DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application is being examined under the pre-AIA first to invent provisions.
Status of the Application
2. Claims 10-12, 16-22, and 39-63 are pending and examined.
Continued Examination Under 37 CFR 1.114
3. A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on May 26, 2026 has been entered.
Claim Rejections - 35 USC § 112 - Indefiniteness
4. The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
5. Claim 10-12, 16-22, and 39-63 remain rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
This rejection has been modified in view of Applicant’s amendments to the claims. Applicant's arguments filed on May 26, 2026 have been fully considered but they are not persuasive.
In claims 10, 16, and 18, as instantly amended, the limitation “having a phytotoxicity index (PI) that is in the range of PI scores for a group of such sunflower plants whose group average is either 2% to 3% phytotoxicity or no more than 3% phytotoxicity” renders the claims indefinite.
First, it is unclear how the terms “phytotoxicity index” and “PI scores” relate the “phytotoxicity” expressed as percentages. The specification refers to “PI” as a “phenotypic scale from 0 to 9 that is assessed for each plant” (page 73, bottom paragraph), but there is no explanation as to how or whether the apparently arbitrarily assigned numbers of the above scale are related to the phytotoxicity expressed as a percentage of injury (see page 54-55), including “2-3% phytotoxicity at 21 DAT” (page 56, first full paragraph).
Second, it is unclear how the “group average” could be applied to “a sunflower plant” recited in the singular in the claim as being used in the method. For example, it is unclear whether some plants in said “group” are meant to not exhibit any symptoms, or what range of statistical significance may be permitted.
Finally, the exemplary term “such” in the phrase “a group of such sunflower plants” introduces further ambiguity into the claim language because it makes it unclear exactly which “sunflower plants” are meant to be included in said “group.” For these reasons, the metes and bounds are unclear.
Given that claims 11-12, 17, 19, 22, 39-55, and 57-63 depend from claims 10, 16, or 18, and fail to recite further limitation overcoming the indefiniteness, they are indefinite as well.
Response to Arguments
Applicant argues that the amendments to the claims overcome the rejection (page 8 of the Remarks). This is not found to be persuasive. Applicant’s amendments are acknowledged and the rejection has been modified accordingly. However, the amended claims remain rejected for the reasons set forth above.
Claim Rejections - 35 USC § 112 - Fourth Paragraph
6. The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
7. Claims 48, 49, 56, and 57 remain rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Applicant's arguments filed on May 26, 2026 have been fully considered but they are not persuasive.
Claims 48 and 49 are directed to the method of claims 10 or 16 and specify the phenotype of the sunflower plant recited in claim 10 or a sunflower plant grown from the seed used in the method of claim 16. The recitation of the phenotype does not introduce any further structural limitations to said plant and thus does not properly further limit the active method steps of claims 10 or 16. The same analysis applies to new claims 56 and 57.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Response to Arguments
Applicant argues that the phenotype of herbicide tolerance structurally limits the claimed plant and cited PTAB Decision 2025-003055 for support (page 8 of the Remarks).
Applicant’s argument is not persuasive. The decision reflects the facts of a specific application drawn to a different invention, in an unrelated crop species. Applicant has provided no explanation as to how the facts of said unrelated application could be applied to the instant scenario. For example, if Applicant’s position is that the recitation of the “phytotoxicity” recited for a “group” of pants in the depended claims, such as, “a group average phytotoxicity of 3%” (claim 46) actually does limit the structure of the sunflower plant recited in part (I) of claim 10, it is unclear how said recitation would limit said structure, as no clarification is supplied. Nor has Applicant provided any evidence that the cited decision is precedential legal authority.
The Examiner maintains that the base claim is drawn to a method of using a product whose structure (and thus patentability) is determined by the presence of the expressly recited mutant AHASL1 alleles. The property recited in the independent claim is inseparable from the product. The recitation of that property in the dependent claim, therefore, does not introduce further limitations to the claimed subject matter. The rejection is maintained.
