A Comprehensive Analysis of Zytron: Disambiguation and Profiling of a Herbicide (DMPA, CAS 299-85-4) and a Pharmaceutical (Ondansetron)

Executive Summary and Disambiguation of "Zytron"

Identification of a Critical Ambiguity

An investigation into the substance designated "Zytron," based on the provided identifiers—specifically CAS Number 299-85-4 and DrugBank ID DB11768—reveals a significant nomenclatural conflict. These identifiers are associated with two distinct and unrelated chemical entities, one an agrochemical and the other a pharmaceutical. The primary objective of this report is to systematically disambiguate these two substances, providing a definitive and comprehensive profile for each to resolve the existing confusion and prevent potential errors in scientific, regulatory, and clinical contexts.

The core of this ambiguity lies in the polysemous use of the trade name "Zytron." In such cases of conflicting information, the Chemical Abstracts Service (CAS) Registry Number serves as the most stable and universally accepted unique identifier for a chemical substance. Therefore, this analysis is anchored to the entity definitively identified by the provided CAS number. The broader implications of this ambiguity extend to the integrity of scientific databases and the systemic risks posed by overlapping commercial branding in disparate industries. The potential for data cross-contamination between agrochemical and pharmaceutical domains highlights a critical need for rigorous adherence to standardized, unique identifiers.

Introduction to Zytron (DMPA): The Herbicide

The CAS Number 299-85-4 unequivocally identifies an organophosphorus compound with the preferred IUPAC name N-propan-2-amine.[1] This substance, commonly known by the synonym DMPA, is the original entity marketed under the trade name Zytron.[1] It is a chlorophenoxy herbicide and insecticide developed for agrochemical applications, primarily for pre-emergent weed control in turf management. Its mechanism of action, toxicological profile, and environmental fate are entirely distinct from any pharmaceutical agent and are characteristic of its classification as a pesticide.

Introduction to Zytron (Ondansetron): The Pharmaceutical

Concurrent with the agrochemical's branding, the name "Zytron" is also used as a commercial trade name for a pharmaceutical product, such as "Zytron 4 MG Tablet".[3] The active pharmaceutical ingredient (API) in this medication is Ondansetron, a potent and widely prescribed antiemetic. Ondansetron is a selective serotonin 5-HT3 receptor antagonist used to prevent nausea and vomiting associated with cancer chemotherapy, radiation therapy, and surgery. The use of the same brand name for this pharmaceutical product is the source of the critical ambiguity addressed in this report.

The Problem of Data Provenance

The provided DrugBank ID, DB11768, further complicates the matter. While external sources link this ID to the herbicide DMPA, direct queries within the DrugBank database do not yield an active, valid entry.[1] Instead, related searches indicate revoked records or point to different, unrelated compounds, suggesting that DB11768 is an erroneous, obsolete, or "ghost" identifier within that specific database ecosystem.[6] This phenomenon of "data echoes," where incorrect information is propagated across interconnected but independently maintained databases, underscores the fallibility of relying on a single, non-primary identifier and reinforces the primacy of the CAS number as the ground truth for chemical identification.

To provide immediate clarity, the fundamental differences between these two substances are summarized in Table 1.

Table 1: Comparative Chemical Identifiers for Zytron (DMPA) vs. Ondansetron

Identifier	Zytron (DMPA)	Zytron (Ondansetron)
Common Name	DMPA	Ondansetron
Synonym(s)	Zytron, Dowco 118, OMS115	Zofran®, Zuplenz®, Zytron Tablet
CAS Number	299-85-4	99614-02-5 (base)
DrugBank ID	DB11768 (erroneous/obsolete)	DB00904
IUPAC Name	N-propan-2-amine	9-methyl-3-[(2-methylimidazol-1-yl)methyl]-2,3-dihydro-1H-carbazol-4-one
Molecular Formula	C10​H14​Cl2​NO2​PS	C18​H19​N3​O
Molar Mass	314.16 g·mol⁻¹	293.36 g·mol⁻¹
Chemical Class	Organophosphorus Herbicide	Carbazole Derivative, 5-HT3 Antagonist

Profile of Zytron (DMPA) - The Organophosphorus Herbicide (CAS 299-85-4)

This section provides a detailed profile of the chemical substance definitively identified by CAS Number 299-85-4. All data herein pertains exclusively to the agrochemical DMPA, also known as Zytron.

