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Herbicide resistant weeds

Jeff L. Gunsolus, Extension agronomist - weed science
Reviewed 2008


Resistance of weeds to herbicides is not a unique phenomenon. In fact, resistance to pesticides is a world wide problem that is not confined to any single pest category. The first report of insects resistant to insecticides was in 1908, of plant pathogens resistant to fungicides in 1940, and of weeds resistant to herbicides (triazines) in 1968. By 1991,120 weed biotypes that were resistant to triazine herbicides and 15 other herbicide families were documented throughout the world. Results of a 1992 North Central Weed Science Society survey of the north central United States and Canada reflect a world wide trend of increasing appearance of herbicide resistance. Twelve states or provinces reported biotypes of 19 weed species resistant to triazine herbicides (Table 7). Five states or provinces reported biotypes of three weed species resistant to lipid biosynthesis inhibitors (Table 4), 10 states or provinces reported biotypes of four weed species resistant to amino acid biosynthesis inhibitors (Table 2), four states or provinces reported biotypes of two weed species resistant to dinitroaniline herbicides (Table 5), and Manitoba reported resistance of a wild mustard biotype to growth regulator herbicides (Table 1). Indeed, pests have proven to be ecologically and biochemically adaptable to agrichemicals.

Why worry about herbicide resistance?

In corn, soybean, and small grains there are many herbicide options. Why then should a crop producer be concerned whether a weed biotype is resistant to a particular herbicide? There are several reasons. Many herbicide options could quickly be lost for several crops if a weed biotype is resistant to more than one herbicide (i.e. cross resistance). Obviously, a loss of herbicide options could have important economic and environmental consequences to agriculture. Also, in an era of high re-registration costs for older herbicides and high development costs for new herbicides, the possibility for replacement of the herbicides lost due to resistance diminishes. Finally, in most cases, it will not be easy nor inexpensive to assess resistant weed biotypes. Due to cross resistance, many resistance problems may have to be solved by trial and error, which could be quite expensive to the crop producer.

The herbicide resistance issue does have solutions and perhaps the best place to start is to consider herbicides as a resource that needs to be preserved. Strategies for resistance prevention follow from there.



Figure 1 Enzymes--Enzymes function as steps in biological processes. Enzymes are also extremely specialized in their function. As a result, many different enzymes are involved with the many different biological processes that occur within a plant. Some herbicides can stop specific enzymes from functioning, resulting in a disruption of specific plant processes; this often leads to the death of the plant. This herbicide-enzyme relationship is very specific and any chemical modification of the herbicide or enzyme can eliminate herbicidal activity.


Figure 2 Photosynthetic Inhibitors--The photosynthetic process occurs within a plant cell's chloroplasts. Certain herbicides can inhibit photosynthesis by binding to specific sites within the chloroplast. The relationship of a herbicide to the chloroplast binding site is very specific and any modification of the herbicide or binding site can eliminate herbicidal activity.

Site of action refers to the biochemical site within the plant with which the herbicide directly interacts. Some herbicide site of action interactions are well understood, others are unknown. Many of the well-known sites of action are enzymes or proteins essential to plant growth and development (Figure 1 and Figure 2). Also, some herbicides are believed to act at multiple sites.

Metabolism refers to the biochemical processes within the plant that generally modify herbicides to less toxic compounds. Differential rates of metabolism between crops and weeds is a primary method of crop selectivity to herbicides. One metabolic process may affect several different families of herbicides.

Herbicide families are a convenient way of organizing herbicides that share a common chemical structure and have similar herbicidal activity. Two or more herbicide families may affect the same site of action and therefore express similar herbicidal activity and injury symptoms.

A biotype is a group of plants within a species that has biological traits that are not common to the population as a whole. For example, the Pursuit resistant corn hybrid Pioneer 3377 IR is a biotype of Pioneer 3377 and atrazine-resistant common lambsquarters is a biotype of common lambsquarters. Therefore, in most instances, specific biotypes are not easily recognizable by casual observation.

