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Review

Lethal Efficacy and Mode of Action of Indian Medicinal Plant Extracts Against Dengue Mosquito Vectors with an Overview of the Disease Burden in India

by
Indra Sarkar
and
Subhankar Kumar Sarkar
*
Entomology Laboratory, Department of Zoology, University of Kalyani, Nadia 741235, WB, India
*
Author to whom correspondence should be addressed.
Green Health 2026, 2(1), 3; https://doi.org/10.3390/greenhealth2010003
Submission received: 13 November 2025 / Revised: 9 January 2026 / Accepted: 12 January 2026 / Published: 22 January 2026
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Abstract

Dengue is the most concerning mosquito-borne neglected tropical disease globally. The disease is caused by the dengue virus (DENV) and transmitted by the vector mosquito species belonging to the genus Aedes Meigen, 1818, particularly Aedes aegypti (Linnaeus, 1762) and Aedes albopictus (Skuse, 1895). In 2024, global cases of dengue exceeded 7.6 million, with India reporting 233,519 cases. These statistics underscore the ongoing challenge of managing dengue outbreaks worldwide. For generations, tribal communities across India have employed medicinal plant-based extracts as mosquito and other insect repellents. Plant-based phytochemicals are largely preferred over synthetic insecticides due to their perceived safety, non-toxicity to non-target organisms, and environmental sustainability. This review provides a comprehensive overview of various phytochemicals extracted from Indian medicinal plants for their larvicidal activity against Aedes mosquitoes. Furthermore, the article also reviews the mode of action of these phytochemicals, including neurotoxicity, mitochondrial dysfunction, sterol carrier protein-2 inhibition, midgut cytotoxicity, insect growth regulation disruption, and antifeedant activity, which aids in formulating dengue vector control strategies. Based on this review, Ecbolin B from Ecbolium viride, Alizarin from Rubia cordifolia, and Azadirachtin from Azadirachta indica exhibited better larval mortality rates against Ae. aegypti, with LC50 values recorded at 0.70, 1.31, and 1.7 ppm, respectively.

1. Introduction

Dengue virus (DENV), classified under the Orthoflavivirus genus in the Flaviviridae family, is characterised as a spherical, enveloped virus with a lipid envelope [1]. The four DENV serotypes (DENV 1–4) are responsible for various dengue-related conditions, including dengue fever, dengue haemorrhagic fever, and dengue shock syndrome [1]. Additionally, in 2007, a new sylvatic strain, the fifth serotype DENV-5, was also detected during the screening of viral samples in a hospital in Sarawak, Malaysia [2]. While infection with one serotype confers long-lasting protective immunity against that specific type, it fails to protect against subsequent infections by the other three serotypes [1,3]. Consequently, individuals residing in areas of hyperendemic dengue are likely to experience multiple and sequential infections with all four dengue serotypes, primarily due to the absence of cross-protective neutralising antibodies [3]. Although all four serotypes can lead to severe dengue, the likelihood of experiencing severe disease markedly rises during a secondary infection with a heterologous serotype, primarily due to immune mechanisms, including antibody-dependent enhancement [4]. Nevertheless, severe dengue may also manifest during primary or subsequent infections, influenced by factors such as host immune status, age, comorbidities, and the virulence characteristics of the virus [5,6]. The genus Orthoflavivirus also consists of other notable human pathogens, such as West Nile virus, Japanese encephalitis virus, and yellow fever virus [7].
Dengue transmission to humans primarily occurs through the bites of infected Ae. aegypti and Ae. albopictus mosquitoes. Currently, dengue is considered the most significant arthropod-borne viral disease in terms of morbidity and mortality rates. Severe dengue, an infrequent outcome of both primary and secondary DENV infections, results from a combination of virological and host factors. These host and viral variables can be viewed as risk factors at the population level. Despite its substantial impact, dengue remains one of the most prevalent neglected tropical diseases worldwide [8].
The origin and development of DENV have been extensively explored. Early theories proposed an African origin with global dissemination through the slave trade. An alternative theory suggests that it originated in a forest cycle involving lower primates and canopy-dwelling mosquitoes in the Malay Peninsula [9]. DENV emerged in human populations from sylvatic precursors several centuries ago [10]. In recent times, the ongoing dengue epidemic has become a significant international public health concern, with more prevalence in the urban and semi-urban cities [11]. This urban prevalence has amplified the disease’s severity, as the densely populated nature of cities makes outbreak management particularly challenging.

1.1. Dengue Epidemic

The World Health Organization (WHO) has identified dengue transmission in all its regions, with over 125 countries considered dengue-endemic [12]. The expansion of dengue has been influenced by various factors, including increased global trade and tourism, urban population growth, inadequate infrastructure for water, sewage, and waste management, ineffective vector control policies, proliferation of Ae. aegypti mosquito vector, and simultaneous circulation of multiple DENV serotypes (hyperendemicity) [12].
During the 18th and 19th centuries, Ae. albopictus was the dominant day-biting mosquito species in most Asian cities. However, with the growth of the shipping industry, Ae. aegypti slowly replaced Ae. albopictus as the leading day-biting mosquito in these urban areas [13]. Initial accounts of significant outbreaks of a disease thought to potentially be dengue were documented on three continents (Asia, Africa, and North America) during the years 1779 and 1780 [14]. This expansion coincided with the circulation of four DENV serotypes and the manifestation of dengue haemorrhagic fever (DHF) [14]. By the mid-1970s, DHF became a leading cause of child mortality in affected areas. Since then, epidemics have grown more frequent, severe, and geographically widespread [13]. While major epidemics were uncommon in African regions before the 1980s, all four DENV serotypes are now present there [11]. Recently, in 2023, due to an ongoing outbreak and unexpected case surge, over five million infections were reported in more than 80 countries, with more than 5000 DENV-related fatalities documented in more than 100 countries throughout five WHO regions [11,15]. In the same year, Brazil, Peru, and Bolivia reported the most instances [11]. Several African nations, including Angola, Burkina Faso, Chad, Côte d’Ivoire, Egypt, Ethiopia, Guinea, Mali, Mauritius, São Tomé and Principe, Senegal, and Sudan, also experienced a dengue epidemic [11]. Pan American Health Organization data shows that case numbers in the first 4.5 months of 2024 are 238% higher than the previous year [16].