Chemical Identification and Physicochemical Properties

The compound with CAS Number 299-85-4 is an organothiophosphate ester with a complex structure. Its unambiguous identification is crucial for toxicological and environmental assessment.

• Synonyms: The compound is known by several names in technical and commercial literature, including: DMPA, O-2,4-Dichlorophenyl O-methyl isopropylphosphoramidothioate, OMS115, Dow-1329, ENT-25647, K-22023, and Dowco 118.[1]
• IUPAC Name: The systematically generated name is N-propan-2-amine.[1]
• Molecular Formula: C10​H14​Cl2​NO2​PS.[1]
• Molar Mass: Calculated values range from 314.16 to 314.18 g·mol⁻¹.[1]
• Structural Identifiers:
• SMILES: CC(C)NP(=S)(OC)Oc1ccc(cc1Cl)Cl.[10]
• InChI: InChI=1S/C10H14Cl2NO2PS/c1-7(2)13-16(17,14-3)15-10-5-4-8(11)6-9(10)12/h4-7H,1-3H3,(H,13,17).[1]
• InChIKey: PJFGPJQBWSEWKX-UHFFFAOYSA-N.[1]

The physical characteristics of a pesticide determine its environmental behavior, mode of application, and potential for human exposure. The key physicochemical properties of DMPA are consolidated in Table 2.

Table 2: Physicochemical Properties of Zytron (DMPA)

Property	Value	Source(s)
Appearance	Solid	1
Melting Point	51.4°C	2
Boiling Point	355.5°C (at 760 mmHg)	2
Density	1.34 g/cm³	2
Vapor Pressure	3.12×10−5 mmHg (at 25°C)	1
Water Solubility	5 mg/L (at 25°C)	2
Flash Point	168.8°C	2

Agrochemical Applications and Historical Context

Zytron (DMPA) was developed as a specialized herbicide with a history of use in professional turf management.

• Primary Use: It functions as a pre-emergent chlorophenoxy herbicide, primarily used to control crabgrass (Digitaria spp.) and other annual weeds in established turfgrass.[1] Its application prevents the germination of weed seeds. In addition to its herbicidal activity, it is also effective against certain turf pests, including ants, chinch bugs, and grubs.[1]
• Historical Context: The compound was tested and became commercially available in the United States in 1959.[1] It was marketed by Dow Chemical Company under trade names such as "Dow Crabgrass Killer," "Dow 1329," and "T-H Crabgrass Killer".[1]
• Application Rates: A notable characteristic of Zytron's use was its high application rate, typically between 10 to 20 pounds per acre on turf.[1] This is a substantial rate compared to many modern herbicides. Experimental applications have been recorded at rates as high as 67 pounds per acre, indicating a wide margin of safety for the target turfgrasses like colonial bentgrass, Kentucky bluegrass, and red fescue.[1]
• Niche Applications: Its efficacy and turf safety profile made it suitable for high-value areas, such as its documented use on baseball pitches in Australia.[1]

Mechanism of Action

The biochemical pathway through which Zytron (DMPA) exerts its herbicidal effect is well-defined and distinct from that of many other herbicide classes.

• Biochemical Pathway: Zytron functions by inhibiting microtubule assembly in plant cells. Microtubules are essential components of the cytoskeleton and are critical for the formation of the mitotic spindle during cell division (mitosis).[1] By disrupting this process, DMPA prevents root and shoot growth in germinating weeds, leading to their death before they can emerge from the soil.
• Herbicide Classification: This mechanism of action places DMPA in the Herbicide Resistance Action Committee (HRAC) Group 3 (or WSSA Group K1). This group includes microtubule assembly inhibitors, such as the dinitroaniline family of herbicides (e.g., trifluralin).[1] This classification is vital for managing herbicide resistance, as it informs rotational strategies to prevent the selection of resistant weed biotypes.

Toxicology, Mammalian Pharmacokinetics, and Environmental Fate

The risk profile of a pesticide is determined by its toxicity to non-target organisms, its behavior within mammals, and its persistence in the environment.