Selection intensity in regard to herbicide resistance is the degree to which weed control measures (e.g. herbicides) in a cropping system give a competitive advantage to a weed or crop biotype resistant to a particular herbicide.

Herbicide susceptibility means a particular weed or crop biotype is killed by the recommended use rate of the herbicide.

Herbicide resistance refers to the inherited ability of a weed or crop biotype to survive a herbicide application to which the original population was susceptible. Currently, the three known resistance mechanisms that plants employ are: an alteration of the herbicide site of action, metabolism of the herbicide, and removal of the herbicide from the target site (sequestration).

Herbicide cross resistance refers to a weed or crop biotype that has evolved a mechanism or mechanisms of resistance to one herbicide that also allows it to be resistant to other herbicides. Cross resistance can occur with herbicides within the same or in different herbicide families and with the same or different sites of action. For example, after the extensive use of herbicide A in a field, selection of a weed biotype resistant to herbicide A is found to also be resistant to herbicide B, although herbicide B was never used in that field.

Herbicide multiple resistance refers to a weed or crop biotype that has evolved mechanisms of resistance to more than one herbicide and the resistance was brought about by separate selection processes. For example, after a weed or crop biotype developed resistance to herbicide A, then herbicide B was used and resistance evolved to herbicide B. The plant is now resistant to herbicides A and B through two separate selection processes.

How does selection of resistant weed biotypes occur?


Figure 3 Selection for herbicide resistance begins when a herbicide resistant biotype survives a particular herbicide application. The resistant biotype survives, matures, and sets seed. If the same herbicide continues to be applied and the resistant weeds reproduce, eventually the majority of the weeds will be resistant to the herbicide.

Selection for change in weed populations begins when a small number of plants (a biotype) within a weed species have a genetic makeup that enables them to survive a particular herbicide application. Where this difference in genetic makeup originated is not clear. However, herbicides are not known to directly cause the genetic change (i.e. mutation) that allows resistance. The resistant biotype, therefore, is present in low numbers in natural populations and when a herbicide is applied, most of the susceptible weeds die but the few resistant weeds survive, mature, and produce seed. If the same herbicide continues to be applied and the resistant weeds reproduce, the percentage of the weed population that is resistant will increase (Figure 3).

It is difficult to predict exactly which weed species will have biotypes resistant to a given herbicide. However, we have learned from previous pesticide resistance problems that the occurrence of herbicide resistant weeds is linked directly to the herbicide program used, the weed species present, and the crop management practices employed.

Selection intensity - the key to prevention

Selection intensity acts, in a sense, like a filter that can screen out susceptible weed biotypes while leaving resistant biotypes. Herbicides by definition are effective weed killers; therefore, they have the potential to exert heavy selection intensity on weeds. The more susceptible a weed species is to a given herbicide (i.e. the greater the weed control) the greater the selection intensity. As a result, the rate of selection for resistance can be quite rapid if the same herbicide or herbicides with the same site of action are repeatedly used in a particular field.


Figure 4 Simulated progression of resistant kochia exposed to repeated annual applications of Glean. This simulation assumes an initial seed population of 100,000/m2 with a 1 in 10,000,000 occurrence of resistant biotypes in the initial population and 90% weed control.

With such highly effective herbicides, one would think that the increase in the number of herbicide resistant biotypes would be readily observable. This is not the case. Resistant biotypes generally are only detectable when they make up about 30% of the population. During the first several years of a weed control program that relies on only one herbicide, the proportion of resistant biotypes is very low (less than 1% of the population). As long as the application of this herbicide continues and the resistant biotypes reproduce, the proportion of the population that is resistant will increase. It is very common to go from excellent control of a particular weed species to very poor control within one growing season. A gradual decline in performance is seldom seen. Figure 4 illustrates the predicted rapid increase in the proportion of a kochia population that is resistant following repeated annual applications of the sulfonylurea herbicide Glean. In field situations, resistance to sulfonylurea herbicides has been reported to occur after 3 to 5 years of repeated use. With triazine herbicides, resistance has generally appeared after seven or more years of repeated use. Therefore, depending upon the proportion of the population that was initially resistant to a herbicide, repeated use of a product for more than two years could develop a herbicide resistance problem.