1.2. India’s Dengue Burden

In India, dengue is endemic in almost all states and has spread significantly in the last two decades (2000–2009 and 2010–2019), with repeated outbreaks and an 11-fold increase in the number of cases [17]. It is a matter of concern that the number of dengue cases is increasing at an alarming rate due to the expansion of the disease to new areas, which eventually causes massive outbreaks [17]. Dengue fever had a predominant urban distribution in the country a few decades earlier, but is now also reported from peri-urban as well as rural areas. Surveillance for dengue fever in India is conducted through a network of more than 600 sentinel hospitals under the National Vector Borne Disease Control Program (NVBDCP), Integrated Disease Surveillance Program (IDSP), and a network of 52 Virus Research and Diagnostic Laboratories (VRDL) established by the Department of Health Research [18]. The 2016 year was marked by widespread dengue outbreaks in India [19]. In 2023, India ranked among the top 20 nations with the highest reported cases and fatalities from dengue, surpassing the annual figures of the past five years [20]. Hence, it may be assumed that the dengue burden is grossly neglected in India [11].
Based on official NCVBDC 2023 data, Uttar Pradesh (35,402 cases) had the highest reported dengue case occurrences, followed by West Bengal (30,683 cases; data till 13 September 2023), Bihar (20,224 cases), Karnataka (19,300 cases), and Maharashtra (19,034 cases) (Figure 1). However, the states with the minimum dengue cases are Meghalaya (114 cases), Arunachal Pradesh (130 cases), Daman and Diu (284 cases), Sikkim (311 cases), and Lakshadweep (445 cases), of which Meghalaya was the safest with only 114 cases. The observed spatial heterogeneity among states illustrates the interplay between urban and peri-urban container-breeding ecology, as well as the patterns of monsoon amplification and the spread of disease across India’s most vulnerable states, which contribute to the emergence of epidemic conditions [21].

1.3. Dengue Vectors

Aedes aegypti (Linnaeus, 1762), commonly referred to as the Egyptian mosquito or yellow fever mosquito, is the main arthropod vector for transmission of dengue viruses. Ae. aegypti is known by two subspecies Ae. aegypti aegypti and Ae. aegypti formosus, each having distinct ecological characteristics and distributional patterns [22]. Ae. aegypti aegypti is a domestic form, whereas Ae. aegypti formosus is a sylvan form, and therefore it may be anticipated that the two subspecies behave differently in terms of the transmission of dengue virus [22]. Unlike other mosquito species, Ae. aegypti feeds during the day, peaking in the early morning and just before dusk [23]. Females typically take multiple blood meals per session, increasing disease transmission efficiency [24]. This species breeds in rainwater or freshwater stored in artificial or natural containers around human dwellings, like buckets, tyres, flower pots, overhead tanks, coconut shells, and discarded items above damp surfaces, making it well-suited for urban areas [23,25]. For this reason, targeting aquatic habitats to eradicate the immature stages of the mosquito is crucial for effectively diminishing population densities in the field.
A second vector, Ae. albopictus, the Asian tiger mosquito, is also reported for dengue transmission, but is considered a low-efficiency vector due to its limited anthropophilic properties [26]. However, an interesting fact about Ae. albopictus is that once it inhabits an area, its eradication becomes difficult, and constant surveillance and appropriate control strategies are required [27]. It may therefore be presumed that its widespread distribution is primarily human-mediated and accidental [28]. Ae. albopictus is currently recognised as one of the top 100 invasive species by the Invasive Species Specialist Group [29]. Additionally, Ae. albopictus exhibits ecological flexibility across various characteristics, including larval breeding habitats, feeding habits, and climatic adaptability, which enhance their capacity for dissemination and adjustment to novel environments, thereby affecting their coexistence with other vector species [30,31].
Moreover, some other species, such as Ae. polynesiensis Marks, 1951 (western Pacific region), Ae. mediovittatus (Coquillett, 1906) (Caribbean), and Ae. niveus (Ludlow, 1903), have been recognised as secondary vectors in specific geographical areas and ecological parameters [25,32].
Adult Aedes mosquitoes are distinct from other mosquito species because they feature slender black bodies that absorb all incoming radiation. Their abdomen, thorax, and legs exhibit unique alternating patterns of light and dark scales. Females have a tapered abdomen and shorter maxillary palps compared to their proboscis, setting them apart from males [33].

1.4. Virus Transmission and Mosquito Developmental Cycle

1.4.1. Virus Transmission

The primary mode of human transmission of the dengue virus is through the bite of an infected female Aedes mosquito. When a female mosquito consumes blood from an individual infected with dengue fever in the initial two to ten days of the disease, the virus infiltrates the cells lining its stomach and successfully infects them [11]. The dengue virus serotype DENV undergoes an incubation period of 7 to 14 days inside the mosquito body during which it spreads systemically from the midgut and migrates to the salivary glands and replicates, thereby enabling the mosquito to transmit the virus [11]. After this period, while biting a new host for a blood meal, the infected mosquito passes the DENV to the latest human host. The DENV must establish a connection, attach, and infiltrate the vulnerable host to access the host’s cellular machinery for its replication [34]. DENV has a broad cellular tropism in both mammalian and invertebrate hosts. In humans, it primarily targets mononuclear phagocyte lineage cells, including monocytes, macrophages, and dendritic cells, including resident Langerhans cells in the skin [11]. This wide range of DENV-permissive cells suggests that the virus requires a cell surface molecule that is universally available or utilises multiple receptors to facilitate infection [35]. In mosquito cells, DENV interacts with receptors like R80, R67, and heat shock protein 70 (Hsp70), while in mammalian cells, it engages with heparan sulphate, Hsp90, CD14, GRP78/BiP, a high-affinity laminin receptor, and several C-type lectin receptors (CLRs) [36].
Several viral factors, host genetic factors, including host genetics and pre-existing immunity, affect viral virulence [37]. Certain DENV strains multiply more easily in humans or in mosquito vectors, and they have a higher potential for spreading epidemics [11]. The accelerated diffusion and reduced extrinsic incubation periods associated with advanced replication in mosquitoes may aid the global spread of a specific strain [11]. Viruses that naturally shift between hosts are thought to evolve more slowly than host-specific viruses [34]. Co-infection rates vary greatly in different nations and areas and show a wide range of 5% to 50%. This has made it more crucial to comprehend how co-infections affect the clinical results of diseases [11].

