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Moxidectin
Moxidectin
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Moxidectin
Structural formula of moxidectin
Ball-and-stick model of the moxidectin molecule
Clinical data
Trade namesCydectin, Equest, ProHeart, Quest.[1]
Other namesCL 301,423;[2] milbemycin B.[2]
AHFS/Drugs.comInternational Drug Names
Routes of
administration
By mouth, topical, subcutaneous
ATC code
Legal status
Legal status
Identifiers
  • (10E,14E,16E,22Z)-(1R,4S,5′S,6R,6′S,8R,13R,20R,21R,24S)-6′-
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
CompTox Dashboard (EPA)
ECHA InfoCard100.163.046 Edit this at Wikidata
Chemical and physical data
FormulaC37H53NO8
Molar mass639.830 g·mol−1
3D model (JSmol)
  • CC(C)\C=C(/C)[C@H]5O[C@@]2(C[C@H]1OC(=O)[C@@H]3/C=C(/C)[C@@H](O)[C@H]4OC/C(=C\C=C\[C@H](C)CC(\C)=C\C[C@H](C1)O2)[C@@]34O)C\C(=N\OC)[C@@H]5C
  • InChI=1S/C37H53NO8/c1-21(2)14-25(6)33-26(7)31(38-42-8)19-36(46-33)18-29-17-28(45-36)13-12-23(4)15-22(3)10-9-11-27-20-43-34-32(39)24(5)16-30(35(40)44-29)37(27,34)41/h9-12,14,16,21-22,26,28-30,32-34,39,41H,13,15,17-20H2,1-8H3/b10-9+,23-12+,25-14+,27-11+,38-31-/t22-,26-,28+,29-,30-,32+,33+,34+,36-,37+/m0/s1 checkY
  • Key:YZBLFMPOMVTDJY-CBYMMZEQSA-N checkY
 ☒NcheckY (what is this?)  (verify)

Moxidectin is an anthelmintic drug used in animals to prevent or control parasitic worms (helminths), such as heartworm and intestinal worms, in dogs, cats, horses, cattle, sheep and wombats.[5] Moxidectin kills some of the most common internal and external parasites by selectively binding to a parasite's glutamate-gated chloride ion channels. These channels are vital to the function of invertebrate nerve and muscle cells; when moxidectin binds to the channels, it disrupts neurotransmission, resulting in paralysis and death of the parasite.

Moxidectin is a therapeutic alternative on the World Health Organization's List of Essential Medicines.[6]

Medical uses

[edit]

Moxidectin was approved for onchocerciasis (river-blindness) in 2018 for people over the age of 11 in the United States based on two studies.[7] There is a need for additional trials, with long-term follow-up, to assess whether moxidectin is safe and effective for treatment of nematode infection in children and women of childbearing potential.[8] Moxidectin is predicted to be helpful to achieve elimination goals of this disease.[9]

Nematodes can develop cross-resistance between moxidectin and other similar parasiticides, such as ivermectin, doramectin and abamectin.[13] The ways in which the parasites evolve resistance to this drug include mutations in glutamate-gated chloride channel genes, GABA-R genes,[14] or increased expression of p-glycoprotein, which is a transmembrane drug efflux pump.[15] Allele frequency changes corresponding to resistance to moxidectin and/or other macrocyclic lactone-class drugs have been observed in the glutamate-gated chloride channel α-subunit gene of Haemonchus contortus and Cooperia oncophora, as well as in the H. contortus genes coding for p-glycoprotein and the GABA-R gene.[15]

Moxidectin is being evaluated as a treatment to eradicate scabies in humans, especially when resistant to other treatments.[16]

Adverse effects

[edit]

Studies of moxidectin show the side effects vary by animal and may be affected by the product's formulation, application method and dosage.[citation needed]. It is however regarded as relatively safe.[17]

An overdose of moxidectin enhances the effect of gamma-aminobutyric acid (GABA) in the central nervous system.[18] In horses, overdose may lead to depression, drooping of the lower lip, tremor, lack of coordination when moving (ataxia), decreased rate of breathing (respiratory rate), stupor and coma.[18]

If a dog licks moxidectin from the skin which was applied as a "spot-on" (topical) treatment, this has the same effect as an overdose, and may cause vomiting, salivation and neurological signs such as ataxia, tremor, and nystagmus.[10] Some Collie dogs can tolerate moxidectin, but other individuals are sensitive and upon ingestion, experience vomiting, salivation or transient neurological signs.[10]

