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Fipronil 20% SC
Good-Job
China Insecticides Fipronil 20% SC manufacturer exporter and Supplier
-CHANGZHOU GOOD-JOB BIOCHEMICAL
Fipronil 20% SC
Fipronil is a broad spectrum Insecticide that disrupts the insect central nervous system by blocking the passage of chloride ions through the GABA receptor and glutamate-gated chloride channels (GluCl), components of the central nervous system. This causes hyperexcitation of contaminated insects’ nerves and muscles. Insect specificity of Fipronil may come from a better efficacy on GABA receptor but also on the fact that GluCl does not exist in mammals.
Fipronil is a slow acting poison. When mixed with a bait it allows the poisoned insect time to return to the colony or harborage. In cockroaches the feces and carcass can contain sufficient residual pesticide to kill others in the same nesting site. In ants, the sharing of the bait among colony members assists in the spreading of the poison throughout the colony. With the cascading effect, the projected kill rate is about 95% in 3 days for ants and cockroaches.
| A. I. Content | 20%, Min. |
| pH | 4.0 – 7.0 |
| Suspensibility | 85%, Min. |
| Wet sieve test(pass 44µm mesh) | 98%, Min. |
| S.G. | 1.120±0.025 |
| Appearance | Light yellow suspension |
Wildlife impacts include the following:
Fipronil is highly toxic to fish and aquatic invertebrates. Its tendency to bind to sediments and its low water solubility may reduce the potential hazard to aquatic wildlife.
Fipronil is toxic to bees and should not be applied to vegetation when bees are foraging.
Fipronil has been found to be highly toxic to upland game birds, but is practically non-toxic to waterfowl and other bird species (2,4). One of the metabolites of Fipronil has a higher toxicity to birds than the parent compound itself.
Mode of Action:
Target and Non-target Organisms
1. Fipronil is toxic to insects by contact or ingestion.
2. Fipronil blocks GABAA-gated chloride channels in the central nervous system. Disruption of the GABAA receptors by Fipronil prevents the uptake of chloride ions resulting in excess neuronal stimulation and death of the target insect.
3.Fipronil exhibits differential binding affinity for GABAA receptor subunits, with a higher binding affinity for insect receptor complexes compared to mammalian complexes. The lower binding affinity for mammalian receptors enhances selectivity for insects and increases the margin of safety for people and animals.
4.Fipronil-sulfone, the primary biological metabolite of Fipronil, is reported to be twenty times more active at mammalian chloride channels than at insect chloride channels. Fipronil-sulfone is reportedly six times more potent in blocking vertebrate GABA-gated chloride channels than Fipronil, but demonstrates similar toxicity to the parent compound in mammals.
5. Fipronil-desulfinyl, the primary environmental metabolite (photoproduct) of Fipronil, is 9-10 times more active at the mammalian chloride channel than the parent compound, reducing the selectivity between insects and humans when exposed to this metabolite.
China Insecticides Fipronil 20% SC manufacturer exporter and Supplier
-CHANGZHOU GOOD-JOB BIOCHEMICAL
Fipronil 20% SC
Fipronil is a broad spectrum Insecticide that disrupts the insect central nervous system by blocking the passage of chloride ions through the GABA receptor and glutamate-gated chloride channels (GluCl), components of the central nervous system. This causes hyperexcitation of contaminated insects’ nerves and muscles. Insect specificity of Fipronil may come from a better efficacy on GABA receptor but also on the fact that GluCl does not exist in mammals.
Fipronil is a slow acting poison. When mixed with a bait it allows the poisoned insect time to return to the colony or harborage. In cockroaches the feces and carcass can contain sufficient residual pesticide to kill others in the same nesting site. In ants, the sharing of the bait among colony members assists in the spreading of the poison throughout the colony. With the cascading effect, the projected kill rate is about 95% in 3 days for ants and cockroaches.
| A. I. Content | 20%, Min. |
| pH | 4.0 – 7.0 |
| Suspensibility | 85%, Min. |
| Wet sieve test(pass 44µm mesh) | 98%, Min. |
| S.G. | 1.120±0.025 |
| Appearance | Light yellow suspension |
Wildlife impacts include the following:
Fipronil is highly toxic to fish and aquatic invertebrates. Its tendency to bind to sediments and its low water solubility may reduce the potential hazard to aquatic wildlife.
Fipronil is toxic to bees and should not be applied to vegetation when bees are foraging.
Fipronil has been found to be highly toxic to upland game birds, but is practically non-toxic to waterfowl and other bird species (2,4). One of the metabolites of Fipronil has a higher toxicity to birds than the parent compound itself.
Mode of Action:
Target and Non-target Organisms
1. Fipronil is toxic to insects by contact or ingestion.
2. Fipronil blocks GABAA-gated chloride channels in the central nervous system. Disruption of the GABAA receptors by Fipronil prevents the uptake of chloride ions resulting in excess neuronal stimulation and death of the target insect.
3.Fipronil exhibits differential binding affinity for GABAA receptor subunits, with a higher binding affinity for insect receptor complexes compared to mammalian complexes. The lower binding affinity for mammalian receptors enhances selectivity for insects and increases the margin of safety for people and animals.
4.Fipronil-sulfone, the primary biological metabolite of Fipronil, is reported to be twenty times more active at mammalian chloride channels than at insect chloride channels. Fipronil-sulfone is reportedly six times more potent in blocking vertebrate GABA-gated chloride channels than Fipronil, but demonstrates similar toxicity to the parent compound in mammals.
5. Fipronil-desulfinyl, the primary environmental metabolite (photoproduct) of Fipronil, is 9-10 times more active at the mammalian chloride channel than the parent compound, reducing the selectivity between insects and humans when exposed to this metabolite.