1.4.2. Mosquito Developmental Cycle (Figure 2)

Aedes mosquitoes go through holometabolous development, transitioning from the immature stages of egg, larva (with four instars), and pupa to the fully developed adult mosquito [38]. The life cycle is influenced by environmental temperature, the availability of food, and the number of larvae present at the same breeding location.
  • Egg: Adult female mosquitoes deposit approximately 100 black-coloured eggs on a wet or moist surface in proximity to a water source, particularly in environments such as marshes, plant axils, tree holes, and even within water containers. Artificial objects like clay pots, bowls, cups, fountains, barrels, vases, and tyres serve as excellent sites for egg deposition [33]. When submerged in water, the eggs normally hatch within a period of 2 to 4 days. However, without water, their significant resistance to desiccation permits the eggs to remain viable for weeks, months, or even up to one year [39]. Their capacity to withstand prolonged periods of desiccation enables them to survive extreme cold and various other challenging climatic conditions.
  • Larva: The egg hatches and gives rise to the first instar larva. This is followed by three successive ecdyses, leading to the corresponding stages of the second, third, and fourth larval instars [23]. The hatching of larvae occurs only when completely immersed in water. This process takes several days to a week. However, some eggs may need multiple soakings before they hatch [33]. The larva positions itself upside down at an angle relative to the water surface. The larval diet consists of microorganisms present in the water. The larva possesses a short respiratory structure known as a siphon located on the eighth abdominal segment to absorb oxygen from the air above the water [23]. After three moults, the larva transforms into a pupa.
  • Pupa: A larva requires five days to transform into a pupa [40]. The pupa stays constantly on the water surface to breathe. At a temperature of around 27 °C, the pupal stage typically lasts for about two days. The mortality rate in pupae is remarkably low, indicating that the quantity of pupae present in the reservoir is directly proportional to the number of adults that have emerged [23]. The pupa undergoes further development until the adult mosquito’s body breaks through the pupal skin and leaves the water [40].
  • Adult: The adult mosquito emerges approximately two to three days after pupation [33]. Within two days of its emergence, mating occurs among adult mosquitoes. Male mosquitoes primarily feed on nectar sourced from flowers, while female mosquitoes exhibit hematophagy, as they aim to extract from the blood meal the essential nutrients required for the maturation of their ovaries and subsequent egg production. Although they are active during the day, their peak activity occurs at dawn and dusk. Following a feeding session, mosquitoes seek out water surfaces to deposit their eggs. They tend to thrive in close proximity to humans, particularly within homes and buildings where windows and doors remain open [41].
Greenhealth 02 00003 g002
Figure 2. Aedes mosquito developmental cycle. Created in BioRender. SARKAR, I. (2026) (Web application, BioRender, Toronto, ON, Canada) (https://BioRender.com/s0ask19, accessed on 28 December 2025) is licensed under CC BY 4.0.
Figure 2. Aedes mosquito developmental cycle. Created in BioRender. SARKAR, I. (2026) (Web application, BioRender, Toronto, ON, Canada) (https://BioRender.com/s0ask19, accessed on 28 December 2025) is licensed under CC BY 4.0.
Greenhealth 02 00003 g002

1.5. Synthetic Insecticides Used in Aedes Mosquito Control and Their Drawbacks

The control of the dengue vector is a critical strive, achievable through environmental, biological, and chemical strategies, such as eliminating breeding sites, leveraging natural predators, and applying insecticides. Among these, synthetic insecticides stand as the cornerstone in the battle against Aedes mosquitoes. The market is saturated with mosquito repellents, mainly featuring active ingredients like N, N-diethyl-meta-toluamide (DEET), IR3535, or picaridin, p-menthane-3, which can be applied to both fabrics and skin [42,43]. A recent study underscores the supremacy of DEET-based sprays, achieving over 70% efficacy in repelling both Ae. aegypti and Ae. albopictus for a minimum of four hours [40]. Although DEET is effective and provides superior protection, it is also toxic to the skin and nervous system, inhibiting ion channels and human acetylcholinesterase, and is involved in the modulation of G-protein-coupled receptors [44]. Research by Corbel et al. (2009) reveals that DEET inhibits cholinesterase and may induce neurotoxic effects in both insect and mammalian nervous systems [45]. Despite apprehensions about DEET’s side effects, with approximately 200 million applications annually, only 14 adverse incidents have been documented, primarily due to overuse [46]. However, the repeated use of all these active ingredients has led to mosquito resistance [42]. Resistance primarily arises from (i) knockdown of the gene encoding the target binding site of the insecticides (knockdown resistance mutation in voltage-gated sodium channel), and (ii) upregulation of mosquito detoxifying enzymes [47]. Regarding insecticides, pyrethroids, a class of WHO-recommended insecticide for indoor use due to their exceptional efficacy, minimal mammalian toxicity, and brief residual action, are the sole insecticides sanctioned for use on long-lasting insecticidal nets against mosquito vectors [47].
Fogging pesticides like malathion has been utilised for fogging purposes to mitigate the transmission of dengue in Southeast Asian nations for more than 25 years [48,49]. It exhibits relatively low toxicity to mammals, but is moderately toxic to some vertebrates such as fish and birds, and is characterised by slight stability, corrosiveness, and an unpleasant odour. Malathion is an insecticide classified as a parasympathetic agent, which irreversibly binds to the cholinesterase enzyme. A key mechanism contributing to the development of insecticide resistance is the enhanced activity of a detoxifying enzyme, specifically the esterase enzyme [48]. However, fogging is not enough to reduce dengue fever transmission since it mainly affects adult mosquitoes, and its effectiveness lasts only two days. Therefore, alternative insecticide methods should be explored to prevent Ae. aegypti mosquitoes from developing immunity.
Similar to mosquito repellents, there have been reports of resistance to larvicides like temephos. Aedes spp. have shown significant resistance to 1% temephos in regions such as Latin America (including Brazil, Cuba, Argentina, Peru, and Colombia), as well as in Thailand, Banjarmasin, and Indonesia [50]. Nevertheless, temephos continues to be the main option for eliminating mosquito larvae.
Consequently, there is an urgent need for the development of natural insecticides to mitigate the extensive dependence on synthetic alternatives, which have resulted in numerous toxicity issues affecting not only humans but also beneficial insects, aquatic organisms, and the environment [51]. For instance, various fish species, including Colossoma macropomum (Cuvier), Hyphessobrycon erythrostigma (Fowler), Paracheirodon axelrodi (Schultz), Nannostomus unifasciatus (Steindachner), and Otocinclus affinis (Steindachner), have demonstrated high sensitivity to the malathion insecticide, with LC50 values ranging from 111 to 1507 ppm. Notably, Nannostomus unifasciatus exhibited the highest sensitivity (LC50 = 111 ppm) [51,52].
Therefore, exploration and recognition of plant-derived substances are crucial for developing an alternative, secure, and sustainable strategy for vector control that also tackles the issue of resistance in mosquito populations.
It is with this background that the present critical review has been taken up to explore the potential of plant-derived molecules from Indian medicinal plants as a better alternative to synthetic insecticides for an effective yet safe and environmentally sustainable control of dengue mosquito vectors. Although adulticidal strategies such as fogging and personal repellents offer prompt relief, they are fundamentally reactive in nature. Focusing on vector mosquitoes during their larval stage is strategically advantageous, as larvae are immobile and found in specific aquatic environments. Eliminating the vector prior to the adult stage and its dispersal more effectively halts the cycle of transmission compared to short-term adulticidal strategies. The focus on phytochemicals tackles the growing issue of resistance. In contrast to single-molecule synthetic compounds, plant extracts comprise intricate combinations of bioactive secondary metabolites (such as alkaloids, terpenoids, and phenolics). These substances frequently produce synergistic, multi-target effects, leading to a considerable reduction in the selection pressure for resistance. Moreover, phytochemicals have better biodegradability, are target specific, show little or no toxicity to non-target organisms, and are environmentally sustainable.