Pharmacology

[edit]

Moxidectin is very lipophilic, which causes it to have a high volume of distribution.[19] Moxidectin concentrates in the animal's adipose tissue, from where it is released for up to two months following administration.[19]

In goats, the oral bioavailability of moxidectin is 2.7 times lower, and the half-life is 1.8 times shorter than in sheep.[20]

Chemistry

[edit]

Moxidectin, a macrocyclic lactone of the milbemycin class,[10] is a semisynthetic derivative of nemadectin, which is a fermentation product of the bacterium Streptomyces cyanogriseus subsp. noncyanogenus.[21]

History

[edit]

In the late 1980s, an American Cyanamid Company agronomist discovered the Streptomyces bacteria from which moxidectin is derived in a soil sample from Australia. Two companies filed patents for moxidectin: Glaxo Group and the American Cyanamid Company;[1] in 1988, all patents were transferred to American Cyanamid.[1] In 1990, the first moxidectin product was sold in Argentina.[1]

For human use, moxidectin was approved by the United States Food and Drug Administration in June 2018, for the treatment of onchocerciasis in adults and adolescents aged 12 years of age and older. This is the first human approval worldwide. The license holder is the nonprofit biopharmaceutical company Medicines Development for Global Health.[4]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
Moxidectin is a macrocyclic lactone drug derived from the actinomycete cyanogriseus, belonging to the milbemycin subclass and primarily used to treat (river blindness) caused by in humans, as well as various internal and external parasitic infections in animals such as heartworm in dogs and gastrointestinal nematodes in cattle. Developed initially as a veterinary parasiticide in the 1980s through fermentation and semisynthetic modification of nemadectin (an avermectin-related compound), moxidectin received U.S. (FDA) approval for human use in June 2018 as an 8 mg single-dose oral tablet for patients aged 12 years and older, marking the first new drug for in over a decade. In February 2025, the FDA expanded its indication to include children as young as 4 years old, weighing at least 13 kg, to address unmet needs in endemic regions. In September 2025, moxidectin was included in the Model List of . For veterinary applications, it is formulated as injectables, pour-ons, and oral suspensions, with the first generic injectable approved in 2023 for beef and nonlactating to control parasites like inhibited larvae of . The drug's mechanism of action involves selective binding to glutamate-gated chloride channels, gamma-aminobutyric acid (GABA) receptors, and transporters in invertebrate parasites, leading to hyperpolarization of and muscle cells, , and of microfilariae while inhibiting embryogenesis and microfilarial release from adult worms. Unlike , another macrocyclic , moxidectin exhibits a longer (approximately 23 days in humans) and greater potency against O. volvulus microfilariae, resulting in sustained reductions in skin microfilarial density for up to 18 months post-treatment. Pharmacokinetically, it is minimally metabolized in the liver (primarily via ) and excreted mostly unchanged in feces, with enhanced when taken with a high-fat . In addition to onchocerciasis, moxidectin is under investigation for , , and soil-transmitted helminths as part of mass drug administration programs in tropical regions, offering potential advantages over due to its extended efficacy and reduced dosing frequency. Common adverse effects in humans include , musculoskeletal pain, and Mazzotti reactions ( and pruritus from dying microfilariae), while veterinary use requires caution to avoid toxicity in certain breeds like collies due to MDR1 gene mutations. Overall, moxidectin's broad-spectrum activity and favorable safety profile position it as a key tool in global efforts to control and animal .