Claim Rejections - 35 USC § 103
8. The following is a quotation of pre-AIA 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negatived by the manner in which the invention was made.
9. Claims 10-12, 16, 17, 39-49, and 52-63 remain rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Jander et al (US Application No. 2003/0097692 A1, published May 22, 2003), in view of Kolkman et al (Theor. and Appl. Genet. (2004) 109:1147-1159), White et al (Weed Science (2003) 51:845-853), Sala et al (US 20110209232, claiming priority to US provisional application 60/695,952, filed July 1, 2005; first published as WIPO publication WO 2007/005581; the citations below are to the WIPO publication), and Kmiec et al (U.S. Patent Application No. 2003/0236208 A1, published December 25, 2003).
Applicant's arguments filed on May 26, 2026 have been fully considered but they are not persuasive.
The claims are drawn to a method of controlling weeds using an effective amount of an AHAS inhibiting herbicide in the vicinity of a sunflower plant, wherein said plant comprises two alleles of the AHASL1 gene, wherein the first one encodes an AHASL1 comprising an alanine to threonine substitution at a position corresponding to position 7 of SEQ ID NO: 20, and wherein the second allele encodes an AHASL1 comprising either an alanine to valine substitution at a position corresponding to position 90 of SEQ ID NO: 20 or a proline to leucine substitution at a position corresponding to position 82 of SEQ ID NO: 20; wherein the sunflower plant has a phenotype of tolerance to an AHAS-inhibiting herbicide such that the sunflower plant has the ability to exhibit phytotoxicity of 2% to 3% or “no more than 3%,” to 200 g AI/ha imazamox, determined at 21 days after treatment.
The following is noted with regard to claim interpretation. Claim 10 requires that the claimed sunflower plants comprising the A107T and the A190V substitutions have a phenotype of tolerance to an AHAS inhibiting herbicide “defined as having a phytotoxicity index (PI) score that is in the range of PI scores for a group of such sunflower plants whose group average is ether 2% to 3% phytotoxicity, or no more than 3% phytotoxicity to 200g AI/ha imazamox determined at 21 days after treatment.” The recitation of said property and does not impart additional limitations to the structure of the sunflower plant beyond the two substitutions. It is also noted that step (II) of the method of claim 10 encompasses applying any effective amount of any AHAS inhibiting herbicide. Similarly, the recitation of the phenotype in claims 48 and 49, as well claims 56 and 57 does not limit the structure of the plant recited in claim 10 or a plant grown from the seed used in the method of claim 16.
The term “phytotoxicity” is not defined in the claims or the specification, and would encompass any method of determining phytotoxicity, so long as that phytotoxicity could be reasonably interpreted as “no more that 3%.” For example, the term would be inclusive of a scenario wherein a resistant plant shows some injury to the herbicide, but because it survived the treatment, is included in a group not showing “phytotoxicity.”
Jander et al teach a nucleic acid molecule encoding functional AHAS that has the A122T (A107T in sunflower) substitution; and an imidazolinone-resistant sunflower plant comprising that nucleic acid (claims 1, 2, 7 and 8). Jander et al teach obtaining non-transgenic plants with imidazolinone resistance obtained by EMS mutagenesis (Example 1, beginning at paragraph 71; Example 2, beginning at paragraph 78). Jander et al teach that imidazolinones, such as imazapyr, could be used alone or in combination with other herbicides for post-emergence control of weeds growing with resistant sunflower; and that a variety of imidazolinone herbicides could be used to protect resistant sunflower plants from weeds (pg. 7, paragraph 68).
Jander et al do not teach a sunflower plant comprising two mutated AHASL alleles, wherein one allele encodes the AHASL with the A107T substitution, and the second one encodes the AHASL with the A190V substitution.