• Acute Toxicity: DMPA exhibits moderate acute oral toxicity in rats, with a reported median lethal dose (LD50​) of 270 mg/kg.[1] It is significantly less toxic to dogs, with an oral LD50​ greater than 1000 mg/kg.[1]
• Mammalian Pharmacokinetics: Despite its organophosphorus structure, metabolic studies reveal a remarkably rapid clearance from the mammalian body. A study involving a lactating cow demonstrated that Zytron disappears almost completely within one hour of exposure.[1] This rapid metabolism and excretion profile is a critical feature, as it strongly mitigates the risk of bioaccumulation in tissues or transfer into milk, even with the high application rates used in turf management.
• Specific Toxicities: As an organophosphorus ester, DMPA belongs to a chemical class known for its potential to cause neurotoxicity, typically through the inhibition of acetylcholinesterase. Specific studies have shown that Zytron can induce neurotoxic effects in chickens, a species often sensitive to this class of compounds. A minimum effective dose of 100 mg/kg administered daily for 10 days was required to produce observable behavioral alterations in hens.[1] This highlights a species-specific sensitivity and confirms the compound's potential for class-related toxicity, though its rapid metabolism in mammals appears to reduce its acute risk compared to other organophosphates.
• Environmental Profile: Research on the environmental fate of Zytron indicates that it does not accumulate in soil and is non-harmful to soil microflora.[1] Studies have confirmed that Zytron and its degradation products have minimal lasting impact on soil microorganisms responsible for processes like cellulose decomposition.[1] This suggests that the compound is effectively broken down by environmental or microbial processes, preventing long-term soil contamination. This favorable environmental profile, combined with its rapid mammalian clearance, helps to explain its historical use in settings with potential for human and animal contact, such as lawns and sports fields.

Profile of Zytron (Ondansetron) - The Antiemetic Pharmaceutical

This section provides a comprehensive profile of the pharmaceutical drug Ondansetron, which is marketed under various brand names, including Zytron. All data herein pertains exclusively to this active pharmaceutical ingredient.

Chemical Identification and Pharmaceutical Formulations

Ondansetron is a synthetic organic compound that represents a major advancement in the management of nausea and vomiting.

• Generic Name: Ondansetron.[4]
• Chemical Class: It is classified as a Carbazole Derivative and, pharmacologically, as a selective Serotonin 5-HT3 Receptor Antagonist.[3]
• Chemical Identifiers:
• IUPAC Name: 9-methyl-3-[(2-methylimidazol-1-yl)methyl]-2,3-dihydro-1H-carbazol-4-one.[13]
• CAS Number: 99614-02-5 (for the free base).[13] The hydrochloride salt is 99614-01-4, and the hydrochloride dihydrate is 103639-04-9.[13]
• DrugBank ID: DB00904.[13]
• Molecular Formula: C18​H19​N3​O.[15]
• Molar Mass: 293.36 g·mol⁻¹.[16]
• Brand Names: The original brand name is Zofran®. Other common brand names include Zofran ODT® (orally disintegrating tablet) and Zuplenz® (oral soluble film).[12] The name "Zytron" is also used for commercial formulations, such as Zytron 4 MG Tablet and Zytron 2 MG Injection.[3]
• Formulations: Ondansetron is available in a wide variety of formulations to suit different clinical needs, including:
• Conventional oral tablets (e.g., 4 mg, 8 mg, 24 mg).[3]
• Orally disintegrating tablets (ODT) that dissolve on the tongue without water.[12]
• Oral solution or syrup.[4]
• Oral soluble film (e.g., Zuplenz®) that dissolves on the tongue.[12]
• Solution for intravenous (IV) or intramuscular (IM) injection.[4]

Clinical Pharmacology: Mechanism of Action

Ondansetron's therapeutic effect is derived from its highly specific interaction with a single subtype of serotonin receptor. This "clean" pharmacological profile is a key reason for its improved tolerability over older, less specific antiemetic agents.

• Primary Mechanism: Ondansetron is a potent, highly selective, and competitive antagonist of the serotonin 5-HT3 receptor.[13] It demonstrates very low affinity for other neurotransmitter receptors, including dopamine D2, histamine H1, adrenergic, and other serotonin receptor subtypes.[16] This specificity is crucial, as it avoids the side effects associated with dopamine blockade (e.g., extrapyramidal symptoms like dystonia and akathisia) that are common with older antiemetics such as metoclopramide.[26]
• Sites of Action: The antiemetic action of ondansetron is mediated through the blockade of 5-HT3 receptors at two primary locations in the body [17]:

1. Peripheral Action: 5-HT3 receptors are densely located on the terminals of the vagus nerve in the gastrointestinal (GI) tract.
2. Central Action: 5-HT3 receptors are also present in the central nervous system (CNS), particularly in the chemoreceptor trigger zone (CTZ) located in the area postrema of the brainstem.