Herbicide factors that increase selection intensity

The herbicide characteristics that affect herbicide resistance are as follows:

  1. Herbicides that act on a single site of action.
  2. Herbicides that are applied multiple times during the growing season.
  3. Herbicides used for several consecutive growing seasons or repeated application of herbicides with the same site of action to the same or different crops.
  4. Herbicides used without other weed control options (e.g. cultivation) and are considered "stand alone" weed control programs.

Single site of action herbicides


Figure 5 Development of resistance to single site of action herbicides is more likely than to multiple site of action herbicides because a change (mutation) in only one gene may be enough to affect a herbicide's binding potential to a single action site. It is less likely that the appropriate mutations will occur at multiple action sites.

Several herbicide families interfere with only a single site of action. Tables 2 - 5 and 7 - 9 list the herbicides associated with specific sites of action. Herbicides that interfere with single sites of action are generally more likely to select for resistant weeds because a change in only one gene may be enough to affect a herbicide's binding potential to the site of action. Therefore, it is more probable that a resistant weed population will develop if a difference of only one gene is required (Figure 5).

Multiple site of action herbicides

Based on the line of reasoning presented for single site of action herbicides, if a herbicide has multiple action sites it is less likely existing biotypes will have the genetic differences at all of the sites of action that will result in resistance (Figure 5). Therefore, it is less likely that weeds will evolve resistance to herbicides with multiple action sites. Tables 1 and 6 list herbicides with multiple sites of action.

Herbicide cross resistance and site of action


Figure 6. Changes (mutations) in a site of action may or may not result in resistance to other herbicides in the same family or that interact at the same site of action. The outcome is dependent upon the herbicide site of action relationship. For example, herbicides A and B may share part of a binding site on a particular enzyme, whereas herbicide C may bind at an entirely different site on the enzyme. Therefore, a genetic change that affects the enzyme may have different effects on any particular herbicide-enzyme relationship and any corresponding effects on crop injury or weed control.

A change in a site of action that results in resistance to a particular herbicide may or may not result in resistance to other herbicides that are active at the same site of action. The reason for this is there can be many different binding sites at a particular site of action (e.g. an enzyme) and those binding sites can be very herbicide specific. Therefore, several different herbicides may bind to the same enzyme but at different sites on the enzyme (Figure 6). As a result, it is not possible to predict herbicide cross resistance; however, the greatest potential for herbicide cross resistance exists among herbicides of the same family and having the same site of action.

To illustrate cross resistance, both the imidazolinone (e.g. Pursuit and Scepter) and sulfonylurea (e.g. Classic) herbicide families are ALS enzyme inhibitors (Table 2). However, imidazolinone resistant (IR) corn hybrids are resistant to imidazolinone herbicides and are cross resistant to the sulfonylurea herbicides. The imidazolinone tolerant (IT) corn hybrids are resistant to Pursuit and soil-applied Scepter but are not cross resistant to sulfonylurea herbicides.

Herbicide resistance via altered metabolism

Regardless of whether a herbicide is active at single or multiple site(s) of action, it is often metabolized by crops or weeds before reaching the primary site(s) of action. Therefore, the rate at which a herbicide is metabolized plays a key role in determining crop injury and weed control. The genetic regulation of a metabolic process will influence the likelihood of developing herbicide resistance due to altered metabolism. For example, a change in only one gene has altered the rate of metabolism of atrazine in some biotypes of atrazine-resistant velvetleaf (Abutilon theophrasti). Most metabolic processes are thought to be controlled by multiple genes, thereby reducing the probability but not eliminating the possibility of weed biotypes that are resistant to herbicides due to enhanced metabolic capabilities or altered metabolic processes. Metabolic resistance could be especially challenging if it were to occur, because a metabolic process often affects several families of herbicides that do not share a common site of action. Regardless of the resistance mechanism, the key to prevention of herbicide resistance is to reduce the selection intensity.