2. Methodology

References for this study were retrieved from Scopus (https://www.scopus.com/, accessed on 12 August 2025), ScienceDirect (http://www.sciencedirect.com/, accessed on 15 August 2025), ISI Web of Science (https://www.isiknowledge.com/, accessed on 16 August 2025), Wiley (https://onlinelibrary.wiley.com/, accessed on 19 August 2025), Springer Link (https://link.springer.com/, accessed on 20 August 2025), and PubMed (http://www.ncbi.nlm.nih.gov/pubmed, accessed on 23 August 2025) databases. Additionally, an open search was also performed on Google (https://www.google.co.in/, accessed on 13 October 2025) for articles not indexed in the above-mentioned databases. Keywords and strings used to search relevant articles include (“Dengue”), (“Dengue virus”), (“DENV”), (“Botanical insecticides”), (“essential oil”), (“sustainable larvicides’’) (“Indian medicinal plant extract”), (“Phytochemicals”), (“larvicidal activity”), (“mosquito”), (“Aedes albopictus”), and (“Aedes aegypti”). Articles were read in full text to screen the year, objective, method of larvicidal assay, and research findings. Furthermore, the references provided in the reviewed literature were cross-examined to acquire more information. The inclusion criteria were as follows: (i) studies including in silico, in vitro, and in vivo assays of Indian ethnomedicinal plants (or plants available within the Indian subcontinent) assessed for their larvicidal efficacy against dengue mosquito vectors, and (ii) studies identifying active metabolites responsible for the larvicidal effects observed in these Indian plant species. The exclusion criteria include (i) research conducted on non-Indian plant species, (ii) clinical case reports and human drug trials, and (iii) publications in languages other than English, unreliable sources, and data that had not been published. A list of Indian ethnomedicinal plants having larvicidal activity against dengue mosquito vectors has been compiled along with the detected metabolites, lethal concentrations, and their mode of action. Studies showing the least value of a lethal concentration of active compounds from the medicinal plant extracts are specifically considered. The lethal concentrations were presented in mg/L or μg·mL−1 or ppm or % as per LC50/LC90/LD50 values and concentration of the active compound in a mixture or solution, respectively. The units mg/L, μg·mL−1, and ppm are essentially the same. In some instances, LC50 or LC90 or LD50 is mentioned in %, where the toxic agent is a mixture, natural product extract, or specific formulation, and is measured as a percentage of the total solution. The taxonomic validity of all plant names was verified with the Botanical Survey of India database. Moreover, the mode of action of all plant extracts, as revealed from the reviewed literature, is graphically presented herein. The graphical illustrations were created online on BioRender (https://biorender.com, accessed on 28 December 2025), and the gradient map depicting dengue cases in India was created utilising the online data visualisation platform Datawrapper (https://www.datawrapper.de/, accessed on 12 November 2025).