Uses

Human indications

Moxidectin is approved for the treatment of , also known as river blindness, caused by the Onchocerca volvulus in adult patients and pediatric patients aged 4 years and older weighing at least 13 kg. The recommended dosage is a single oral dose of 8 mg (four 2 mg tablets) for adults and patients weighing 30 kg or more; for pediatric patients weighing 15 kg to less than 30 kg, the dose is 6 mg (three tablets); and for those weighing 13 kg to less than 15 kg, it is 4 mg (two tablets). This indication was initially approved by the U.S. (FDA) in 2018 for patients aged 12 years and older, with expansion in February 2025 to include younger children following pediatric pharmacokinetic and safety trials that confirmed comparable exposure and tolerability at these weight-based doses of 4 to 8 mg. Treatment targets microfilariae but does not eliminate adult worms, necessitating follow-up evaluations and potential retreatment. Clinical trials have demonstrated moxidectin's superior microfilaricidal efficacy over , the standard treatment, with a single 8 mg dose achieving undetectable skin microfilarial densities in 83.4% of patients at 1 month post-treatment compared to 42.9% with (p < 0.0001). This effect persists longer, maintaining significantly lower skin microfilarial densities for up to 18 months after administration, reducing the parasite transmission reservoir by an average of 97-98% annually versus 88% for . These outcomes support moxidectin's role in mass drug administration programs for onchocerciasis control and potential elimination in endemic regions. Beyond its approved use, moxidectin is being investigated for scabies infestations caused by Sarcoptes scabiei. A completed phase 2b clinical trial, such as MDGH-MOX-2002, evaluated the efficacy and safety of single oral doses ranging from 8 mg to 32 mg in achieving complete cure at day 28, aiming to provide a simpler alternative to topical treatments. Preliminary dose-finding studies have established proof-of-concept for its parasiticidal activity against scabies mites in humans. Moxidectin is also under investigation for lymphatic filariasis caused by Wuchereria bancrofti. A 2025 clinical trial demonstrated that moxidectin combined with albendazole achieved superior clearance of microfilariae compared to ivermectin-based regimens, with complete data supporting its use in mass drug administration at 36 months post-treatment. For soil-transmitted helminths, particularly trichuriasis caused by Trichuris trichiura, a 2025 randomized trial showed that moxidectin co-administered with albendazole was superior to albendazole monotherapy in school-aged children, with higher cure rates (e.g., 45% vs. 15% for trichuriasis). Recent preclinical research in 2025 has highlighted moxidectin's potential repositioning for cutaneous leishmaniasis, showing significant reductions in Leishmania tropica cell counts across promastigote and amastigote stages, with IC50 values of 0.58 μM and 0.94 μM, respectively, and a selectivity index of 63.49 indicating low host cell toxicity. In vivo models using Galleria mellonella larvae demonstrated a marked decrease in parasite burden (AUC 19.32 vs. 57.37 in controls, p < 0.05), suggesting promise for further clinical development. Moxidectin is administered in 2 mg tablet form, which can be taken with or without food to enhance patient compliance in field settings. Prior screening for co-infection with is recommended to avoid risks like .

Veterinary applications

Moxidectin serves as a broad-spectrum in , primarily employed for the prevention and control of internal and external parasitic infections in companion animals and livestock. In dogs and cats, it is widely used to prevent heartworm disease caused by , with formulations providing monthly protection against larval stages. For horses, it targets intestinal nematodes including small strongyles (cyathostomins) and large strongyles, reducing parasite burdens and associated clinical signs like . In ruminants such as , sheep, and goats, moxidectin effectively controls gastrointestinal nematodes, lungworms, and certain ectoparasites, supporting overall animal health and productivity in farming operations. Available formulations of moxidectin are tailored to species and administration preferences, enhancing ease of use in veterinary practice. For cattle, injectable solutions at 0.2 mg/kg subcutaneously treat and control gastrointestinal roundworms, including inhibited Ostertagia ostertagi, while pour-on topicals at 0.5 mg/kg provide broad-spectrum coverage against nematodes, grubs, and lice. Horses receive oral gels or pastes at 0.4 mg/kg for deworming, offering a convenient single-dose option that minimizes handling stress. In sheep and goats, oral drenches at 0.2–0.4 mg/kg address roundworms and lungworms, though extra-label dosing may be applied in goats due to metabolic differences. Dogs typically receive extended-release injectables like ProHeart 6 (0.17 mg/kg) for six-month heartworm prevention, or topical applications combined with other actives for monthly use in cats. Moxidectin exhibits prolonged activity in ruminants, providing persistent protection against reinfection for 21–28 days post-treatment for key parasites like Ostertagia ostertagi and Dictyocaulus viviparus, with efficacy extending to hypobiotic larvae stages that other macrocyclic lactones may not fully address. This long-acting profile, up to 4–5 months in some extended formulations against certain nematodes, reduces treatment frequency and supports strategic parasite control programs. In wildlife conservation, moxidectin has been applied off-label for treating sarcoptic mange (Sarcoptes scabiei) in bare-nosed wombats (Vombatus ursinus), where topical pour-on administration at approximately 0.2–0.5 mg/kg in multiple doses effectively eliminates mites and promotes recovery without significant adverse effects. Emerging concerns include potential cross-resistance with ivermectin in equine nematodes, particularly cyathostomins, necessitating fecal egg count monitoring and rotation of anthelmintics to preserve efficacy. Veterinary guidelines recommend resistance surveillance through diagnostic testing to guide sustainable use.