Kolkman et al teach a sunflower plant comprising at least one copy of an AHASL polynucleotide encoding an herbicide resistance AHASL1 protein (Fig. 2 on pg. 1152). Kolkman et al teach that the A190V of sunflower AHASL1 confers resistance to imidazolinone herbicides, such as imazethapyr, and to chlorimuron (pg. 1153, right col; pg. 1157). Kolkman et al teach introgressing resistance genes to AHASL inhibiting herbicides from resistant populations into sunflower lines for the purpose of developing herbicide resistant sunflower cultivars and hybrids (pg. 1148, left col., second full paragraph).
Kolkman et al teach an amino acid sequence that is 99.7% identical to the instant SEQ ID NO: 20. The instant specification defines SEQ ID NO: 20 as truncated sunflower AHASL with an A107T mutation (in sunflower AHASL numbering), which corresponds to position 7 in SEQ ID NO: 20 (see pg. 11, lines 20-22). The sequence of Kolkman et al differs from the instant SEQ ID NO: 20 at a single amino acid residue: the sequence of Kolkman et al has an alanine at position 107. As one skilled in the art would recognize, the amino acid sequence of Kolkman et al corresponds to the non-mutated form of the instant SEQ ID NO: 20, and position 107 of the sequence of Kolkman et al corresponds to position 7 of the instant SEQ ID NO: 20. The sequence alignment is set forth below:
DT 07-DEC-2004, integrated into UniProtKB/TrEMBL.
DT 07-DEC-2004, sequence version 1.
DT 28-FEB-2018, entry version 66.
DE RecName: Full=Acetolactate synthase {ECO:0000256|RuleBase:RU003591};
DE EC=2.2.1.6 {ECO:0000256|RuleBase:RU003591};
GN Name=AHAS1 {ECO:0000313|EMBL:AAT07322.1};
OS Helianthus annuus (Common sunflower).
OC Eukaryota; Viridiplantae; Streptophyta; Embryophyta; Tracheophyta;
OC Spermatophyta; Magnoliophyta; eudicotyledons; Gunneridae;
OC Pentapetalae; asterids; campanulids; Asterales; Asteraceae;
OC Asteroideae; Heliantheae alliance; Heliantheae; Helianthus.
OX NCBI_TaxID=4232 {ECO:0000313|EMBL:AAT07322.1};
RN [1] {ECO:0000313|EMBL:AAT07322.1}
RP NUCLEOTIDE SEQUENCE.
RX PubMed=15309298; DOI=10.1007/s00122-004-1716-7;
RA Kolkman J.M., Slabaugh M.B., Bruniard J.M., Berry S., Bushman B.S.,
RA Olungu C., Maes N., Abratti G., Zambelli A., Miller J.F., Leon A.,
RA Knapp S.J.;
RT "Acetohydroxyacid synthase mutations conferring resistance to
RT imidazolinone or sulfonylurea herbicides in sunflower.";
RL Theor. Appl. Genet. 109:1147-1159(2004).
CC -!- CATALYTIC ACTIVITY: 2 pyruvate = 2-acetolactate + CO(2).
CC {ECO:0000256|RuleBase:RU003591}.
CC -!- COFACTOR:
CC Name=Mg(2+); Xref=ChEBI:CHEBI:18420;
CC Evidence={ECO:0000256|RuleBase:RU003591};
CC Note=Binds 1 Mg(2+) ion per subunit.
CC {ECO:0000256|RuleBase:RU003591};
CC -!- COFACTOR:
CC Name=thiamine diphosphate; Xref=ChEBI:CHEBI:58937;
CC Evidence={ECO:0000256|RuleBase:RU003591};
CC Note=Binds 1 thiamine pyrophosphate per subunit.
CC {ECO:0000256|RuleBase:RU003591};
CC -!- PATHWAY: Amino-acid biosynthesis; L-isoleucine biosynthesis; L-
CC isoleucine from 2-oxobutanoate: step 1/4.
CC {ECO:0000256|RuleBase:RU003591}.
CC -!- PATHWAY: Amino-acid biosynthesis; L-valine biosynthesis; L-valine
CC from pyruvate: step 1/4. {ECO:0000256|RuleBase:RU003591}.
CC -!- SIMILARITY: Belongs to the TPP enzyme family.