• Pathophysiology of Emesis: In the context of chemotherapy and radiotherapy, cytotoxic agents cause damage to the enterochromaffin cells lining the GI tract. This damage triggers a massive release of the neurotransmitter serotonin (5-hydroxytryptamine, or 5-HT).[4] The released serotonin then binds to and activates the 5-HT3 receptors on the vagal afferent nerves, sending a powerful emetic signal to the vomiting center in the medulla. Serotonin also acts on 5-HT3 receptors within the CTZ. By blocking these receptors at both the peripheral and central sites, ondansetron effectively interrupts the vomiting reflex at its origin.[11]

Clinical Pharmacology: Pharmacokinetics and Pharmacodynamics

The pharmacokinetic profile of ondansetron is characterized by rapid absorption, extensive hepatic metabolism, and a relatively short half-life. A key pharmacodynamic feature is its effect on cardiac repolarization.

• Absorption: Following oral administration, ondansetron is rapidly and completely absorbed from the GI tract. However, it undergoes significant first-pass metabolism in the liver, resulting in an absolute bioavailability of approximately 60%.[28] The presence of food slightly enhances its bioavailability.[32] Peak plasma concentrations (Tmax) are typically achieved within 0.5 to 2 hours after an oral dose.[29]
• Distribution: Ondansetron is widely distributed throughout the body, with a volume of distribution (Vd) of approximately 160 L or 1.9 L/kg.[29] It is moderately bound to plasma proteins (70-76%).[15]
• Metabolism: The drug is extensively metabolized in the liver, with hepatic processes accounting for over 95% of its clearance.[17] The primary metabolic pathway is hydroxylation on the indole ring, followed by glucuronide or sulfate conjugation.[16] This metabolism is carried out by a multiplicity of cytochrome P450 (CYP) enzymes, predominantly CYP3A4, but also involving CYP1A2 and CYP2D6.[16] This metabolic redundancy is a significant clinical advantage, as it means that genetic variations in a single enzyme (e.g., CYP2D6 "poor metabolizers") or inhibition of one pathway by a co-administered drug has little overall effect on ondansetron clearance. This makes its pharmacokinetic profile more predictable across diverse patient populations.[16]
• Excretion: Less than 5% of an administered dose is excreted unchanged in the urine.[30] The elimination half-life ( t1/2​) in healthy adults is approximately 3 to 4 hours.[29] This half-life is prolonged in elderly patients (to ~5.5 hours) and significantly prolonged in patients with severe hepatic impairment (up to 20 hours), necessitating dose adjustments in the latter group.[28]
• Pharmacodynamics: Ondansetron produces a dose-dependent prolongation of the QT interval on an electrocardiogram (ECG).[3] The QT interval represents the time taken for ventricular depolarization and repolarization. Prolongation of this interval is a risk factor for a potentially fatal ventricular arrhythmia called Torsade de Pointes. This effect prompted the U.S. Food and Drug Administration (FDA) to issue a safety warning and mandate the withdrawal of the 32 mg single intravenous dose from the market, recommending that no single IV dose should exceed 16 mg.[13]

Therapeutic Indications and Clinical Use

Ondansetron is a cornerstone of supportive care in oncology and surgery, with a well-established set of approved indications and several common off-label applications.

• FDA-Approved Indications: The U.S. FDA has approved ondansetron for the following uses [30]:

1. Chemotherapy-Induced Nausea and Vomiting (CINV): Prevention of nausea and vomiting associated with both highly emetogenic (e.g., high-dose cisplatin) and moderately emetogenic cancer chemotherapy in adults and pediatric patients.
2. Radiation-Induced Nausea and Vomiting (RINV): Prevention of nausea and vomiting in patients receiving radiotherapy, particularly total body irradiation or radiation to the abdomen.
3. Postoperative Nausea and Vomiting (PONV): Prevention of nausea and/or vomiting following surgical procedures.