Weed characteristics that favor resistance

Weeds, by their nature, have a diverse genetic background that gives them the ability to adapt to many different environments. For example, the repeated mowing of a lawn selects for low growing plants that avoid or are not affected by repeated cutting. Therefore, it should not be surprising that weeds can adapt to certain herbicide programs. Weeds with a diverse genetic background may have a resistant biotype that has a 1 in 1 million chance of occurring within a weed population. Although these odds sound remote, a 1 in 1 million chance of occurrence can translate into a high probability of selecting for a herbicide resistant weed biotype unless proper methods to reduce selection intensity are used.

As a herbicide resistant biotype becomes more predominant in the weed population, two factors increase in importance:

  1. Weed reproductive capability.
  2. Weed seed dispersal mechanisms.

The greater the reproductive success of the resistant biotype, the greater its potential to spread and become a dominant part of the population. Due to the extended viability of most weed seeds, once established, a herbicide resistant biotype will be difficult to eliminate from the population, even if extensive remedial weed control measures are used. Weeds such as kochia can tumble for miles spreading seed onto previously uninfested land. As a result of the diverse seed dispersal mechanisms of weeds, it is apparent that a farm manager must always use good herbicide resistance management strategies to prevent resistant biotypes from developing on the land and prohibit the establishment of resistant weed biotypes spreading from adjacent lands or from custom harvesting equipment and other machinery.

Diagnosing herbicide resistant weeds

Before assuming that any weeds surviving a herbicide application are resistant, rule out other factors that might have affected herbicide performance. Several factors would be misapplication, unfavorable weather conditions, improper timing of herbicide application, and weed flushes after application of a non-residual herbicide. If resistance appears to be a likely possibility, check for the following:

  1. Are other weeds listed on the product label controlled satisfactorily? Chances are only one weed species will show herbicide resistance in any given field situation. Therefore, if several normally susceptible weed species are present, reconsider factors other than herbicide resistance as the cause of the lack of weed control.
  2. Did the same herbicide or herbicide with the same site of action fail in the same area of the field in the previous year?
  3. Do field histories indicate extensive use of the same herbicide or herbicide site of action year after year?

If one or more of these three situations apply, it is possible that the weeds are resistant to the herbicide. If resistance is suspected, control the weeds with a labeled herbicide having another site of action or use appropriate nonchemical weed control methods to prevent the weeds from going to seed. Next, contact your local crop consultant or extension agent, state weed specialist, and the appropriate chemical company to develop a comprehensive weed control program to manage the problem.

Herbicide resistant crops

Recent research efforts have been directed at breeding herbicide resistance into crops. For minor-use crops it may be more economical to breed herbicide resistance into a crop than to develop new selective herbicides for current crop varieties. For major-use crops such as corn, soybeans, and wheat, herbicide resistant crops may be useful where difficult to control weeds or environmental conditions dictate the use of specific herbicides to which the crop is normally susceptible.

The use of herbicide resistant crops could enhance the potential for selecting for herbicide resistant weeds unless careful management practices are followed. The key, once again, is selection intensity. Misuse of herbicide resistant crops could encourage the use of a single herbicide or herbicide family over several crop rotations, thereby enhancing the selection intensity for herbicide resistant weeds.

Herbicide resistant crop varieties or hybrids need to be carefully evaluated for other performance characteristics (e.g. yield) and these characteristics should be compared to all other suitable hybrids or varieties in the marketplace, whether they have herbicide resistance or not. This will ensure that crop producers are getting the best overall agronomic value for their money. It will also be very important that accurate records be kept of the exact planting location of the herbicide resistant crops to avoid herbicide misapplication.

