DETAILED ACTION
Claims 1, 2, 5-7, 9, 11, 13, 15, 17, 18, 22, 25, 27, 28, 45, 49, 53, 60 and 61 are currently pending in the instant application and are rejected.
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant’s election without traverse of the species polydopamine in the reply filed on 11 June 2026 is acknowledged.
According to MPEP 803.02, the examiner has determined whether the elected species is allowable. Applicants’ elected species does not appear allowable. Therefore, the search and examination has not been extended.
Claims 1, 2, 5-7, 9, 11, 13, 15, 17, 18, 22, 25, 27, 28, 45, 49, 53, 60 and 61 have been examined to the extent that they are readable on the elected embodiment, the elected species.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claim(s) 1, 2, 5-7, 9, 11, 13, 15, 17, 18, 22, 25, 27, 28, 45, 49, 53, 60, 61 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Yang et al. Structural and Functional Tailoring of Melanin-Like Polydopamine Radical Scavengers, CCS Chem, 2020, 2, 128-138, published 26 February 2020. (Form 892).
Yang et al. provides a synthetic analogue of melanin, polydopamine (PDA) nanospheres, page 129, which can be utilized as free-radical scavengers for the treatment of a series of diseases, including reactive oxygen and nitrogen species-induced ischemic stroke, acute inflammation induced injury, oxidative stress-induced periodontal diseases, and osteoarthritis. Scheme 1, page 129 provides conventional polydopamine (PDA-O) and amino acid-doped PDA as free-radical scavengers. In vivo cutaneous wound model is found on page 131 where the wounds were smeared with PDA-O or PDA-2 twice a day using the same dose. Page 131 provides nanoparticles with uniform size, such as arginine-doped PDA could be rigorously controlled and finely tuned from 80-240nm, see also figure 1 (d), page 132. Page 133 provides similar sized PDA nanoparticles of 130nm and testing free-radical scavenging activities. Page 134 provides figure 2, which has PDA-O with 0% arginine content with size of 140nm. Figure 2(e) provides scavenging activity of conventional PDA-O and amino acid-doped PDA with all samples exhibiting free-radical scavenging. Reactive Oxygen species (ROS) scavenging properties of PDA-O and PDA-2 are provided in Figure 3, page 135. Figure 4A on page 136 provides data for wound healing with PDA-O and PDA-2 with both promoting wound healing. Page 137 provides that arginine-doped PDA nanoparticles can protect cells from ROS-induced damage and accelerate the wound healing process both in vitro and in vivo.
Yang et al. corresponds to the instant method of treatment of a subject by topically administering a melanin formulation having an artificial melanin material to damaged skin wherein the artificial melanin material comprises an extracellular artificial melanin material which facilitates skin healing by performing a therapeutic extracellular activity (instant claims 1, 22, 25, 27, and 28) as Yang et al. provides the in vivo cutaneous wound model on page 131 where wounds are smeared with PDA-O or TDAS-2. The wound model in Yang et al. corresponds to the types of damaged skin in instant claim 2 along with page 129 which discusses acute inflammation induced injury. The limitation wherein at least a portion of the extracellular melanin material is in the stratum corneum of the damaged skin (instant claim 5) is met as the PDA-O and PDA-2 are smeared in the wound model as the stratum corneum is the outermost layer of the epidermis. The limitations of instant claims 6 and 7 is met as Yang et al. provides reactive oxygen species (ROS), in Figure 3, page 135. The limitations of instant claims 9, 11,and 13 are met as the at least a portion of the administered artificial melanin material directly and/or indirectly reduces inflammation by absorbing one or more inflammatory factors as seen by the ROS scavenging properties of PDA-O and PDA-2 in Figure 3, page 135 and page 134 which provides scavenging activity of conventional PDA-O and amino acid-doped PDA with al samples exhibiting free-radical scavenging. Additionally, page 129 provides the treatment of acute inflammation induced injury. The limitations of instant claim 15 are met as at least a portion of the administered artificial melanin directly and/or indirectly downregulates inflammation-related gens and/or apoptosis-related genes compared to when the artificial melanin materials is absent as seen in Yang et al. page 135, Figure 3 which compares negative control (without any treatment) with ROS levels. The limitations of claims 17 and 18 are met as an intracellular activity is provided in Figure 3 which provides antioxidant effects in in vitro cell data Page 131 also provides intracellular oxidative stress of hDPSCs, The limitations of claim 45 is met as seen in Yang et al. page 131 provides particle size of 80-240 nm with page 133 providing 130nm and page 134 providing 140nm. The limitations of claims 49 and 53 are met as no other therapeutic agents are provided in the PDA-O. The limitations of claims 60 and 61 are met as the administered artificial melanin is the extracellular artificial melanin material, the PDA gels of Yang et al. which are present extracellularly as they are topical, see the wound model..
Claim(s) 1, 2, 5-7, 9, 11, 13, 15, 17, 18, 22, 25, 27, 28, 45, 49, 53, 60, 61 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wang et al. Adv. Funct. Mater. 2018, 28, 1802127, pages 1-9 (IDS filed 7/10/2024, Doc. No. C259).
