Tebuconazole
DMI (demethylation inhibitors) Folicur 250EW
Squalene
1. IMIDAZOLES: thiobendazole, Flutriafol
Cell membrane carbendazim, prochloraz – Botrytis,
Septoria, Fusarium
Impact 125SC
Epoxiconazole
(ergosterol) 2. PYRIMIDINES
3. TRIAZOLES: Protective;
Opus 125SC
Propiconazole
(Curative); leaf greening Tilt 125SC
Rust > Septoria > (Erysiphe)
Resistance - single site-of-action C14
demethylase
Combat resistance by introducing
additional sites-of-action, increase
effect against Erysiphe and reduce
total cost of application.
Inh. of steroid reduction
MORPHOLINES: Δ14 reductase
Protective; (Curative)
Fenpropidin Tern 750
Erysiphe > rust Fenpropimorph Corbel
Two sites-of-action 750EC
Inh. of steroid isomerization
Oomycetes Δ8-Δ7 isomerase
partially systemic
Ergosterol
DIMETHOMORPH
Cellulose
Cell wall
biosynth.
(chitin; cellulose) inh.
Cell wall and -
membrane
• Electron transport complexes I-IV or ATP synthase
inhibitors starve cells of energy by preventing ATP
formation
• True Fungi AND Oomycetes
• Narrow spectrum, single-site MOA (resistance)
• Generally newer chemistries; lower rate
• Generally effective: inhibit spore germination,
penetration, mycelial growth (protective & curative)
• MOA cascades => synergy?
Complex I: Diflumetorim, Complex II: CARBOXAMIDES
(Tolfenpyrad, INS) PM Rust Boscalid, Bixafen Botrytis H+
FADH O2 H2O ADP ATP
Qi: Cyazofamid
NADH
Residual Oomycetes
In
II
SDH Qi
ATPsynth
I III IV ATP synthase
Q cyt bc1 Cyt c
NADH CoQ inhibitors
oxidoreductase oxidase
Qo
Cyt c
Out
H+ uncouplers: PYRIDINES
H+ H+ H+ H+ Protective Contact, good
Qo: STROBILURINS Protective; some curative (spore germ. residual effect. Mildew,
& mycelial growth, residual. Leaf greening Septoria > Rust blight & moulds Fluazinam
> (Erysiphe) Kresoxim methyl Mentor KrM150 Shirlan, Foliar. DP, WP, SC
Azoxystrobin Amistar 250SC Pyraclostrobin Comet 250EC
Energy
metabolism
glyphosate
EPSP inh
Glucose
Aromatic E4P F6P
EPSP
amino acids
isoxaflutole RuBP Rub CO2
sulcotrione HPPD HPPD Aclonifen
mesotrione inh PQ
PDS inh clomazone
Vit E DFF
PDS
H+ ATP PPOinh DXP
Bleaching
fomesafen
ROS
CHL
ATPsynth
PQ
PSII PSI
Thylakoid
H+ H2O PSII inh PSI inh membrane
Pigment diquat
diuron
atrazine synthesis paraquat ROS burning
NH4+
GluS Glutamine
GluS inh glufosinate
Light activation of ROS
florasulam, imazapyr,
non-SU imazethapyr
Glucose metsulfuron, tribenuron
SU thifensulfuron, rimsulfuron
NIC
Pyruvate ALS Br. chain Cytosol
ROS burning Stunting amino acids
Rub
CO2
Acetyl coA
Anthocyanin Twisting
ACC ACCase inh
ROS
FOPS: fenoxaprop, clodinafop
DIMS: clethodim
PSII PQ PSI
Fatty acid Plastid &
non- cytosol , ER
synthesis ACCase
Thiocarbamates: prosulfocarb.
H2O Thylakoid
membrane VLCFA
Chloracetamides metazachlor
Isoxazolines pyroxasulfone
Cellular metabolism
Neural (synaptic) inhibitors; Na K Cl channel modulators
(Inhibitory synapse) (Activatory synapse)
GABA synapse Cholinergic (ACh) synapse
Nerve impulse
Nerve impulse
Pyrethroids
Na+
Choline
Choline
transporter
GABA ACh Acetyl coA
Phenylpyrazoles Choline Phosphates
Avermectins Cl- AChE
GABA Neonicotinoids ACh
AcOH Carbamates
GABA
receptor Ach receptor
GABA activated
chloride channel
Nerve impulse
Nerve impulse
Hyperpolarization; Stimulated nerve
decreased nerve transmission transmission => tremors and
=> flaccid paralysis and death uncontrolled movement
Nerve or muscle
action
• Energy metabolism inhibitors starve cells of energy by
preventing ATP formation, resulting in paralysis.
• Fast to moderately fast acting
• MOA cascades => synergy?
Complex II
Beta-ketonitrile derivatives
Complex III Qi inh
ADP H ATP
Carboxanilides +
Flometoquin O2 H2O
FADH
In NADH
II
SDH Qi
Inhibitors of ATP synthase
ATPsynth
I III IV Diafenthiuron
NADH CoQ Q cyt bc1 Cyt c Organotin miticides
oxidoreductase oxidase Propargite, Tetradifon
Qo Cyt c
Out
Proton gradient
H+ H+ H+ H+ uncouplers
Chlorfenapyr
Complex I inh Complex III inh Complex IV inh
DNOC
METI acaricides Acequinocyl, Fluacrypyrim Aluminium
Rotenone Hydramethylnon phosphide
Cyanide, Phosphine
Energy
metabolism
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