3. Indian Ethnomedicinal Plants as Sustainable Larvicides Against Aedes Mosquitoes

India’s extensive biodiversity and ethnobotanical heritage offer a robust foundation for sustainable vector control strategies, particularly mosquitoes, which are vectors for dengue, chikungunya, and Zika viruses. The country’s rich flora provides numerous plant-derived compounds with significant larvicidal activity, operating through diverse biochemical and physiological mechanisms.
The wide range of phytochemicals from Indian ethnomedicinal plants exhibits diverse modes of action, which primarily include the inhibition of critical enzymes, particularly those involved in detoxification and neuromuscular regulation (Table 1) (Figure 3, Figure 4 and Figure 5).
Table 1. List of Indian-origin ethnomedicinal plants having larvicidal activity against Aedes mosquitoes with their extracted lead compound/s and mode of action.
Table 1. List of Indian-origin ethnomedicinal plants having larvicidal activity against Aedes mosquitoes with their extracted lead compound/s and mode of action.
Plant Species (Family)
Common Name		Plant
Parts Used		Type of Extract (Solvent)Active Compound/s
(Chemical Formula)		Test Larval StageMode of ActionLethal ConcentrationsReference
Carica papaya Linnaeus
(Caricaceae)
Papeeta, Papaya		LeafLeaf extract
(Ethanol)		Carpaine
(C28H50N2O4)
(Figure 4A)		3rd and 4th instar larvae of Ae. aegyptiAChE inhibitionLC50-215.96 ppm[53]
Piper sarmentosum Roxb.
(Piperaceae)
Tippili, Pipul		RootsRoot extract
(Hexane)		Asaricin 1
(C11H12O3)
(Figure 4B),
Isoasarone 2
(C12H16O3)
(Figure 4C),
Trans-asarone 3
(C12H16O3)
(Figure 4D)		Late 3rd or early 4th larvae of Ae. aegypti, Ae. albopictusAcetylcholinesterase (AChE) inhibitionIC50-
0.73–2.24 μg/mL		[54]
Prangos pabularia Lindl.
(Apiaceae)
Komal		FruitsFruit oil extract
(Hydrodistillation)		Suberosin
(Figure 4E)		1-day-old Ae. aegypti larvaeSimilar to Coumarin, i.e., AChE inhibition.LC50-8.1 ppm[55]
Myristica fragrans Houtt.
(Myristicaceae)
Jaiphal, Jayapatri		SeedsSeed essential oil (Acetone)Sabinene
(C10H16)
(Figure 4F)		3rd instar larvae of Ae. aegyptiInhibition of AChE and butyrylcholinesterase (BChE)LC50-
28.2 μg/mL		[56]
Syzygium zeylanicum (Linnaeus) DC.
(Myrtaceae)
Bhedas (Mar.)		LeavesEssential oil (DMSO)α-humulene (C15H24)
(Figure 4G) and
β-elemene
(C15H24)
(Figure 4H)		Early 3rd instar larvae of Ae. albopictusDisrupts the function of cell membranes and enzymes, NeurotoxicLC50-
6.86 μg/mL (α-humulene)
and 11.15 μg/mL (β-elemene)		[57,58]
Euphorbia hirta Linnaeus
(Euphorbiaceae)
Dudhia		Leaf and stem barkPetroleum etherQuercitrin
(C21H20O11)
(Figure 4I)		Early 4th instar larvae of Ae. aegyptiDisrupt physiological processes and metabolic functions of larvae, neurotoxic,LC50-272.36 ppm[59,60]
Curcuma longa Linnaeus
(Zingiberaceae)
Haldi, Halada		RhizomesEssential oil
(Ethanol)		Ar-turmerone
(C15H20O)
(Figure 4J)		4th instar larvae of Ae. aegyptiInfluences
olfactory system mechanism, either in the periphery or in the
central nervous system.		LC50-2.5 ppm[61,62]
Annona muricata Linnaeus
(Annonaceae)
Mamphal		SeedSeed extract (Ethanol)Annonacin
(C35H64O7)
(Figure 4K)		4th instar larvae of Ae.
aegypti and
Ae. albopictus		Inhibition of
Complex I (NADH dehydrogenase) in the mitochondrial electron transport chain.		LC50-2.65 μg/mL
(Ae. aegypti),
8.34 μg/mL
(Ae. albopictus).
LC 90-4.83 μg/mL
(Ae. aegypti), 16.30 μg/mL
(Ae. albopictus).		[63]
Aegle marmelos (Linnaeus)
Corrêa
(Rutaceae)
Bel		LeafLeaf extract (Petroleum ether: Ethyl acetate)β-sitosterol
(C29H50O)
(Figure 4L)		Early 3rd instar larvae of Ae. aegyptiInhibition of the sterol carrier protein-2 (SCP-2)LC50-480.19 ppm[64]
Tinospora cordifolia (Willd.) Hook.f. & Thomson
(Menispermaceae)
Amrita, Giloe		Stem and leavesStem and leaf extract
(Ethanol)		Berberine
(C20H18NO4+)
(Figure 5A)		3rd instar larvae of Ae. aegyptiInhibition of Sterol Carrying Protein (SCP)-2LC50-100.64 ppm,
LC90-
386.37 ppm		[65]
Areca catechu Linnaeus
(Arecaceae)
Supari, Chaali		NutNut extract (Methanol)Arecaidine
(C7H11NO2)
(Figure 5B),
Dodecanoic acid (C12H24O2) (Figure 5C), Methyl tetradecanoate (C15H30O2)
(Figure 5D),
n-Tetradecanoic acid (C14H28O2)
(Figure 5E), and n-Hexadecanoic acid (C16H32O2)
(Figure 5F)		Early 4th instar larvae of Ae. aegypti and Ae. albopictsMidgut damageLC50-621
mg/L (Ae. aegypti), 636 mg/L (Ae. albopictus)		[66]
Acorus calamus Linnaeus
(Araceae)
Bach, Gora-bach		LeavesLeaf extract
(Hexane)		Asarone
(C12H16O3)
(Figure 5G)		3rd instar larvae of Ae. aegyptiMassive damage to midgut epithelial columnar cells and rupture of the peritrophic membrane.LC50-151.86 ppm
LC90-536.36 ppm		[67]
Limonia acidissima Linnaeus
(Rutaceae)
Kavat, Kadbel		LeavesFormulated essential oil (Steam distillation)Estragole
(C10H12O)
(Figure 5H)		3rd instar larvae of Ae. AegyptiAlters the level of major detoxifying enzymes, Glutathione S-transferases and CYP450, which is strongly deleterious to the survival of larvae.LC50-65.24 ppm
LC90-179.3 ppm		[68]
Ocimum sanctum Linnaeus
(Lamiaceae)
Tulsi		LeafLeaf extract (Methanol)Eugenol
(C10H12O2)
(Figure 5I)		4th instar larvae of Ae. aegyptiDamage to midgut epithelial cellsLC50-0.66%; LC90-1.38%).[69]
Ecbolium viride
(Forssk.) Alston
(Acanthaceae)
Udajati		RootsRoot extract (Ethyl acetate)Ecbolin B
(C22H22O8)
(Figure 5J)		3rd instar larvae of Ae. aegyptiSevere damage to midgut epithelial columnar cells and rupture of the peritrophic membrane.LC50-0.70 ppm
LC90-1.42 ppm		[70]
Leucas aspera (Willd.) Link
(Lamiaceae)
Safed Halkusa, Thumbai		Whole plantWhole plant
(Methanol)		Catechin
(C15H14O6)
(Figure 5K)		4th instar larvae of Ae. aegyptiDisruption of ion transport by inducing damage to the anal papillae and outer cuticular layer, mainly affecting the epithelial layer of the midgutLC50-3.05 ppm
LC90-8.25 ppm		[71]
Vitex trifolia Linnaeus
(Verbenaceae)
Pani-ki-sanbhalu, Sufed-sanbhalu		LeavesLeaf extract (Methanol)Methyl-p-hydroxybenzoate
(C8H8O3)
(Figure 5L)		Early 4th instar larvae of Ae. aegyptiDisruption of midget epithelial cellsLC50-4.74 ppm[72]
Andrographis paniculata (Burm. fil.) Nees
(Acanthaceae)
Kirayat		LeafLeaf extract (Ethanol)Andrographolide
(C20H30O5)
(Figure 6A)		4th instar larvae of Ae. aegyptiReduction in the regulation of detoxification enzymes α and β carboxylesterasesLC50-12 ppm [66]
Piper nigrum Linnaeus (Piperaceae)
Kala maricha		FruitsFruit extract
(Petroleum ether)		Pipnoohine
(C24H43NO)
(Figure 6B)
And pipyahyine (C24H33NO3)
(Figure 6C)		4th instar larvae of Ae. aegyptiInhibition of the activity of α- and β-carboxylesterase.LC50-35.0 ppm for Pipnoohine and LC50-30.0 ppm for pipyahyine[73,74]
Rubia cordifolia Linnaeus
(Rubiaceae)
Manjit, Manjitha		RootsRoot extract (Methanol)Alizarin (C14H8O4)
(Figure 6D)		3rd instar larvae of Ae. aegyptiStomach poisonLC50-1.31 ppm
LC90-6.04 ppm		[75]
Polygonum hydropiper Linnaeus
(Polygonaceae)
Pani-mari		LeavesEssential Oil (Hexane)Confertifolin (C15H22O2)
(Figure 6E)		2nd and 4th instar larvae of Ae. aegypti and Ae. albopictusDiscolouration, unnatural positions, incoordination, or rigour of the larvaeFor Ae. aegypti, 2.90 ppm (2nd instar) and 2.96 ppm (4th instar).
For Ae. albopictus, 2.02 ppm (2nd instar) and 3.16 ppm (4th instar)		[76,77]
Azadirachta indica
A. Juss. (Meliaceae)
Nim		Neem oilNeem oil formulation (with a mixture of polyoxyethylene ether,
sorbitan dioleate and epichlorohydrin)		Azadirachtin (C35H44O16)
(Figure 6F)		Late 3rd and 4th instar larvae of Ae. aegyptiGrowth inhibition by impacting the neuroendocrine regulatory pathways (blocking of prothoracicotropic hormone production and release, ecdysone production, oxidation of ecdysone to 20-hydroxyecdysone, and Juvenile hormone production and release).LC 50-1.7 ppm[78,79]
Catharanthus roseus (Linnaeus) G. Don
(Apocynaceae)
Nayantara		LeafLeaf extract (Chloroform)Ursolic acid (C30H48O3)
(Figure 6G)		3rd instar larvae of Ae. aegyptiAs a strong antifeedant and insect growth regulatorLC50-
40.09 ppm,
LC90-
189.15 ppm		[80]
Zingiber officinale Roscoe
(Zingiberaceae)
Adrak		RhizomeRhizome extract
(Petroleum ether)		4-gingerol
(C15H22O4)
(Figure 6H)		4th instar larvae of Ae. aegyptiAs an insect growth regulator (IGR) and insect antifeedantLC50-4.25 ppm[81]
Acacia nilotica (Linnaeus) Willd. ex Delile (Mimosaceae)
Kirkar, Babula		SeedSeed hydrodistilled essential
Oil (distilled water)		Hexadecane (C16H34)
(Figure 6I), Heptacosane (C27H56)
(Figure 6J)		4th instar larvae of Ae. aegyptiDisruption of the respiratory system by blocking the respiratory spiracles of larvaeLC50-3.174 mg/L
LC90-11.739 mg/L		[82,83,84]
Psidium guajava Linnaeus
(Myrtaceae)
Amrud, Safed safari		LeafLeaf extract
(Ethanol)		Quercetin
(C15H10O7)
(Figure 6K)		4th instar larvae of Ae. aegyptiInhibit reverse transcriptase enzyme activityLD50-11.384%.[85]
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Figure 6. Chemical structures of major secondary metabolites detected in medicinal plants: (A) Andrographolide, (B) Pipnoohine, (C) Pipyahyine, (D) Alizarin, (E) Confertifolin, (F) Azadirachtin, (G) Ursolic acid, (H) 4-gingerol, (I) Hexadecane, (J) Heptacosane, and (K) Quercetin.
Figure 6. Chemical structures of major secondary metabolites detected in medicinal plants: (A) Andrographolide, (B) Pipnoohine, (C) Pipyahyine, (D) Alizarin, (E) Confertifolin, (F) Azadirachtin, (G) Ursolic acid, (H) 4-gingerol, (I) Hexadecane, (J) Heptacosane, and (K) Quercetin.
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The diverse modes of action of different phytochemicals extracted from medicinal plants of Indian origin are discussed below.