Safety profile

Adverse effects in humans

Moxidectin is generally well tolerated in humans, with most adverse effects being mild to moderate and transient. Common adverse reactions in adults and adolescents treated for include (58%), musculoskeletal pain (64%), pruritus (65%), and (12%), often occurring within days of administration and resolving without specific intervention. In patients with , these symptoms are frequently associated with the , an inflammatory response triggered by the death of microfilariae, manifesting as itchiness, rash, fever, , and ; such reactions occurred in up to 99% of treated individuals in phase III trials but were comparable in frequency and severity to those seen with . In pediatric clinical trials conducted in 2025 for children aged 4-11 years receiving 6-8 mg doses, the most frequently reported adverse reactions were and , each affecting 8% of participants, with no new safety signals observed compared to older age groups. Overall, no severe adverse events have been reported in human trials across doses up to 36 mg, and mild to moderate events typically resolve spontaneously or with supportive care. To manage inflammatory responses, particularly in patients with high microfilarial loads, symptomatic treatment with antihistamines or corticosteroids may be used, alongside monitoring for orthostatic hypotension. In special populations, no new safety concerns have emerged for children aged 4 years and older based on recent trial data, though ongoing studies continue to evaluate long-term effects. Limited human data exist for pregnant women, with animal studies indicating no major risks to embryo-fetal development, but use is not recommended unless benefits outweigh potential unknowns. Moxidectin should be used with caution or avoided in patients with known co-infection with Loa loa, particularly those with high microfilarial loads, due to the risk of serious encephalopathy; screening for loiasis is recommended in endemic areas before treatment.

Adverse effects in animals

Moxidectin is generally well-tolerated by animals at recommended therapeutic doses, with a wide margin in most , often exceeding 10-fold the standard dose before significant occurs. In dogs, mild gastrointestinal effects such as (reported in 14.3% of cases) and (13.2%) are the most common adverse reactions when administered topically or orally at labeled doses. Overdose in dogs can lead to neurological symptoms including tremors, , depression, , seizures, , and , primarily due to enhanced inhibitory neurotransmission via potentiation. These signs are more pronounced in cases of ingestion or high-dose exposure, but most affected dogs respond to supportive treatment such as intravenous fluids, activated charcoal for , and monitoring for respiratory support. In horses, therapeutic doses rarely cause issues, but overdose may result in , tremors, depression, lip droop, and recumbency, particularly in young foals where even slight overdoses can be neurotoxic and potentially fatal. Dogs with the MDR1 (common in breeds like Collies) exhibit increased sensitivity to macrocyclic lactones, yet moxidectin demonstrates a wider safety margin compared to , with no neurotoxic effects observed even at 30 times the therapeutic dose in affected Collies. Nonetheless, caution is advised in these breeds, and is recommended prior to use. Cattle and sheep show minimal adverse effects at therapeutic levels, benefiting from a higher safety margin (up to 20-fold in some studies), with rare reports limited to transient or only in very young or overdosed individuals. Injectable formulations in have occasionally been associated with anaphylactic reactions if administered concurrently with , emphasizing the need for separate timing. Precautions include avoiding use in animals with known to macrocyclic lactones and monitoring for overdose, where treatment focuses on symptomatic care without specific antidotes. No teratogenic or has been reported in animal studies at doses up to several times the therapeutic level.

Pharmacology

Mechanism of action

Moxidectin exerts its effects primarily by binding to glutamate-gated channels (GluCl) in the and muscle cells of , such as nematodes and arthropods. This binding increases the permeability of the channels to ions, leading to an influx of that hyperpolarizes the and disrupts normal . The hyperpolarization inhibits electrical activity in the parasite's cells, resulting in and eventual death of the organism, without directly killing it through . This mechanism targets parasites selectively because mammalian cells lack these specific GluCl channels, and moxidectin exhibits minimal interaction with mammalian GABA receptors at therapeutic doses. Selective toxicity in mammals is further enhanced by the blood-brain barrier, where (P-gp), an efflux transporter, actively pumps moxidectin out of the , limiting its penetration and preventing neurotoxic effects. In P-gp-deficient models, such as certain strains, moxidectin shows comparable brain penetration to related drugs but with a lower neurotoxic potential, approximately 2.7-fold less than , due to reduced affinity for mammalian receptors. Compared to , another macrocyclic lactone with a similar mechanism, moxidectin demonstrates higher potency and greater efficacy against certain parasites, such as Onchocerca volvulus microfilariae, often reducing parasite loads to undetectable levels where ivermectin falls short, owing to differences in binding affinity to GluCl subunits.