CC {ECO:0000256|RuleBase:RU362132}.
CC -----------------------------------------------------------------------
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DR EMBL; AY541451; AAT07322.1; -; Genomic_DNA.
DR ProteinModelPortal; Q5VB49; -.
DR UniPathway; UPA00047; UER00055.
DR UniPathway; UPA00049; UER00059.
DR GO; GO:0003984; F:acetolactate synthase activity; IEA:UniProtKB-EC.
DR GO; GO:0050660; F:flavin adenine dinucleotide binding; IEA:InterPro.
DR GO; GO:0000287; F:magnesium ion binding; IEA:UniProtKB-UniRule.
DR GO; GO:0030976; F:thiamine pyrophosphate binding; IEA:UniProtKB-UniRule.
DR GO; GO:0009097; P:isoleucine biosynthetic process; IEA:UniProtKB-UniPathway.
DR GO; GO:0009099; P:valine biosynthetic process; IEA:UniProtKB-UniPathway.
DR InterPro; IPR012846; Acetolactate_synth_lsu.
DR InterPro; IPR029035; DHS-like_NAD/FAD-binding_dom.
DR InterPro; IPR029061; THDP-binding.
DR InterPro; IPR012000; Thiamin_PyroP_enz_cen_dom.
DR InterPro; IPR012001; Thiamin_PyroP_enz_TPP-bd_dom.
DR InterPro; IPR000399; TPP-bd_CS.
DR InterPro; IPR011766; TPP_enzyme-bd_C.
DR Pfam; PF02775; TPP_enzyme_C; 1.
DR Pfam; PF00205; TPP_enzyme_M; 1.
DR Pfam; PF02776; TPP_enzyme_N; 1.
DR SUPFAM; SSF52467; SSF52467; 1.
DR SUPFAM; SSF52518; SSF52518; 2.
DR TIGRFAMs; TIGR00118; acolac_lg; 1.
DR PROSITE; PS00187; TPP_ENZYMES; 1.
PE 3: Inferred from homology;
KW Amino-acid biosynthesis {ECO:0000256|RuleBase:RU003591};
KW Branched-chain amino acid biosynthesis
KW {ECO:0000256|RuleBase:RU003591};
KW Magnesium {ECO:0000256|RuleBase:RU003591};
KW Metal-binding {ECO:0000256|RuleBase:RU003591};
KW Thiamine pyrophosphate {ECO:0000256|RuleBase:RU362132};
KW Transferase {ECO:0000256|RuleBase:RU003591,
KW ECO:0000313|EMBL:AAT07322.1}.
FT DOMAIN 83 247 TPP_enzyme_N. {ECO:0000259|Pfam:PF02776}.
FT DOMAIN 275 407 TPP_enzyme_M. {ECO:0000259|Pfam:PF00205}.
FT DOMAIN 469 624 TPP_enzyme_C. {ECO:0000259|Pfam:PF02775}.