3.1. Neurotoxicity: Acetylcholinesterase (AChE) Inhibition (Figure 7)

Several phytochemicals extracted from Indian medicinal plants, such as Carpaine (from Carica papaya), Asaricin 1, Isoasarone 2, Trans-asarone 3 (all from Piper sarmentosum), Suberosin (from Prangos pabularia), Sabinene (from Myristica fragrans), Arecoline (from Areca catechu), α-humulene and β-elemene (from Syzygium zeylanicum), Quercitrin (from Euphorbia hirta), inhibit the AChE activity [53,54,55,56,57,58,59,60,86]. Niloticin, derived from Limonia acidissima, also demonstrates significant efficacy as an AChE1 inhibitor against the larvae of Ae. aegypti [87]. AChE is an enzyme crucial for neuromuscular signalling. These compounds function as potent agonists of acetylcholine receptors, effectively mimicking the natural neurotransmitter to trigger continuous, uncontrolled nerve firing [88]. This is additionally reinforced by a secondary action where the compounds inhibit the AChE enzyme, causing a detrimental accumulation of acetylcholine [54,89,90]. The interplay of these synergistic mechanisms results in a fatal overstimulation of the larva’s nervous system, resulting in spasms, paralysis, and ultimately, death [87]. Larvicides targeting the olfactory and nervous systems provide another axis of mosquito control. Curcuma longa essential oil, rich in ar-turmerone, β-turmerone, and vanillin, interferes with the olfactory receptors of Ae. aegypti, affecting their behaviour and sensory-driven survival strategies [61,62]. These volatile compounds also exhibit neurotoxic properties, possibly by modulating synaptic transmission.
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Figure 7. Mechanism of inhibition of Acetylcholinesterase (AChE). Inhibitors like Azadirachtin and Carpaine block AChE activity, preventing the breakdown of ACh. This inhibition results in the accumulation of neurotransmitter within the synaptic cleft (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/mp9gjox, accessed on 14 October 2025) is licensed under CC BY 4.0.
Figure 7. Mechanism of inhibition of Acetylcholinesterase (AChE). Inhibitors like Azadirachtin and Carpaine block AChE activity, preventing the breakdown of ACh. This inhibition results in the accumulation of neurotransmitter within the synaptic cleft (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/mp9gjox, accessed on 14 October 2025) is licensed under CC BY 4.0.
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3.2. Mitochondrial Dysfunction (Figure 8)

Phytochemicals from plants like Annona muricata exhibit notable larvicidal effects against Aedes species by inducing significant mitochondrial dysfunction. The primary mechanism involves acetogenins, especially annonacin [63], which act as strong inhibitors of Complex I NADH dehydrogenase in the mitochondrial electron transport chain [91]. This targeted inhibition disrupts the entire respiratory process, leading to a marked reduction in Adenosine Triphosphate (ATP) production and depriving the larval cells of essential energy [92]. Furthermore, this blockage causes an ‘electron leak,’ which leads to an excess of reactive oxygen species (ROS). The rise in ROS results in considerable oxidative damage to cellular components and triggers apoptotic pathways, ultimately causing cell death and the demise of the larvae [92]. The LC50 values indicate significant potency: the fraction rich in acetogenins exhibited greater activity against Ae. albopictus (LC50 3.41 μg·mL−1) in comparison to Ae. aegypti (LC50 12.41 μg·mL−1), which signifies low concentrations necessary for effective larval control [63].
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Figure 8. Mechanism of mitochondrial dysfunction in the Aedes mosquito by Annonacin. Annonacin primarily inhibits Complex I within the electron transport chain (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/1k9088y, accessed on 11 October 2025) is licensed under CC BY 4.0.
Figure 8. Mechanism of mitochondrial dysfunction in the Aedes mosquito by Annonacin. Annonacin primarily inhibits Complex I within the electron transport chain (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/1k9088y, accessed on 11 October 2025) is licensed under CC BY 4.0.
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3.3. Sterol Carrier Protein-2 (SCP-2) Trafficking Inhibition (Figure 9)

Insects are unable to synthesize cholesterol de novo; instead, they are required to absorb phyto sterols and transport them through the midgut epithelium utilising sterol carrier proteins (particularly SCP-2), which is crucial for sterol absorption, growth, and reproductive success. The SCP-2 also plays a crucial role in steroid biosynthesis by facilitating the transfer of cholesterol to the mitochondria [64]. The inhibition of SCP-2 by β-sitosterol extracts derived from Aegle marmelos and Berberine extracts from Tinospora cordifolia is regarded as a promising therapeutic target for managing mosquito populations during their larval stage [64,65]. The inhibition of SCP-2 prevents mosquitoes from synthesising cholesterol from plant sterols, ultimately causing developmental deformities that result in larval mortality [64].
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Figure 9. Mechanism of sterol carrier protein-2 (SCP-2) inhibition in mosquito larvae by phytocompounds. Compounds like β-sitosterol and berberine inhibit SCP-2, leading to a cholesterol deficiency (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/l4z2hxs, accessed on 10 November 2025) is licensed under CC BY 4.0.
Figure 9. Mechanism of sterol carrier protein-2 (SCP-2) inhibition in mosquito larvae by phytocompounds. Compounds like β-sitosterol and berberine inhibit SCP-2, leading to a cholesterol deficiency (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/l4z2hxs, accessed on 10 November 2025) is licensed under CC BY 4.0.
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3.4. Epithelial Targets: Midgut Cytotoxicity and Peritrophic Membrane Failure