• Prominent Off-Label Uses: Due to its efficacy and favorable safety profile compared to older agents, ondansetron is frequently used for indications not formally approved by regulatory agencies. These include:
• Pregnancy-Related Nausea: Treatment of nausea and vomiting of pregnancy ("morning sickness") and its severe form, hyperemesis gravidarum. It is typically reserved as a second-line agent after other treatments have failed.[30]
• Gastroenteritis: To reduce vomiting, prevent dehydration, and facilitate oral rehydration therapy, especially in pediatric patients in the emergency department setting.[42]
• Other Conditions: It is also used in the management of cyclic vomiting syndrome, to control symptoms in irritable bowel syndrome with diarrhea (IBS-D), and has been investigated as an adjunctive therapy for treatment-resistant obsessive-compulsive disorder (OCD).[30]

The approved dosing regimens vary significantly by indication, patient age, and route of administration, as summarized in Table 3.

Table 3: Summary of FDA-Approved Indications and Dosages for Ondansetron (Adults)

Indication	Route	Recommended Dosage Regimen
Highly Emetogenic CINV	Oral	A single 24-mg dose administered 30 minutes before chemotherapy.
Moderately Emetogenic CINV	Oral	8 mg administered 30 minutes before chemotherapy, followed by another 8-mg dose 8 hours later. Then, 8 mg every 12 hours for 1 to 2 days.
Moderately Emetogenic CINV	IV	0.15 mg/kg over 15 minutes, 30 minutes before chemotherapy, repeated at 4 and 8 hours after the first dose. (Single doses not to exceed 16 mg).
Radiation-Induced Nausea/Vomiting	Oral	8 mg administered 1 to 2 hours before radiotherapy, with subsequent doses every 8 hours for the duration of treatment and 1-2 days after.
Postoperative Nausea/Vomiting	Oral	16 mg administered 1 hour before induction of anesthesia.
Postoperative Nausea/Vomiting	IV/IM	4 mg administered immediately before anesthesia or postoperatively.

Note: Pediatric dosing is typically weight-based. Dosing for patients with severe hepatic impairment should not exceed 8 mg per day.[19]

Safety, Regulation, and Risk Profile of Ondansetron

The safety profile of ondansetron is well-characterized after decades of widespread clinical use. While generally well-tolerated, it carries specific risks, contraindications, and a complex regulatory history reflecting the evolution of post-marketing safety surveillance.

Adverse Effects and Tolerability

• Common Side Effects: The most frequently reported adverse events are generally mild to moderate in severity. These include headache, constipation, diarrhea, fatigue or a feeling of malaise, drowsiness, and dizziness.[3] In the postoperative setting, hypoxia and fever have also been noted as common side effects.[46]
• Serious Adverse Events: Although less common, ondansetron is associated with several potentially serious risks:
• Cardiovascular Effects: The most significant risk is dose-dependent QT interval prolongation, which can lead to the life-threatening ventricular arrhythmia Torsade de Pointes.[3] Cases of myocardial ischemia, believed to be caused by coronary artery spasm, have also been reported, with symptoms sometimes appearing immediately after IV administration.[51]
• Hypersensitivity Reactions: Severe allergic reactions, including anaphylaxis and bronchospasm, can occur. Cross-sensitivity has been observed, meaning patients with a known hypersensitivity to other selective 5-HT3 antagonists (e.g., granisetron) may also react to ondansetron.[3]
• Neurological Effects: Serotonin Syndrome is a rare but serious condition that can occur when ondansetron is used, particularly in combination with other serotonergic drugs (e.g., SSRI antidepressants). Symptoms include a combination of mental status changes (agitation, hallucinations), autonomic instability (tachycardia, fever, sweating), and neuromuscular hyperactivity (tremor, hyperreflexia).[46] While ondansetron's selectivity largely prevents the extrapyramidal symptoms seen with dopamine antagonists, rare cases of seizures and movement disorders (e.g., oculogyric crisis, dystonic reactions) have been reported.[36]
• Gastrointestinal Effects: Because ondansetron can slow large bowel transit time, it may mask the signs of a progressive ileus or gastric distention in postoperative patients. Careful monitoring of bowel activity is warranted in this population.[32]