SQ SEQUENCE 655 AA; 71322 MW; 3AF7DF2D81C31752 CRC64;
Query Match 99.8%; Score 2026; DB 40; Length 655;
Best Local Similarity 99.7%;
Matches 391; Conservative 0; Mismatches 1; Indels 0; Gaps 0;
Qy 1 FAYPGGTSMEIHQALTRSSTIRNVLPRHEQGGVFAAEGYARASGLPGVCIATSGPGATNL 60
|||||| |||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 101 FAYPGGASMEIHQALTRSSTIRNVLPRHEQGGVFAAEGYARASGLPGVCIATSGPGATNL 160
Qy 61 VSGLADALLDSVPMVAITGQVPRRMIGTDAFQETPIVEVTRSITKHNYLVLDVEDIPRIV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 161 VSGLADALLDSVPMVAITGQVPRRMIGTDAFQETPIVEVTRSITKHNYLVLDVEDIPRIV 220
Qy 121 REAFYLASSGRPGPVLIDVPKDIQQQLVVPKWDEPMRLPGYLSRMPKPQYDGHLEQIVRL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 221 REAFYLASSGRPGPVLIDVPKDIQQQLVVPKWDEPMRLPGYLSRMPKPQYDGHLEQIVRL 280
Qy 181 VGEAKRPVLYVGGGCLNSDDELRRFVELTGIPVASTLMGLGAYPASSDLSLHMLGMHGTV 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 281 VGEAKRPVLYVGGGCLNSDDELRRFVELTGIPVASTLMGLGAYPASSDLSLHMLGMHGTV 340
Qy 241 YANYAVDKSDLLLAFGVRFDDRVTGKLEAFASRAKIVHIDIDPAEIGKNKQPHVSICGDI 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 341 YANYAVDKSDLLLAFGVRFDDRVTGKLEAFASRAKIVHIDIDPAEIGKNKQPHVSICGDI 400
Qy 301 KVALQGLNKILEEKNSVTNLDFSTWRKELDEQKMKFPLSFKTFGEAIPPQYAIQVLDELT 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 401 KVALQGLNKILEEKNSVTNLDFSTWRKELDEQKMKFPLSFKTFGEAIPPQYAIQVLDELT 460
Qy 361 GGNAIISTGVGQHQMWAAQFYKYNKPRQWLTS 392
||||||||||||||||||||||||||||||||
Db 461 GGNAIISTGVGQHQMWAAQFYKYNKPRQWLTS 492
White et al teach herbicide resistant sunflower plants comprising a gene encoding the AHASL protein with the A205V (in Arabidopsis, corresponding to A190V in sunflower) substitution (Abstract; pg. 852, left col. first full paragraph). White et al teach that the A205V substitution in sunflower resulted in resistance to both imazethapyr and chlorimuron-ethyl (paragraph spanning pages 849 and 850). White et al teach that multiple mutations conferring resistance to AHASL-inhibitors have been found at position A205 (in Arabidopsis, corresponding to P182 and A190, respectively, in sunflower; White et al, pg. 850, left col; Table 4).
Sala et al teach a sunflower plant comprising an AHASL polynucleotide encoding a herbicide-resistance AHASL with a threonine at position 107, said protein further comprising a valine at position 190 (Sala et al, claims 1-7). Sala et al teach that sunflower plants comprising the A122T or the A205V substitutions both showed significantly reduced sensitivity to imazamox, at 100 g ai/ha and at 200 g ai/ha (Figures 4 and 5; Tables 3).
Sala et al teach a method for controlling weeds in the vicinity of the herbicide resistant sunflower plants of their invention, comprising applying an effective amount of an herbicide, including an imidazolinone or sulfonylurea herbicide, to the weeds and the herbicide resistant plant (pg. 9, lines 11-20; claims 16-18). Sala et al teach applying an herbicide pre-emergence, post-emergence, pre-planting, or at planting (pg. 46, lines 6-18). Sala et al teach applying herbicides as seed treatment (pg. 51, lines 17-23; paragraph spanning pages 54 and 55).
Sala et al teach that the weeds in said method comprise dicot and monocot weeds, including those from the genera Sinapis and Echinochloa (page 56, lines 22-33). Sala et al teach that AHAS inhibiting herbicide formulations can be used in solutions, emulsions, dusts, powders, among others (page 49, lines 1-5). Sala et al teach that the formulations can include solvents such as xylene; and comprise carriers, such as ground natural minerals (page 49, lines 6-26). Sala et al teach that the formulations of their inventions can comprise 0.01% to 95% as well as 90% to 100% of an AHAS-inhibiting herbicide, by weight (page 51, lines 17-23). Sala teach that the herbicide preparations could be wet or dry and can include flowable powders, emulsifiable concentrates, and liquid concentrates (page 46, lines 6-18). Sala et al teach that herbicides can be applied by “spraying, irrigation, dusting, or the like” (page 46, lines 16-18). Sala et al teach spraying imidazolinones “over the top of a wide area of vegetation” (page 2, lines 5-13). Sala et al teach herbicidal compositions comprising “other herbicides” and detergents (paragraph 150).