Another significant mechanism involves midgut disruption, which adversely affects nutrient absorption, digestion, and immune function. Notable examples include Areca catechu, Acorus calamus, Limonia acidissima, Ocimum sanctum, Ecbolium viride, Leucas aspera, and Vitex trifolia [66,67,68,69,70,71,72]. Andrographolide, derived from Andrographis paniculata, and Estragole, derived from Limonia acidissima, induce extensive midgut damage, characterised by epithelial cell vacuolation, peritrophic membrane disruption, and misalignment of the gut lining, alongside modulation of enzymes such as carboxylesterase (CoE), glutathione-S-transferase (GST), and cytochrome P450 (CYP450) [68,69,70,71,72,73]. Similar midgut lesions and swelling are observed in larvae treated with Acorus calamus, where cuticle transparency and gut bloating indicate internal haemorrhage and digestive failure [67]. O. sanctum primarily exerts its effects through saponins, which compromise the midgut epithelium, interfere with cholesterol in cell membranes, and reduce larval appetite and digestion, ultimately leading to starvation [69]. Ecbolium viride is particularly noteworthy in this context. Its active constituent, ecbolin B, results in malformed larvae and pupae, incomplete transitions between developmental stages, and damage to the peritrophic membrane. Cellular leakage and membrane rupture allow midgut contents to spill into inappropriate compartments, causing systemic failure and death [70]. Piper nigrum also causes epithelial erosion and impairs the regulation of detoxifying enzymes in the gut, resulting in the loss of digestive and protective functions [73,74]. Alizarin extracted from Rubia cordifolia Linnaeus shows stomach toxicity against 3rd instar larvae of Ae. aegypti [75]. Similarly, Confertifolin inflicts considerable harm on Ae. aegypti larvae by damaging their anal papillae, resulting in a shrunken cuticle and a compromised surface characterised by the loss of ridge-like reticulum [76,77].

3.5. Insect Growth Regulation (IGR) Disruption (Figure 10)

Azadirachtin functions as a potent insect growth disruptor by antagonising the two principal hormones that regulate insect development, 20-hydroxyecdysone (20E) and juvenile hormone (JH), thereby disrupting the critical hormonal balance necessary for proper developmental transitions [93]. The mechanism is complex, mainly characterised by the reduction in haemolymph ecdysteroid and juvenile hormone (JH) levels through the inhibition of the release of morphogenetic peptide hormones such as prothoracicotropic hormone (PTTH) and allatotropins. This disruption of the neuroendocrine system is further exacerbated by degenerative structural alterations that occur in the primary endocrine glands, namely the prothoracic gland, corpus allatum, and corpus cardiacum [78,94]. In addition to inhibiting hormone release, azadirachtin specifically affects the hormonal activation pathway by blocking ecdysone 20-monooxygenase, a cytochrome P450-dependent enzyme responsible for converting ecdysone into its more biologically active form, 20E [95]. This particular enzymatic inhibition has been shown in vitro, where the abdomens of the adult female mosquito, Ae. aegypti, incubated with radiolabelled ecdysone and azadirachtin, exhibited a dose-dependent decrease in ecdysone 20-monooxygenase activity [95]. The culmination of these disruptive actions on the endocrine system results in significant growth deregulation effects, which are typically characterised as diminished pupation, developmental abnormalities, and an inability for adults to emerge [93]. Similarly, ursolic acid from Catharanthus roseus and 4-gingerol from Zingiber officinale function as insect growth regulators (IGRs), inhibiting cuticle development and disrupting juvenile hormone balance [80,81].
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Figure 10. Mechanism of action of phytochemicals as insect growth regulators (IGRs) on the mosquito neuroendocrine system. Plant-derived compounds like azadirachtin, 4-gingerol, and ursolic acid disrupt the hormonal pathway that regulates moulting and metamorphosis (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/h7zx9sy, accessed on 14 October 2025) is licensed under CC BY 4.0.
Figure 10. Mechanism of action of phytochemicals as insect growth regulators (IGRs) on the mosquito neuroendocrine system. Plant-derived compounds like azadirachtin, 4-gingerol, and ursolic acid disrupt the hormonal pathway that regulates moulting and metamorphosis (for details, see text). Created in BioRender. SARKAR, I. (2026) (https://BioRender.com/h7zx9sy, accessed on 14 October 2025) is licensed under CC BY 4.0.
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3.6. Antifeedant Activity

Insects utilise an olfactory system to search out and identify potential food sources, subsequently engaging in chemoreception, referred to as primary antifeedant, which can validate the quality of the food and serve as a foundation for food selection and discrimination [96]. A signal sent to the brain triggers a response that leads to avoidance of further approach or feeding. The main antifeeding action of azadirachtin appears to be facilitated by gustatory chemosensilla and is associated with a reduction in the firing rate of sugar-sensitive cells within the gustatory chemoreceptors, which is triggered by the activation of bitter-sensitive gustatory cells [96]. Similarly, ursolic acid from Catharanthus roseus and 4-gingerol from Zingiber officinale exhibit antifeedant activity [80,81].