Contraindications, Warnings, and Drug Interactions

• Absolute Contraindications: The use of ondansetron is strictly contraindicated in two situations:

1. Patients with a known history of hypersensitivity (e.g., anaphylaxis) to ondansetron or any of its formulation components.[3]
2. Concomitant use with apomorphine, a dopamine agonist used for Parkinson's disease. This combination has been associated with profound hypotension and loss of consciousness.[3]

• Warnings and Precautions:
• Congenital Long QT Syndrome: Ondansetron should be avoided in patients with this inherited condition due to the high risk of inducing a fatal arrhythmia.[49]
• High-Risk Cardiac Patients: ECG monitoring is recommended for patients with pre-existing risk factors for QT prolongation, such as electrolyte imbalances (hypokalemia, hypomagnesemia), congestive heart failure, and bradyarrhythmias, or those taking other QT-prolonging medications.[3]
• Drug Interactions: Ondansetron has numerous clinically significant drug interactions, which can be broadly categorized by their mechanism. A flat list of all 364 known interacting drugs is not practical for clinical decision-making; understanding the underlying pharmacology is key.[55] Table 4 organizes these interactions into actionable categories.

Table 4: Major Drug Interactions with Ondansetron, Categorized by Mechanism

Interaction Mechanism	Drug Class / Specific Examples	Clinical Consequence and Recommendation
Pharmacodynamic (Additive Risk of QT Prolongation)	Antiarrhythmics: Amiodarone, Dronedarone, Sotalol Antipsychotics: Haloperidol, Ziprasidone, Quetiapine Antibiotics: Fluoroquinolones (e.g., Ciprofloxacin), Macrolides (e.g., Azithromycin) Antidepressants: Citalopram, Escitalopram, Amitriptyline Other: Methadone, Tramadol	Increased risk of Torsade de Pointes. Avoid combination if possible, especially in high-risk patients. If co-administration is necessary, ECG monitoring is recommended. Dronedarone is contraindicated.
Pharmacodynamic (Additive Risk of Serotonin Syndrome)	SSRIs: Sertraline, Fluoxetine SNRIs: Venlafaxine, Duloxetine MAOIs: Phenelzine, Methylene Blue Opioids: Tramadol, Fentanyl Other: Lithium, Mirtazapine	Increased risk of serotonin syndrome. Monitor patients for signs and symptoms (mental status changes, autonomic instability, neuromuscular symptoms). If symptoms occur, discontinue both agents and provide supportive care.
Pharmacokinetic (Altered Ondansetron Metabolism)	Potent CYP3A4 Inducers: Phenytoin, Carbamazepine, Rifampicin CYP3A4 Inhibitors: Ketoconazole, Itraconazole	Inducers: Increase the clearance and decrease the blood concentration of ondansetron, potentially reducing its efficacy. Inhibitors: May decrease clearance and increase ondansetron concentration, though the clinical impact is often limited due to redundant metabolic pathways.

Global Regulatory Status and History

The regulatory journey of ondansetron is a salient example of how the understanding of a drug's risk-benefit profile evolves over its lifecycle through post-marketing pharmacovigilance.

• Development and Initial FDA Approval: Ondansetron was developed by Glaxo (now GlaxoSmithKline) in the mid-1980s and received its first U.S. patent in 1987.[42] The FDA granted its initial approval in January 1991 for the intravenous formulation to treat CINV.[13] An oral tablet form was approved in 1993.[59] After its patent expired, generic versions became available in the U.S. around 2007.[58]
• Key FDA Safety Actions: The most significant regulatory action concerned its cardiac effects.
• In September 2011, the FDA issued a Drug Safety Communication highlighting the risk of QT interval prolongation and abnormal heart rhythms.[50]
• In December 2012, following a thorough review, the FDA announced that the 32 mg single intravenous dose would no longer be marketed and should not be used. This action was taken to mitigate the risk of Torsade de Pointes. The agency clarified that no single IV dose should exceed 16 mg.[13] This is sometimes referred to as a "black box warning" in legal and patient-facing literature, reflecting the severity of the risk identified.[60]
• European Medicines Agency (EMA): The EMA has taken a notably cautious stance regarding ondansetron use during pregnancy. In July 2019, the agency's Pharmacovigilance Risk Assessment Committee (PRAC) reviewed epidemiological data and concluded that first-trimester use was associated with a small increased risk of orofacial clefts (cleft lip/palate). Consequently, the EMA recommended that the Summary of Product Characteristics (SmPC) for all ondansetron-containing products be updated to state that it should not be used during the first trimester of pregnancy.[63] This strong recommendation has been debated by some clinical organizations, who argue that the absolute risk increase is very small and must be weighed against the benefits of treating severe nausea and vomiting in pregnancy.[63]
• Therapeutic Goods Administration (TGA, Australia): In Australia, ondansetron is regulated as a Schedule 4 (Prescription Only Medicine).[66] It is approved for the management of CINV, RINV, and PONV.[66] In 2020, the TGA considered and ultimately rejected an application to down-schedule ondansetron to Schedule 3 (Pharmacist Only Medicine). The delegate's decision was based on the grounds that the approved indications require a medical diagnosis, and there were significant safety concerns related to off-label use without medical supervision, particularly the known risk of QT interval prolongation.[69] This decision reflects a regulatory philosophy that prioritizes physician oversight for this medication, in contrast to a model that would permit wider access through pharmacists.