Sala et al teach no apparent statistically significant difference in phytotoxicity index at 14 DAT, in plants comprising the individual A122T and A205V substitutions and treated with the 1X or lower application rate of imazapic (Figure 10).
Kmiec et al teach methods and oligonucleotides for targeted modification of AHASL genes (Table 11 on pg. 19-28; claim 1 and 12). Kmiec et al teach making alterations at several positions of the AHASL of Arabidopsis and a number of other species (Table 11, beginning at pg. 19, paragraph 120). Kmiec et al teach using the methods of their invention in sunflower (pg. 4, paragraph 19).
At the time the invention was made, it would have been prima facie obvious to use the oligonucleotide-based mutagenesis method of Kmiec et al or the EMS-based mutagenesis method of Jander et al and introduce the A122T (A107T) substitution into the AHASL1 gene of a sunflower plant; including wherein the plant comprises the sequence of Kolkman et al.
It would have been obvious to use the introgression methods taught by Kolkman et al, and to cross the resultant sunflower plants comprising the A107T mutation with the sunflower plants of White et al (comprising the A190V mutation), thus obtaining sunflower plants comprising these two mutations on different AHASL1 alleles. As a result of the introgression of the A107T mutant allele into a plant comprising another mutant allele, such as A190V, at least some progeny plants would be heterozygous for the two mutations.
It would have been obvious to use the resultant sunflower plants or their seeds in any standard method of weed control, including those taught by Sala et al and Jander et al, wherein the herbicide is applied either post-emergence or pre-emergence, and including wherein the seeds of the resistant sunflower plant are coated with an AHAS inhibiting herbicide. Using said plants in a method of controlling dicot and monocot weeds, including those from the genera recited in the instant claims 40 and 41, as well as using standard herbicide formulations, such as dry, wet, or powder formulations, recited in the instant claims 58 and 59, would have been prima facie obvious in view of the teachings of Sala et al. Applying the herbicide via spraying or dusting would have been obvious in view of Sala et al (instant claims 60 and 61). Applying the herbicide in a formulation comprising a detergent or an additional herbicide would have also been obvious in view of the teachings Sala et al (instant claims 62 and 63).
Given the teachings of Kmiec et al and Jander et al, and given the routine nature of the introgression methods of Kolkman et al, one would have had reasonable expectation of success in obtaining said plants comprising two AHASL1 alleles each comprising a different herbicide resistance mutation. Given the teachings of Kolkman et al, Jander et al, Sala et al, and White et al, one would have reasonably expected that the sunflower plants comprising the A107T allele along with the A190V one would be resistant to both sulfonylureas and imidazolinones.
Given that both, A122T and A205V confer tolerance to imidazolinones (see Kolkman et al, Sala et al), and in view of the teachings of Sala et al, one would reasonably expect that at least under some conditions, sunflower plants comprising both substitutions would exhibit the phenotype of tolerance an imidazolinone herbicide that would be “the same as” that of the A122T/A122T homozygous plants. Specifically, in view of the teachings of Sala et al (see Figures 4 and 6; Table 3, for example), and given the above claim interpretation, it would not have been unexpected that at least some of the resultant plants to show phytotoxicity that is 2-5% at 200 g ai/ha of imazamox.
It is also noted that “The fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious.” Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985). It is also noted that the active steps of the instantly claimed methods encompass application of any effective amount of any AHAS inhibiting herbicide, and are not limited to 200 g ai/ha of imazamox.
One would have been motivated to combine said teachings because of the agronomic desirability of sunflower plants resistant to both sulfonylureas and imidazolinones, and because Sala et al expressly teach sunflower plants comprising the two claimed point mutations on the same AHASL protein.