Moxidectin exhibits rapid absorption following in humans, with median peak plasma concentrations (T_max) achieved in 3-4 hours under fasted conditions. The absolute has not been directly determined in humans, but exposure is dose-proportional across 2-8 mg doses, and a high-fat increases the area under the curve (AUC) by approximately 44% and maximum concentration (C_max) by 34%, likely due to enhanced solubilization. The drug is highly lipophilic (log P = 5.4), resulting in a large apparent (V_z/F) of 2000-3000 L, which facilitates extensive tissue penetration and concentration in . This property enables slow release from stores, contributing to moxidectin's prolonged lasting up to 2 months post-dose. Metabolism of moxidectin is minimal (<10% of dose), occurring primarily in the liver via and enzymes to form hydroxylated metabolites, with no significant non-CYP pathways identified. Elimination is predominantly fecal, with the majority of the dose excreted unchanged via biliary routes independent of efflux, and negligible renal clearance. The terminal elimination in humans ranges from 20-35 days, substantially longer than that of , supporting extended parasite suppression. In pediatric patients aged 4 to 17 years weighing at least 13 kg, are similar to adults when dosed on a weight-based schedule (4 mg for 13 to <15 kg, 6 mg for 15 to <30 kg, 8 mg for ≥30 kg). Mean C_max values range from 39.5 ng/mL (4 mg dose) to 70.3 ng/mL (8 mg dose), with median T_max of 3.0 to 4.0 hours, AUC_inf from 3064 to 6980 day·ng/mL, and terminal approximately 18 to 28 days, based on data from a study of 36 patients as of 2025. In animals, pharmacokinetic profiles vary by species. Dogs show faster clearance with a terminal half-life of 10-26 days following oral or subcutaneous administration. In cattle, elimination is slower, with half-lives of 9-25 days in tissues such as fat and plasma after subcutaneous dosing, reflecting greater persistence.

Chemistry

Structure and properties

Moxidectin is a semi-synthetic macrocyclic belonging to the milbemycin subclass, derived from the natural product nemadectin produced by cyanogriseus subsp. noncyanogenus through chemical modification involving methoximation. Its molecular formula is C₃₇H₅₃NO₈, and it features a 16-membered pentacyclic ring system fused to an oxahydrindane spiroketal moiety, without the disaccharide substituent found in avermectins. Key structural elements include a methoxime group at carbon 23, a methyl functionality, and a substituted (E)-1,3-dimethylbut-1-enyl side chain at carbon 25, contributing to its lipophilic nature. Physically, moxidectin appears as a white to pale yellow crystalline powder with a of 145–154 °C. It is highly lipophilic, with an (logP) of approximately 5.4, and exhibits low water solubility at 0.51 mg/L ( 7, 20 °C), rendering it sparingly soluble in aqueous media but readily soluble in organic solvents such as and . Moxidectin is sensitive to degradation by ultraviolet and oxidation, which can lead to loss of potency; therefore, it is typically stored protected from in sealed containers at low temperatures, often formulated as capsules, oral solutions, or pour-on liquids to enhance stability and .

Production

Moxidectin is produced via a semi-synthetic that begins with the of the actinomycete bacterium cyanogriseus subsp. noncyanogenus, which naturally yields nemadectin as the key precursor compound. This step leverages the bacterium's metabolic pathways to generate nemadectin, a milbemycin-class macrocyclic , under controlled aerobic conditions in nutrient-rich media. Nemadectin undergoes chemical modification to form moxidectin, primarily through the addition of a methoxime group at the C-23 position, which enhances the molecule's and broadens its potency against parasitic nematodes and arthropods. This semi-synthetic alteration improves the precursor's pharmacokinetic properties without altering its core macrocyclic structure. At industrial scale, moxidectin production employs large bioreactors for high-yield of the strain, typically achieving nemadectin titers suitable for commercial output, followed by solvent extraction from the , chromatographic purification to isolate the desired fractions, and to yield the final active pharmaceutical ingredient. Key patents on this process, originally held by (now part of ), expired between 2010 and 2016, facilitating the entry of generic manufacturers and increased global supply. Quality control measures during production ensure moxidectin purity exceeds 94%, meeting pharmacopeial standards such as those of the , with residual solvents and impurities tightly regulated through validated analytical methods like HPLC. For veterinary applications, the purified moxidectin is formulated by blending with excipients—such as solvents, stabilizers, and carriers like or —to produce injectable suspensions or pour-on topicals, optimizing and shelf-life.