Management strategies for avoiding and managing herbicide resistant weeds

The North Central Weed Science Society (NCWSS) Herbicide Resistance Committee has developed the following list of strategies for avoiding and managing problems with herbicide resistant weed biotypes. Keep in mind that reliance upon any one strategy is not likely to be effective. The crop producer must use the following strategies in carefully selected combinations if herbicide resistant weed problems are to be avoided or properly managed.

  1. Use herbicides only when necessary. Where available, herbicide applications should be based on economic thresholds. Continued development of effective economic threshold models should be helpful.
  2. Rotate herbicides (sites of action). Do not make more than two consecutive applications of herbicides with the same site of action to the same field unless other effective control practices are also included in the management system. Two consecutive applications could be single annual applications for two years, or two split applications in one year.
  3. Apply herbicides in tank-mixed, prepackaged, or sequential mixtures that include multiple sites of action. Both herbicides, however, must have substantial activity against potentially resistant weeds for this strategy to be effective. Remember that in the past, weeds that were selected for herbicide resistance often were not the primary target species. It may be expensive to apply herbicide combinations that duplicate a wide spectrum of weed control activity. Many of the more economical herbicide combinations may not be adequate. Table 10 is a cross reference list of package mixtures and their corresponding sites of action.
  4. Rotate crops, particularly those with different life cycles (e.g. winter annuals such as winter wheat, perennials such as alfalfa, summer annuals such as corn or soybeans). At the same time, remember not to use herbicides with the same site of action in these different crops against the same weed unless other effective control practices are also included in the management system.
  5. Planting new herbicide resistant crop varieties should not result in more than two consecutive applications of herbicides with the same site of action against the same weed unless other effective control practices are also included in the management system.
  6. Combine, where feasible, mechanical weed control practices such as rotary hoeing and cultivation with herbicide treatments.
  7. Include, where soil erosion potential is minimal, primary tillage as a component of the weed management program.
  8. Scout fields regularly and identify weeds present. Respond quickly to changes in weed populations to restrict spread of weeds that may have been selected for resistance.
  9. Clean tillage and harvest equipment before moving from fields infested with resistant weeds to those that are not.
  10. Encourage railroads, public utilities, highway departments and similar organizations that use total vegetation control programs should be encouraged to use vegetation management systems that do not lead to selection of herbicide resistant weeds. Resistant weeds from total vegetation control areas frequently spread to cropland. Chemical companies, state and federal agencies, and farm organizations can all help in this effort.


The author would like to acknowledge the members of the 1991 and 1992 North Central Weed Science Society (NCWSS) Herbicide Resistance Committees who developed the ten management strategies for avoiding and managing herbicide resistant weeds listed in this publication and extensively reviewed this publication. The members are as follows: Thomas Bauman, T. Robert Dill, Ray Forney, R. Gordon Harvey (Chair-1991), Nick Jordan, Rex Liebl, Michael Owen, Jamie Retzinger, Dave Stoltenberg, G. Chris Weed, Phil Westra, Gail Wicks, and Bill Witt. It has been my pleasure to serve as Vice-chair and Chair of this committee in 1991 and 1992, respectively, and to work with these dedicated people.

The author would also like to thank the American Cyanamid Company for the use of Figures 3 and 5, B.D. Maxwell for Figure 4, and J.J. Kells for Figure 6.


Green, M.B., H.M. LeBaron, and W.K. Moberg (Editors), 1990. Managing Resistance to Agrochemicals: From Fundamental Research to Practical Strategies. American Chemical Society, Symposium Series No. 421. 496 pp.

Gressel, J. 1992. Addressing Real Weed Science Needs with Innovations. Weed Technology. Vol 6:509-525.

Gunsolus, J.L., and W.S. Curran. 1992 (revised). Herbicide Mode of Action and Injury Symptoms CD-ROM.

Maxwell, B.D., M.L. Roush, and S.R. Radesevich. 1990. Predicting the Evolution and Dynamics of Herbicide Resistance in Weed Populations. Weed Technology. Vol. 4:2- 13.