10. Claims 18-22 and 51 remain rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Jander et al (US Application No. 2003/097692 A1, published May 22, 2003), Kolkman et al (Theor. and Appl. Genet. (2004) 109:1147-1159), White et al (Weed Science (2003) 51:845-853), Sala et al (US 20110209232, claiming priority to US provisional application 60/695,952, filed July 1, 2005; first published as WIPO publication WO 2007/005581), and Kmiec et al (U.S. Patent Application No. 2003/0236208 A1, published December 25, 2003), as applied to claims 10-13, 16, and 17, above, further in view of Alonso et al (Helia (1998) 21:45-54) and Costejon-Munos et al (Weed Research (1998) 33:171-176), taken with the evidence of Schneiter et al (Stages of Sunflower Development document, NDSU extension, 2013).
Applicant's arguments filed on May 26, 2026 have been fully considered but they are not persuasive.
The claims are drawn to a method for controlling broomrape, including Orobanche cumana or O. cernua, comprising applying imidazolinone herbicides to a resistant sunflower plant and said broomrape, including a plant comprising an allele encoding the AHASL with the A107T substitution and an allele encoding the AHASL with the A205V substitution; wherein the sunflower plan has a phenotype of tolerance to an AHAS-inhibiting herbicide that is equivalent to a level of tolerance of a sunflower plant that is homozygous for the alanine to threonine substitution at the position corresponding to position 7 of SEQ ID NO: 20. The claims are drawn to said method and the method of claim 10, wherein the herbicide is imazapyr and the growth stage at which it is applied is R1.
The teachings of Jander et al, Kolkman et al, White et al, Sala et al, and Kmiec et al have been set forth above. The references do not teach applying an imidazolinone herbicide to a resistant sunflower plant and the broomrape parasitic plant.
Alonso et al teach a method of post-emergence control of O. cernua in sunflower resistant to imazethapyr, an imidazolinone (Abstract). Alonso et al teach that imazapyr was used to control broomrape in sunflower (page 46, second paragraph). Alonso et al teach applying imazethapyr to 40-day old plants that had 5 pairs of leaves (page 47). Alonso et al teach that between the day of treatment and day 65 of plant growth, O. cernua continued germinating and attaching to the sunflower roots (page 50, first paragraph).
Costejon-Munos et al teach the developmental stages of O. cernua and teach that it shows extensive, but subterranean, development at the early heading stage of sunflower (pg. 175, left col.). Costejon-Munos et al teach that at this stage, O. cernua begins to reduce sunflower plant growth (pg. 171, left col.).
Schneiter et al provide evidence that in sunflower a miniature floral head is formed at Reproductive Stage 1 (R1) (see both pages of the document).
At the time the invention was made, it would have been prima facie obvious to modify the method made obvious by the teachings of Kolkman et al, Jander et al, White et al, and Sala et al, and apply any imidazolinone to which the plants are resistant, including imazapyr or imazethapyr, to said plant and the broomrape, as taught by Alonso et al. It would have been obvious to apply the imidazolinone at the vegetative stages or at later stages, including the stage of had formation, R1, as evidenced by Schneiter et al. It is noted that the resultant method would also read on the method of claim 51.
One would have been motivated to combine said teachings given that imidazolinones control O. cernua, a major sunflower parasitic weed. One would have been specifically motivated to apply the herbicide at the early heading stage of sunflower (R1) because at that stage O. cernua begins to reduce the growth of the infected sunflower, as taught by Costejon-Munos. Given that the plants made obvious by Kolkman et al, Jander et al, White et al, and Sala et al would be resistant to imidazolinones, and given the teachings of Alonso et al, one would have had reasonable expectation of success.
11. Claim 50 remains rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Jander et al (US Application No. 2003/097692 A1, published May 22, 2003), Kolkman et al (Theor. and Appl. Genet. (2004) 109:1147-1159), White et al (Weed Science (2003) 51:845-853), Sala et al (US 20110209232, claiming priority to US provisional application 60/695,952, filed July 1, 2005; first published as WIPO publication WO 2007/005581), and Kmiec et al (U.S. Patent Application No. 2003/0236208 A1, published December 25, 2003), as applied to claim 10, and further in view of Fernandez-Martinez et al (Euphytica (1989) 41:39-51).