This divergence in regulatory actions between major global agencies—particularly regarding pregnancy and accessibility—demonstrates that the interpretation of risk-benefit data is not monolithic. It is influenced by regional healthcare systems, legal precedents, and differing philosophies on public health risk management.

Synthesis, Data Integrity Analysis, and Concluding Remarks

Critical Assessment of Database Discrepancies

The initial query presented a classic data integrity challenge, stemming from the collision of a polysemous trade name ("Zytron") and an erroneous database identifier (DrugBank ID DB11768). A critical analysis of the provided sources confirms that DB11768 is not a valid, active entry for any compound in the DrugBank database. Its linkage to the herbicide DMPA appears to be a propagated error, or "data echo," within tertiary information sources that may not be subject to the same rigorous curation as primary databases.[1]

This situation serves as a powerful illustration of the critical importance of data provenance and the use of primary, unique identifiers in scientific research and communication. While trade names are useful in a commercial context, they lack the specificity required for unambiguous scientific identification. Similarly, while database-specific IDs are useful within their native systems, they can become corrupted or obsolete. The CAS Registry Number, in contrast, remains the gold standard for uniquely and permanently identifying a specific chemical substance.

Comparative Summary and Recommendations

This report has systematically disambiguated and profiled two fundamentally different substances that share the name "Zytron":

1. Zytron (DMPA, CAS 299-85-4): An organophosphorus herbicide and insecticide used in turf management. It acts by inhibiting microtubule assembly in plants. It possesses moderate acute toxicity, is rapidly metabolized by mammals, and does not persist in the soil environment. Its use is strictly limited to agrochemical applications.
2. Zytron (Ondansetron, CAS 99614-02-5): A selective 5-HT3 receptor antagonist and a cornerstone antiemetic medication in human medicine. It is used to prevent nausea and vomiting from chemotherapy, radiotherapy, and surgery. Its safety profile is well-defined, with the most significant risks being dose-dependent QT prolongation and serotonin syndrome.

Based on this comprehensive analysis, the following recommendations are made to prevent future ambiguity:

• Prioritize Definitive Identifiers: In all scientific, regulatory, clinical, and legal documentation, the CAS Number should be used as the primary identifier to specify a chemical substance. For pharmaceuticals, this should be supplemented with the non-proprietary generic name (i.e., Ondansetron).
• Use Trade Names with Caution: The trade name "Zytron" should be considered ambiguous and should always be qualified with a definitive identifier (e.g., "Zytron herbicide, CAS 299-85-4") or by its context of use (e.g., "the pharmaceutical Zytron containing ondansetron").
• Verify Database Information: Researchers and professionals should practice due diligence by cross-referencing information from aggregated databases against primary sources or other authoritative registries to identify and correct for potential data propagation errors.

In conclusion, the name "Zytron" applies to two vastly different worlds of chemistry and application. One is a tool for agriculture, designed to be toxic to specific plants, with a corresponding toxicological profile. The other is a vital tool for supportive medical care, designed to interact with specific human neuroreceptors, with a complex but well-understood profile of therapeutic benefits and risks. The distinction is absolute, and maintaining this clarity through the disciplined use of standardized identifiers is paramount for safety and accuracy across all domains.

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