Wang et al. provides polydopamine (PDA) gels using PDA nanoparticles which resulting polydopamine (PDA) sunscreens are bioadhesive, water resistant, and no skin penetration and have superior UV shielding properties, page 1 and page 4. Page 2 provides Figure 1, which has gels 1-3, as PDA sunscreen. Page 2 provides that PDA NPs can protect skin cells from UV damaging rays that undergo similar pathways as natural melanins perform. Page 2 provides PDA NO’s mixed with different hydrophilic polymers with Gel 3 complexed with PDA NPs via hydrophilic bonding interactions to form thermosensitive hydrogels. PDA NP’s used for gelation have particle size, similar to 100nm and uniformity are provided on page 3. Page 4 provides the three PDA gels for anti-UV protection and in vitro inhibition against UV exposure-induced reactive oxygen species (ROS) generation. Pages 4 and 5 provide how ROS generated by UV irradiation could alter the intracellular redox balance and induce the translocation of p53 to mitochondria where the Lys residues of p53 protein were acetylated activation and the increased permeability of mitochondrial membrane could cause depolarization, finally leading to apoptosis. The ROS inhibition efficiencies of the sunscreens provide protection effects on preventing ROS-induced mitochondrial damage. Figure 3 provides in vitro UV protection for all three PDA gel sunscreens. Page 6 provides superior protection against ROS mediated DNA double-strand breaks (DSBs) of biofriendly PDAS gels along with no keratin overproduction preventing skin irritation and keratosis pilaris with epidermal hypertrophy diminished.
Wang et al. corresponds to the instant method of treatment of a subject by topically administering a melanin formulation having an artificial melanin material to damaged skin wherein the artificial melanin material comprises an extracellular artificial melanin material which facilitates skin healing by performing a therapeutic extracellular activity (instant claims 1, 22, 25, 27, and 28) as Wang et al. provides the application of three polydopamine (PDA) nanopartical hydrogels (page 2), see for example, Figure 5, where different topical interventions are received after 7 days UV irradiation, Figure 6, Figure 4, and Figure 3 which provides PDA gels for keratinocyte protection and inhibition against UV-induced ROS generation. The UV irradiation in Wang et al. corresponds to radiation-induced damage (instant claim 2). The limitation wherein at least a portion of the extracellular melanin material is in the stratum corneum of the damaged skin (instant claim 5) is met as the PDA hydrogels are applied topically and the stratum corneum is the outermost layer of the epidermis. The limitations of instant claims 6 and 7 is met as Wang et al. provides reactive oxygen species (ROS), see pages 4-6. The limitations of instant claims 9, 11,and 13 are met as the at least a portion of the administered artificial melanin material directly and/or indirectly reduces inflammation by absorbing one or more inflammatory factors such as one or more proteins associated with the MAPK-ERK pathway as excessive ROS from mitochondrial dysfunction can trigger p53 activation and inflammatory responses that contribute to cell death as seen in Wang et al. as Wang et al. provides how ROS generated by UV irradiation could alter the intracellular redox balance and induce the translocation of p53 to mitochondria where the Lys residues of p53 protein were acetylated activation and the increased permeability of mitochondrial membrane could cause depolarization, finally leading to apoptosis. The ROS inhibition efficiencies of the sunscreens provide protection effects on preventing ROS-induced mitochondrial damage, see pages 4 and 5. The limitations of instant claim 15 are met as at least a portion of the administered artificial melanin directly and/or indirectly downregulates inflammation-related gens and/or apoptosis-related genes compared to when the artificial melanin materials is absent as seen in Wang et al. pages 4-5 which provides how ROS generated by UV irradiation could alter the intracellular redox balance and induce the translocation of p53 to mitochondria where the Lys residues of p53 protein were acetylated activation and the increased permeability of mitochondrial membrane could cause depolarization, finally leading to apoptosis. The ROS inhibition efficiencies of the sunscreens provide protection effects on preventing ROS-induced mitochondrial damage. Figure 3 provides in vitro UV protection for all three PDA gel sunscreens and inhibition against UV-induced ROS generation. The limitations of claims 17 and 18 are met as an intracellular activity as pages 4-5 provide how ROS generated by UV irradiation could alter the intracellular redox balance and induce the translocation of p53 to mitochondria where the Lys residues of p53 protein were acetylated activation and the increased permeability of mitochondrial membrane could cause depolarization, finally leading to apoptosis. The limitations of claim 45 is met as seen in Wang et al. page 3 wherein particle size is 100nm. The limitations of claims 49 and 53 are met as no other therapeutic agents are provided in the three gels of Wang et al. as PDA is mixed only with hydrophilic polymers, page 2. The limitations of claims 60 and 61 are met as the administered artificial melanin is the extracellular artificial melanin material, the PDA gels of Wang et al. which are present extracellularly as they are topical, see figure 5 and they do not penetrate the skin, page 1.
Conclusion
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/REBECCA L ANDERSON/Primary Examiner, Art Unit 1626 ____________________ 9 September 2026
Rebecca Anderson
Primary Examiner
Art Unit 1626, Group 1620
Technology Center 1600
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