final order effective June 7, 2017 (Federal Register 2017 [Ref 29]; PMID 28591974)
- **Rationale:** Required under US obligations to the 1961 Single Convention on Narcotic Drugs; no accepted medical use; high abuse potential; documented fatalities (≥57 confirmed US deaths at time of permanent scheduling)
- **Analog Act:** Prior to 2015 temporary scheduling, potentially subject to Federal Analogue Act as substantially similar to fentanyl

### Canada
- **Current status:** Controlled under CDSA Schedule I, item 16 (fentanyl and analogue provision)
- Acetylfentanyl is not explicitly named but is captured under the **structural analogue provision** for fentanyl derivatives (Health Canada 2024 [Ref 32])
- 3 kg seizure in 2013 preceded scheduling

### United Kingdom
- **Current status:** Uncertain from available sources. The UK Government controlled drugs list does not explicitly name acetylfentanyl (confirmed via GOV.UK list lookup). However, acetylfentanyl would be covered by:
  1. The **Psychoactive Substances Act 2016** (blanket prohibition on novel psychoactive substances)
  2. Potentially by fentanyl analog scheduling provisions under the Misuse of Drugs Act 1971 if UK has enacted a generic fentanyl analog order
- 2 deaths documented in UK by August 2015 (EMCDDA 2016 [Ref 31])
- ⚠️ **FLAG:** UK classification requires direct verification against current Misuse of Drugs Act schedules

### European Union
- Multiple EU member states scheduled acetylfentanyl following the EMCDDA-Europol joint risk assessment (September 2015) and joint report publication (June 2016) [Ref 31]
- Sweden, Germany, Poland all had documented fatalities and implemented controls
- Under EU Council Decision 2005/387/JHA framework, EU members can be required to subject new psychoactive substances to control measures

### Australia
- **Current status:** Expected to be Schedule 9 (Prohibited Substance) under the Poisons Standard (SUSMP) based on class membership and documented illicit use, but explicit confirmation from the Office of Drug Control database was not retrievable during research. ⚠️ **FLAG:** Requires direct verification against ODC controlled substances list.

### Japan
- Documented fatalities and illicit market detections (Takase et al. 2016 [Ref 14]); scheduled under Japanese narcotics law. Specific scheduling date not confirmed.

---

## Clinical Trials

**No registered clinical trials for acetylfentanyl found on ClinicalTrials.gov** (search returned 0 results). This is consistent with acetylfentanyl's Schedule I status and complete absence of any approved medical or veterinary use globally.

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## Community Feedback Analysis

**No community feedback submitted.** Part A2 of the brief was empty. Standard research directives followed.

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## Gaps & Flags

### Data Gaps
1. **No Ki/EC50 values** for acetylfentanyl at mu-opioid receptor (or any receptor) available in peer-reviewed literature. All pharmacological potency data derives from in vivo animal studies.
2. **No human pharmacokinetic studies** published for acetylfentanyl. Half-life, bioavailability, Tmax, and volume of distribution are all extrapolated from fentanyl class data.
3. **No controlled human studies** on subjective effects, dose-response, or psychoactive properties exist.
4. **SMILES string** was not returned by PubChem API call; should be separately retrieved from PubChem CID 527015.
5. **Melting point, solubility, and log P** data not identified from published sources.
6. **No acetylfentanyl-specific CYP enzyme data** — CYP3A4 involvement is class inference only.
7. **Tolerance timelines** (5-day half-life, 1.5-week reset) in seed data are not verified against published acetylfentanyl-specific literature.
8. **ED50/LD50 values** cited from web-retrieved DEA source — not directly extractable from the PDF; should be considered provisional until the DEA document is confirmed.

### Safety-Critical Flags
9. **Dose ranges** (threshold 2 mg; light 5–10 mg; common 10–15 mg; strong 15–20 mg for both ROAs) are **not verified against published pharmacological data**. With a therapeutic index 23× narrower than fentanyl, these values carry extreme safety implications. They appear plausible given the ~15–16× potency vs. morphine, but any dose data requires explicit editorial review before publishing.
10. **Skin absorption fatal risk** claim in seed data (toxicity notes) is consistent with fentanyl class properties but not confirmed by acetylfentanyl-specific peer-reviewed case reports.
11. **Interaction severities** for Nitrous oxide and PCP listed as "unknown" in seed data — could not be upgraded from published literature.

### Legal Status Flags
12. **UK scheduling status**: Acetylfentanyl not found on the current UK controlled drugs list. Status should be confirmed with UK Home Office. It is almost certainly controlled (PSA 2016 or MDA 1971 generic provision) but the specific class and schedule need verification.
13. **Australia scheduling status**: Could not confirm Schedule 9 classification from ODC database lookup — timeout error. Requires direct verification.

### Seed Data Discrepancies
14. **PubChem CID was blank** in seed data — confirmed as CID 527015 via API.
15. **Molecular formula, weight, InChIKey, SMILES were all blank** in seed data — formula, weight, and InChIKey now confirmed; SMILES still missing.
16. **Street name candidates blank**: Acetylfentanyl is commonly referred to as "acetyl fentanyl" (two words), "AF" in forensic literature; may also be encountered labelled as heroin or fentanyl.