4. Discussion

A comparison between synthetic insecticides and plant-derived compounds for vector mosquito control reveals a trade-off between period of action and efficacy versus harmlessness and sustainability. Synthetic insecticides continue to be regarded as the benchmark for large-scale emergency interventions, owing to their swift “knockdown” effect and significant environmental stability. Their extended half-lives guarantee residual persistence, which is crucial for controlling mosquito populations in both urban and semi-urban settings. Additionally, synthetic insecticides are advantageous due to their standardised production processes and compatibility with current methods and equipment, including modern sprayers and thermal foggers. Nevertheless, these benefits are progressively undermined by the rising issue of physiological resistance and adverse impacts on non-target organisms. Conversely, phytochemicals offer a sustainable, multi-target alternative that significantly minimises the risk of resistance. Although they exhibit high bioactivity in laboratory environments, their implementation in field applications faces several critical challenges. Many potent botanical agents, including essential oils and terpenoids, possess a natural volatility and are highly susceptible to rapid photodegradation. As a result of this brief environmental half-life, there is a requirement for more regular re-application, significantly raising the labour costs and logistical demands associated with vector management programs in comparison to their synthetic alternatives. Furthermore, the utilisation of botanical larvicides in large urban areas commonly referred to as “megacities” introduces distinct challenges, frequently necessitating the use of specialised delivery mechanisms such as nano-encapsulation to prevent premature degradation in extreme, high-temperature aquatic environments. In contrast to synthetic chemicals, the effectiveness of plant extracts varies according to their geographical source and the season in which they are harvested, resulting in a significant industrial challenge for large-scale standardisation and scalability. In conclusion, although synthetic substances deliver enhanced immediate control and stability, phytochemicals play a crucial role in facilitating long-term resistance management. As innovative formulation technologies such as nano-encapsulation start to address these stability challenges, the shift towards plant-derived agents evolves from being a secondary option to becoming a primary requirement. Synthetic insecticides have long been used commercially on a large scale due to their rapid and cost-effectiveness, but these have significant drawbacks in terms of widespread resistance, human safety, and environmental sustainability. On the other hand, phytochemicals offer a safer, environmentally friendly, consistent, and sustainable alternative to synthetic insecticides for vector mosquito control.
Synthetic insecticides have been the backbone of mosquito control for decades. Common synthetic insecticides fall into four main classes, viz., pyrethroids, organophosphates, organochlorines, and carbamates. Most of these insecticides act as neurotoxins, disrupting the mosquito’s nervous system and leading to paralysis and death, providing rapid knockdown and effective mosquito population control. However, these synthetic insecticides have severe drawbacks as their continuous and heavy use led to widespread and increasing insecticide resistance in the global mosquito population. These synthetic insecticides also contaminate soil and water on a large scale and induce toxicity to non-target organisms, thereby posing health risks to humans and other animals, and also causing chronic ecological degradation, which is a matter of serious concern.
By contrast, well-known phytochemicals with medicinal properties include essential oils, neem-based compounds, pyrethrins, alkaloids, and flavonoids. Phytochemicals have a synergistic and more complex mode of action encompassing neurotoxicity, mitochondrial dysfunction, sterol carrier protein-2 inhibition, midgut cytotoxicity, insect growth regulation disruption, and antifeedant activity. These multiple modes of action offer a more flexible and easier alternative for the formulation of strategies to control mosquito populations, including dengue vectors.
For example, several phytochemicals have been identified as particularly effective, including Ecbolin B (from Ecbolium viride), Alizarin (from Rubia cordifolia), and Azadirachtin (from Azadirachta indica), which exhibit low LC50 values against Ae. aegypti larvae at 0.70, 1.31, and 1.7 ppm, respectively. The review also emphasises other highly potent compounds, such as Ar-turmerone (from Curcuma longa), with an LC50 of 2.5 ppm, and Annonacin (from Annona muricata), with an LC50 of 2.65 μg/mL. This notable lethality is attributed to their unique and potent biological disruptive properties. For instance, Alizarin functions as a direct stomach poison, while Azadirachtin acts as a robust insect growth regulator (IGR) and antifeedant by disrupting the neuroendocrine system. In addition to these compounds, the review delineates several other potent mechanisms of action. Neurotoxicity is a common mechanism, with compounds such as Carpaine (from Carica papaya) and Sabinene (from Myristica fragrans) inhibiting acetylcholinesterase (AChE). Other compounds induce fatal mitochondrial dysfunction, such as Annonacin, which inhibits Complex I of the electron transport chain. Midgut cytotoxicity is another critical pathway; Ecbolin B causes severe damage to midgut epithelial cells, as do Catechin (from Leucas aspera, LC50 3.05 ppm) and Methyl-p-hydroxybenzoate (from Vitex trifolia, LC50 4.74 ppm). Additionally, some compounds interfere with essential metabolic processes, such as β-sitosterol (Aegle marmelos) and Berberine (Tinospora cordifolia), which inhibit the sterol carrier protein-2 (SCP-2).
While the phytochemicals discussed in this study demonstrate significant potential, there are still various limitations that need to be addressed before these phytochemicals can be effectively used as insecticidal products.
Various factors may contribute to this discrepancy, including (i) the complex regulatory procedures associated with the registration of a pesticide product; (ii) the amount of raw material biomass necessary to yield an adequate extract and/or its isolated active ingredient; and (iii) the majority of research is performed at the laboratory level, frequently lacking field assessments to validate the application of the product.
Although researchers have found that various plants possess multiple compounds that serve as a powerful solution for eliminating mosquitoes. However, by prioritizing field effectiveness and exploring innovative formulations, such as botanical-derived nanoparticles, these phytochemicals could become the next generation of effective, environmentally friendly, and safe tools for addressing the global dengue challenges.

Author Contributions

I.S.: Conceptualisation, Methodology, Data curation, Data analysis and interpretation, Map and graphics preparation, Writing—Original draft. S.K.S.: Supervision, Conceptualisation, Visualisation, Data analysis and interpretation, Writing—Reviewing and editing final draft. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analysed in this study. Data sharing is not applicable to this article.

Acknowledgments

Authors are indebted to all researchers for their literature support.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. A gradient map of the number of dengue cases in India in 2023 (based on data retrieved from NCVBDC). Map: Indra Sarkar. Source: National Center for Vector-Borne Diseases Control (NCVBDC). Created with Datawrapper (Web application, Datawrapper GmbH, Berlin, Germany). (https://www.datawrapper.de/, accessed on 12 November 2025).
Figure 1. A gradient map of the number of dengue cases in India in 2023 (based on data retrieved from NCVBDC). Map: Indra Sarkar. Source: National Center for Vector-Borne Diseases Control (NCVBDC). Created with Datawrapper (Web application, Datawrapper GmbH, Berlin, Germany). (https://www.datawrapper.de/, accessed on 12 November 2025).
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Figure 3. Flow diagram outlining the review step by step and selection methodology.
Figure 3. Flow diagram outlining the review step by step and selection methodology.
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Figure 4. Chemical structures of major secondary metabolites detected in medicinal plants: (A) Carpaine, (B) Asaricin 1, (C) Isoasarone 2, (D) Trans-asarone 3, (E) Suberosin, (F) Sabinene, (G) α-humulene, (H) β-elemene, (I) Quercitrin, (J) Ar-turmerone, (K) Annonacin, and (L) β-sitosterol.
Figure 4. Chemical structures of major secondary metabolites detected in medicinal plants: (A) Carpaine, (B) Asaricin 1, (C) Isoasarone 2, (D) Trans-asarone 3, (E) Suberosin, (F) Sabinene, (G) α-humulene, (H) β-elemene, (I) Quercitrin, (J) Ar-turmerone, (K) Annonacin, and (L) β-sitosterol.
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Figure 5. Chemical structures of major secondary metabolites detected in medicinal plants. (A) Berberine, (B) Arecaidine, (C) Dodecanoic acid, (D) Methyl tetradecanoate, (E) n-Tetradecanoic acid, (F) n-Hexadecanoic acid, (G) Asarone, (H) Estragole, (I) Eugenol, (J) Ecbolin B, (K) Catechin, and (L) Methyl-p-hydroxybenzoate.
Figure 5. Chemical structures of major secondary metabolites detected in medicinal plants. (A) Berberine, (B) Arecaidine, (C) Dodecanoic acid, (D) Methyl tetradecanoate, (E) n-Tetradecanoic acid, (F) n-Hexadecanoic acid, (G) Asarone, (H) Estragole, (I) Eugenol, (J) Ecbolin B, (K) Catechin, and (L) Methyl-p-hydroxybenzoate.
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Sarkar, I.; Sarkar, S.K. Lethal Efficacy and Mode of Action of Indian Medicinal Plant Extracts Against Dengue Mosquito Vectors with an Overview of the Disease Burden in India. Green Health 2026, 2, 3. https://doi.org/10.3390/greenhealth2010003

AMA Style

Sarkar I, Sarkar SK. Lethal Efficacy and Mode of Action of Indian Medicinal Plant Extracts Against Dengue Mosquito Vectors with an Overview of the Disease Burden in India. Green Health. 2026; 2(1):3. https://doi.org/10.3390/greenhealth2010003

Chicago/Turabian Style

Sarkar, Indra, and Subhankar Kumar Sarkar. 2026. "Lethal Efficacy and Mode of Action of Indian Medicinal Plant Extracts Against Dengue Mosquito Vectors with an Overview of the Disease Burden in India" Green Health 2, no. 1: 3. https://doi.org/10.3390/greenhealth2010003

APA Style

Sarkar, I., & Sarkar, S. K. (2026). Lethal Efficacy and Mode of Action of Indian Medicinal Plant Extracts Against Dengue Mosquito Vectors with an Overview of the Disease Burden in India. Green Health, 2(1), 3. https://doi.org/10.3390/greenhealth2010003

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