Table 1. Cross reference list of herbicide trade names and common names classified as growth regulators

Trade * Name Common Name Trade * Name Common Name
Banvel Dicamba Stinger Clopyralid
Butyrac 2,4-DB Tordon 22K ** Picloram
Clarity Dicamba 2,4-D Amine, others 2,4-D Amine
MCPA Amine, others MCPA Amine 2,4-D Ester, others 2,4-D Ester
MCPA Ester, others MCPA Ester 2,4-DB 2,4-DB

Table 2. Cross reference list of herbicide trade names and common names classified as amino acid synthesis (ALS synthase enzyme) inhibitors.

Trade * Name Common Name Trade *Name Common Name
Accent Nicosulfuron Express Tribenuron
Ally Metsulfuron Glean Chlorsulfuron
Amber Triasulfuron Harmony Thifensulfuron
Assert Imazamethabenz Harmony Extra Tribenuron + Thifensulfuron
Beacon Primisulfuron Pinnacle Thifensulfuron
Broadstrike Flumetsulam Pursuit Imazethapyr
Classic Chlorimuron Scepter Imazaquin

Table 3. Cross reference list of herbicide trade names and common names classified as amino acid synthesis (EPSP synthase enzyme) inhibitors.

Trade * Name Common Name Trade * Name Common Name
Honcho Glyphosate Rodeo Glyphosate
Jury Glyphosate Roundup Glyphosate
Mirage Glyphosate Ruler Glyphosate
Ranger Glyphosate Show-Off Glyphosate
Rattler Glyphosate Silhouette Glyphosate

Table 4. Cross reference list of herbicide trade names and common names classified as lipid (Acetyl-CoA carboxylase enzyme) inhibitors.

Trade * Name Common Name Trade * Name Common Name
Assure II Quizalofop Option II Fenoxaprop
Fusilade 2000 Fluazifop Poast Sethoxydim
Fusilade DX Fluazifop Poast Plus Sethoxydim
Fusion Fluazifop + Fenoxaprop Select Clethodim
Hoelon ** Diclofop Whip Fenoxaprop

Table 5. Cross reference list of herbicide trade names and common names classified as seedling root (tubulin protein) inhibitors.

Trade * Name Common Name Trade * Name Common Name
Balan Benefin Treflan Trifluralin
Basalin Fluchloralin Trific Trifluralin
Prowl Pendimethalin Trillin Trifluralin
Sonalan Ethalfluralin

Table 6. Cross reference list of herbicide trade names and common names classified as seedling shoot inhibitors.

Trade * Name Common Name Trade * Name Common Name
Arena ** Alachlor Frontier Dimethenamid
Confidence ** Alachlor Harness Plus ** Acetochlor + Safener
Cropstar ** Alachlor Judge ** Alachlor
Dual Metolachlor Lasso ** Alachlor
Eptam EPTC Partner ** Alachlor
Eradicane EPTC + Dichlormid Ramrod Propachlor
Eradicane Extra EPTC + Dichlormid + Dietholate Stall ** Alachlor
Far-Go Triallate Surpass ** Acetochlor + Dichlormid
Sutan Butylate + Dichlormid

Table 7. Cross reference list of herbicide trade names and common names classified as photosynthesis (D-1 quinone-binding protein) inhibitors.

Trade * Name Common Name Trade * Name Common Name
Atrazine ** Atrazine Lexone Metribuzin
Basagran Bentazon Linex Linuron
Bladex ** Cyanazine Lorox Linuron
Buctril Bromoxynil Princep Simazine
Buctril-Atrazine ** Bromoxynil + Atrazine Sencor Metribuzin
Evik Ametryn Sinbar Terbacil
Extrazine II ** Cyanazine + Atrazine Spike Tebuthiuron
Hyvar XL Bromacil Tough Pyridate
Laddok ** Bentazon + Atrazine Velpar Hexazinone

Table 8. Cross reference list of herbicide trade names and common names classified as cell membrane disrupters.