History

Discovery and early development

Moxidectin was isolated in the late 1980s from the bacterium cyanogriseus subsp. noncyanogenus, discovered in a sample collected from by an agronomist at the Company (now part of Animal Health). This strain, designated NRRL 15773, was identified through routine screening of environmental samples for novel antiparasitic compounds, building on the success of earlier -derived macrocyclic lactones like avermectins. The precursor to moxidectin, nemadectin (also known as LL-F28249α), was first identified in 1983 as a natural product of S. cyanogriseus subsp. noncyanogenus. Researchers at developed moxidectin as a semisynthetic derivative of nemadectin by introducing a methoxime group at the 23-position, aiming to broaden its spectrum of activity and extend its duration of action against nematodes. This modification enhanced the compound's potency while maintaining its milbemycin core structure, positioning it as a promising endectocide for veterinary applications. Early preclinical evaluation involved in vitro assays against helminth larvae and ectoparasites, demonstrating potent and lethality through glutamate-gated modulation. studies in and models further confirmed broad efficacy against gastrointestinal nematodes like Haemonchus contortus and external parasites such as ticks and mites, with low toxicity profiles. These results prompted the prototyping of initial veterinary formulations, including injectable and oral prototypes, by the late . Intellectual property for moxidectin's synthesis and use was secured through filed by in 1987 and 1988, following independent discoveries by Glaxo Group (later transferred to ). Key filings, such as U.S. 4,916,154, detailed the chemical derivatization and biological assays supporting its .

Regulatory milestones

Moxidectin was first approved for veterinary use by the U.S. (FDA) in 1998 for cattle under the brand name Cydectin as a pour-on to treat internal and external parasites. Subsequent expansions included approvals for injectable solutions in beef and nonlactating in 2005, qualifying for seven years of exclusive marketing rights due to its demonstration of safety and efficacy in food-producing animals. In the , moxidectin was included in Annex III of Regulation (EEC) No 2377/90 in November 1994, establishing maximum residue limits for cattle, sheep, and goats, which facilitated its marketing authorization for use across multiple species and . Development for human use began with preclinical research initiated by the World Health Organization's Special Programme for Research and Training in Tropical Diseases (WHO/TDR) in the late , focusing on its potential against filarial parasites. Phase 1 and 2 clinical trials were launched in 2006, led by WHO/TDR in collaboration with Medicines Development for (MDGH), evaluating , tolerability, and in onchocerciasis-endemic areas such as . Phase 3 trials, conducted from 2015 to 2017 across , , and the , compared a single 8 mg dose of moxidectin to , establishing its superior microfilaricidal activity while maintaining a comparable profile. The FDA granted approval for moxidectin tablets (8 mg) on June 13, 2018, as the first new treatment for due to in over two decades, initially indicated for patients aged 12 years and older. This approval was supported by the phase 3 data and leveraged a voucher, enabling expedited review. In February 2025, the FDA expanded the indication to include children aged 4 years and older weighing at least 13 kg, based on pharmacokinetic, safety, and efficacy data from studies in younger populations. Although not centrally authorized by the (EMA) for human use, moxidectin has been incorporated into national programs in endemic regions following FDA approval. In September 2025, moxidectin was added to the 2025 WHO Model List of (core list) for the treatment of , recognizing its role in accelerating elimination efforts in endemic areas. MDGH has supported access through donation programs and pilot implementations, including a community-directed treatment initiative launched in Ghana's Twifo Atti-Morkwa district in January 2025, providing biannual doses to residents of the district (population approximately 101,000) to evaluate integration into mass drug administration strategies. These efforts, funded by a US$1 million grant, aim to ensure affordable supply in low-resource settings while monitoring long-term safety and effectiveness.

References

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