Clomazone Mode of Action

Clomazone is a “bleaching” herbicide used mainly pre-emergence. Inside the plant it converts to 5-ketoclomazone, which inhibits DXS (1-deoxy-D-xylulose-5-phosphate synthase)—the first, rate-limiting enzyme of the chloroplast MEP/DOXP isoprenoid pathway. That pathway makes carotenoids (the “sunscreen” that protects chlorophyll). When carotenoids drop, chlorophyll photo-oxidizes: new leaves turn pale/white, growth stalls, seedlings die. HRAC/WSSA classifies clomazone as Group 13 (DXS inhibitors).

How clomazone works (mechanism made practical)

• Pro-herbicide: The parent clomazone is weakly active; plant metabolism oxidizes it to 5-ketoclomazone, the form that binds and inhibits DXS.

• Upstream blockade: Because DXS is the first step in the MEP pathway, inhibition starves multiple chloroplast isoprenoids—most visibly carotenoids.

• Visible outcome: Without carotenoids, chlorophyll can’t handle light; new tissue bleaches first (growing points, unfolding leaves), then plants stunt and collapse.

Not all “bleaching herbicides” are the same

Bleaching symptoms can look alike, but targets differ:

• Clomazone = Group 13 (DXS) — very upstream in the pathway.

• HPPD inhibitors = Group 27 — block the homogentisate/tyrosine branch downstream.

• PDS inhibitors = Group 12 — block phytoene desaturase further along the carotenoid branch.
  Takeaway: same look, different lock. Correct grouping matters for rotation and diagnostics.

Why many crops tolerate clomazone (selectivity)

• Metabolic selectivity: Tolerant crops detoxify/partition clomazone faster into low-activity metabolites; sensitive weeds do not.

• Formulation advances: Microencapsulation/low-volatility formulations reduce vapor drift and “phantom” whitening on neighboring crops.

• Physiology: Young tissues are the main targets; placement in the seed zone protects crops when labels are followed.

Absorption, movement, and the right timing

• Uptake & movement: Primarily root uptake with short-distance upward movement—hence the new-leaf bleaching signature.

• Best use window: Pre-emergence / pre-plant incorporated fits the biology—build a protective layer where weeds germinate.

• Soils & moisture: Soil texture, organic matter, and moisture influence the treated layer’s stability and persistence; follow label guidance for your conditions.

Field diagnosis: what you’ll see

• Typical: New leaves lose green → turn pale → white, often starting at tips/edges; plants stunt at higher exposure.

• Differentiate from other causes: Compare history (what and when was applied), symptom location (new vs. old leaves), and pattern (treated zone vs. drift edges). HPPD/PDS drift can look similar—timing and placement usually separate them.

Resistance risk and how to manage it

• Risk profile: DXS is a multi-cofactor, rate-limiting enzyme; resistance tends to emerge slower than with single-site post-emergence chemistries, but it can still develop (enhanced metabolism, target changes) under heavy, repeated use.

• Program design: Rotate Group 13 with different MOA groups (e.g., 27/12/5/15 as labels allow), mix with partners when permitted, and pair with non-chemical tactics (seedbed prep, cover, row closure, timely mechanical control).

Safety, stewardship, and compliance (non-negotiables)

• People: Clomazone products are often suspension concentrates or microcaps; during mixing/loading, manage dust/aerosol, wear basic PPE (gloves, long sleeves, eye protection; respirator if dusty), and follow the REI.

• Environment: Respect wind, temperature, and buffers to prevent vapor/drift onto sensitive crops. Never rinse equipment to drains/waterways.

• Records: Keep block, soil condition, planting depth, formulation, weather, and partner products in your log for audits and troubleshooting.

• No rates here: Always follow the registered label and local regulations for rates, intervals, and permitted uses.

Practical application playbook (no rates—just the logic)

1. Pre-emergence baseline: After planting and covering seed, establish the treated soil band per label; maintain seed-zone moisture for consistent uptake.

2. Post scenarios (only when labeled): Choose low-volatility formulations and tight weather windows; manage downwind boundaries near sensitive crops.

3. Neighbors & greenhouses: Be conservative around leafy veg, cucurbits, tobacco, and other sensitive plants; align applications with wind and temperature to avoid off-target whitening.

Quick FAQ (client-facing)

Does clomazone burn leaves?
Not a burn. It depletes carotenoids, so chlorophyll photo-oxidizes—seen as bleaching, not necrotic scorch.

Is it the same as HPPD herbicides?
No. Similar look, different target. Clomazone is Group 13 (DXS); HPPDs are Group 27.

How do I avoid crop injury?
Use labeled crops/timings, select low-volatility formulations, manage seed depth and treated layer, avoid hot, bright hours, and separate from oils/sulfur where cautioned.

How do I slow resistance?
Rotate MOA groups, mix with non-Group 13 partners when allowed, and integrate cultural/mechanical controls.

Why is pre-emergence preferred?
Because clomazone focuses on new tissue. A seed-zone barrier hits weeds at germination and aligns with the mode of action.

Take-home for buyers and agronomy teams

• Value proposition: Upstream DXS inhibition gives strong preventive control with clear, visible diagnostics (bleaching), ideal for pre-emergence weed programs.

• Risk control: Modern microcaps mitigate vapor drift; pair with boundary/weather checks and compliant intervals to protect neighbors and crops.

• Program fit: Position clomazone as the pre base, rotate MOA, and document decisions. That’s how you keep performance high and risk low over many seasons.