Applicant's arguments filed on May 26, 2026 have been fully considered but they are not persuasive.
The claim is drawn to the method of claim 10, wherein the sunflower plant produces seeds comprising extractable seed oil comprising at least 85% oleic acid.
The teachings of Jander et al , Kolkman et al, White et al, Sala et al, and Kmiec et al have been set forth above. The references do not expressly teach a sunflower plant producing seed comprising at least 85% oleic acid.
Fernandez-Martinez et al teach sunflower lines that are true breeding for high oleic acid content (average of higher than 85%) (Abstract; pg. 41, both col.).
At the time the invention was made, it would have been prima facie obvious to further modify the method made obvious by the teachings of Jander et al , Kolkman et al, White et al, Sala et al, and Kmiec et al, and introduce the above substitutions into the plant of Fernandez-Martinez et al, and use the resultant plant in the method of controlling weeds with reasonable expectation of success. One would have been motivated to combine said teachings in view of the desirability of a sunflower plant comprising high oleic content (as taught by Fernandez-Martinez et al and known in the art), which plant is also tolerant to AHAS inhibiting herbicides.
Response to Arguments
Applicant argues that the phenotype of herbicide tolerance structurally limits the claimed plant and cited PTAB Decision 2025-003055 for support. Applicant argues that the decision is applicable to the instant case (page 9 of the Remarks).
Applicant’s argument is not persuasive. The cited PTAB decision reflects the facts of a specific application drawn to a different invention, in an unrelated crop species. Applicant has provided no explanation as to how the facts of said unrelated application could be applied to the instant scenario. For example, if Applicant’s position is that the recitation of the “phytotoxicity” recited for a “group” of pants in the depended claims, such as, “a group average phytotoxicity of 3%” (claim 46) actually does limit the structure of the sunflower plant recited in part (I) of claim 10, it is unclear how said recitation would limit said structure, as no clarification is supplied.
Applicant argues that “the PTAB's decision does not rely on the identity of the herbicide tolerance trait nor on the plant species, but instead enunciates a principle applicable to any species of herbicide-tolerant plants and seeds.” (page 9 of the Remarks).
This is not found to be persuasive. Applicant has provided no explanation as to what portions of the opinion provide support for Applicant’s broad generalization regarding the applicability of the Board’s decision. This deficiency in Applicant’s position is particularly relevant given that the claims in the application at issue on appeal were much narrower, and unliked the instant invention, required the full-length amino acid sequence of the mutant AHASL protein. Applicant has also supplied no evidence that the cited decision is precedential legal authority.
Moreover, the teachings of the prior art regarding the two AHASL substitutions at issue (both of which are located in well-recognized conserved AHASL domains) are extensive, including where they are present in sunflower, specifically. This is illustrated by the teachings of Sala et al, above, who expressly teach combining the A122T and A205V substitutions on the same sunflower AHASL molecule.
The Examiner maintains that the two individual AHASL substitutions at issue here were not only well-known in the art at the time of invention but also used commercially to confer herbicide tolerance to crops. For example, Tan et al, Pest Manag Sci (2005) 61: 246-257; pg. 248, right col., under “Commercialized Imidazolinone-Tolerant Crops” - pg. 249, right col.; Table 1; of record. The rejection is maintained.
Conclusion
12. No claims are allowed.
13. All claims are identical to or patentably indistinct from, or have unity of invention with claims in the application prior to the entry of the submission under 37 CFR 1.114 (that is, restriction (including a lack of unity of invention) would not be proper) and all claims could have been finally rejected on the grounds and art of record in the next Office action if they had been entered in the application prior to entry under 37 CFR 1.114. Accordingly, THIS ACTION IS MADE FINAL even though it is a first action after the filing of a request for continued examination and the submission under 37 CFR 1.114. See MPEP § 706.07(b). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/MYKOLA V. KOVALENKO/Primary Examiner, Art Unit 1662
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