Trade * Name Common Name Trade * Name Common Name
Activated by Photosystem I Inhibit Protoporhyrinogen Oxidase
Avenge Difenzoquat Blazer Acifluorfen
Cyclone ** Paraquat Cobra Lactofen
Gramoxone Extra ** Paraquat Reflex Fomesafen

Table 9. Cross reference list of herbicide trade names and common names classified as pigment inhibitors.

Trade * Name Common Name Trade * Name Common Name
Command Clomazone Zorial Norflurazon

Table 10. Cross reference list of package mixture trade names and common names and their corresponding sites of action.

Trade * Name Common Name Reference Table Trade * Name Common Name Reference Table
Bicep ** Atrazine + Metolachlor 7 + 6 Galaxy Bentazon + Acifluorfen 7 + 8
Broadstrike + Dual Flumetsulam + Metolachlor 2 + 6 Gemini Linuron + Chlorimuron 7 + 2
Broadstrike + Treflan Flumetsulam + Trifluralin 2 + 5 Harmony Extra Tribenuron + Thifensulfuron 2 + 2
Bronate Bromoxynil + MCPA 7 + 1 Laddok ** Bentazon + Atrazine 7 + 7
Bronco ** Alachlor + Glyphosate 6 + 3 Landmaster Glyphosate + 2,4-D 3 + 1
Buckle Triallate + Trifluralin 6 + 5 Lariat ** Alachlor + Atrazine 6 + 7
Buctril-Atrazine ** Bromoxynil + Atrazine 7 + 7 Lasso + Atrazine ** Alachlor + Atrazine 6 + 7
Bullet ** Alachlor + Atrazine 6 + 7 Lorox Plus Linuron + Chlorimuron 7 + 2
Cannon ** Alachlor + Trifluralin 6 + 5 Marksman ** Dicamba + Atrazine 1 + 7
Canopy Chlorimuron + Metribuzin 2 + 7 Passport Trifluralin + Imazethapyr 5 + 2
Cheyenne TP ** Fenoxaprop + MCPA ester + Thifensulfuron + Tribenuron 4 + 1 + 2 +2 Preview Metribuzin + Chlorimuron 7 + 2
Commence Clomazone + Trifluralin 9 + 5 Prozine ** Pendimethalin + Atrazine 5 + 7
Concert Chlorimuron + Thifensulfuron 2 + 2 Pursuit Plus Imazethapyr + Pendimethalin 2 + 5
Crossbow Triclopyr + 2,4-D ester 1 + 1 Ramrod + Atrazine ** Propachlor + Atrazine 6 + 7
Curtail Clopyralid + 2,4-D amine 1 + 1 Salute Trifluralin + Metribuzin 5 + 7
Curtail M Clopyralid + MCPA ester 1 + 1 Squadron Imazaquin + Pendimethalin 2 + 5
Cycle ** Metolachlor + Cyanazine 6 + 7 Storm Acifluorfen + Bentazon 8 + 7
Dakota TP Fenoxaprop + MCPA ester 4 + 1 Sutazine ** Butylate + Atrazine 6 + 7
Extrazine II ** Cyanazine + Atrazine 7 + 7 Synchrony STS Chlorimuron + Thifensulfuron 2 + 2
Fallow Master Glyphosate + Dicamba 3 + 1 Tiller Fenoxaprop + 2,4-D + MCPA 4 + 1 +1
Finesse Chlorsulfuron + Metsulfuron 2 +2 Tornado Fluazifop + Fomesafen 4 + 8
Freedom ** Alachlor + Trifluralin 6 + 5 Tri-Scept Imazaquin + Trifluralin 2 + 5
Fusion Fluazifop + Fenoxaprop 4 + 4 Turbo Metolachlor + Metribuzin 6 + 7

* Reference to commercial products or trade names is made with the understanding that no discrimination is intended and no endorsement by the University of Minnesota Extension is implied.

** Restricted Use Herbicide

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