The Dawning of a New Enterprise: RNA Therapeutics for the Skin

Rachel E. Kieser1,2,5#, Shaheerah Khan1,2,5#, Nada Bejar1,2,5#, Daniel L. Kiss1,2,3,4,5*

1Center for RNA Therapeutics,

2Department of Cardiovascular Sciences,

3Weill Cornell Medical College, New York, NY, USA

4Houston Methodist Cancer Center, Houston, TX, USA

5Houston Methodist Academic Institute, Houston Methodist Research Institute, 6670 Bertner Ave, R10‑113, Houston 77030, TX, USA

#These authors have contributed equally

Despite being under development for decades, RNA therapeutics have only recently emerged as viable drug platforms. The COVID-19 mRNA vaccines have demonstrated the promise and power of the platform technology. In response, novel RNA drugs are entering clinical trials at an accelerating rate. As the skin is the largest and most accessible organ, it has always been a preferred target for drug discovery. This holds true for RNA therapies as well, and multiple candidate RNA-based drugs are currently in development for an array of skin conditions. In this mini review, we catalog the RNA therapies currently in clinical trials for different dermatological diseases. We summarize the main types of RNA-related drugs and use examples of drugs currently in development to illustrate their key mechanism of action.


The discovery and development of novel RNA therapy candidates has accelerated since the success of the COVID-19 mRNA vaccines 1. RNA therapeutics have been tapped to provide novel approaches to treat various dermatological conditions where conventional treatments have offered little success. For example, diabetic patients suffer from poor wound healing, which correlates with an increased chance of infections leading to amputation. In addition, metastatic melanoma is one of the deadliest forms of skin cancer with a 5-year survival rate of less than 5% 2. It is inherently resistant to radiotherapy and chemotherapy with median survival reduced to approximately 10 months 2. Novel therapies are vital to treat these patients, with several candidate RNA therapies showing promising results.

The rapid advancement of RNA-based therapies underlines their inherent advantages. For example, (1) they have a transient effect, (2) present no risk of insertional mutagenesis, (3) are easy to develop and manufacture, and (4) are cost-effective. These traits make them attractive options for development. Here we summarize the RNA-based therapies currently in clinical trials for skin conditions (Table 1), described are the main categories of RNA therapeutics: RNAi (siRNA and miRNA), antisense oligonucleotides (ASO), messenger RNA (mRNA), and provide examples detailing their mechanisms of action (Figure 1).

Table 1: RNA-based therapies currently in clinical trials for skin conditions

Drug name

Trial Phase

Clinical trial #

Status (Jan, 2023)

Skin Condition


Mechanism of action

Alternative names of drug [38, 39]


RNA interference (RNAi)

LEM S401

Phase I



Hypertrophic Scar & Keloid


Encapsulated siRNA targeting CTGF to reduce fibrosis

LEM-S401; siRNA encapsulated in DegradaBALL


PH 762

Phase I

CSET 3432


Malignant melanoma & Squamous cell cancer

Phio Pharmaceuticals

Self-delivering siRNA reducing the expression of PD-1 to enhance T-cells anti-tumor activity (also tested as an Adoptive Cell Therapy)

PH 762 adoptive cell therapy; PH-762; PH762-ACT; RXI 762-ACT



Phase I



Pachyonychia Congenita

Transderm/International Pachyonychia

siRNA targeting one disease-causing mutation of keratin 6a (K6a), the N171K mutant

Pachyonychia congenita siRNA; Reveker; sdTD-K6a.513a.12; siRNA sdTD101; TD-K6a.513a.12; TD101


MRX 34

Phase I/II




Mirna therapeutics (Synlogic)

Encapsulated synthetic miR-34a mimic- Tumour suppressor gene modulators

miR-34 - Synlogic; miR-34 mimic - Synlogic; MRX-01; MRX34


BMT101 or OLX101A

Phase II



Hypertrophic scars


Cell penetrating asymmetric siRNA targeting human CTGF to reduce fiborsis

asiRNA therapeutics - OliX Pharmaceuticals; BMT 101; cp-asiRNA therapeutics - OliX Pharmaceuticals; OLX 10020; OLX 103; OLX 201; OLX 301; OLX 401; OLX 701;OLX10010; OLX101


STP 705

Phase II



Squamous Cell Carcinoma, Keloids & hypertrophic scar, Fat sculpting


Two encapsulated siRNAs targeting TGF-β1 and Cox-2 to reduce fibrogenic response

Anti-fibrosis RNA interference therapeutic - Sirnaomic; Cotsiranib; STP-705; STP-705LU; STP-705LV; STP705L



Phase II



Pathological fibrosis, Fibrous scar & Keloid

miRagen Therapeutics (Viridian)

miR-29b mimic to reduce collagen and other scarring proteins

miR-29 replacement; MRG-201



Phase II



Hypertrophic Scars & Keloids

RXi Pharmaceuticals (Phio Pharmaceuticals)

Self-delivering siRNA targeting CTGF to reduce fibrosis

RXI 109; PH-109


Antisense Oligonucleotides (ASOs)


Phase I




Purdue Pharma,Exicure

Nanoparticle-based spherical nucleic acid (SNA) to knockdown a tumor necrosis factor gene; Tumour necrosis factor inhibitors



MRG 110

Phase I



wound healing

Viridian Therapeutics; miRagen Therapeutics, Inc.

Inhibitor of microRNA-92

Anti Mir92a; MRG-110; S95010



Phase I



Alopecia; Netherton syndrome; Psoriasis

Dermelix Biotherapeutics; Exicure

SNA targeted to mRNA encoding interleukin 17 receptor alpha (IL-17RA)



QR 313

Phase I/II



Epidermolysis bullosa

Phoenicis Therapeutics; ProQR Therapeutics

Designed to exclude exon 73 from the mRNA (exon skipping) and produce a functional C7 protein, thereby restoring the functionality of the anchoring fibrils

PTW-002; QR-313; QRX-313


QR 313

Phase I/II



Fibrous scar & Keloid

Phoenicis Therapeutics

Designed to exclude exon 73 from the mRNA (exon skipping) and produce a functional C7 protein, thereby restoring the functionality of the anchoring fibrils

PTW-002; QR-313; QRX-313



Phase II



Atopic dermatitis

Sterna Biologicals GmbH & Co. KG

DNAzyme hgd40 targeting GATA3, a highly mutated transcription factor

hgd40; SB-010; SB-011; SB-012



Phase II



Cutaneous T-Cell Lymphoma; Dystropic Epidemolysis Bulosa

Viridian Therapeutics

Inhibitor of miR-155




Phase II



Hypertrophic scar


Anti-CTGF antisense oligonucleotide

EXC-001; PF-06473871; PF-6473871



Phase II/III




Oncotelic Therapeutics

mRNA of the human TGF-β2 gene

AP 2/09-DS; AP-12009; AP-2/09; OT-101; OT-201; Personalised dosing TGF-beta antisense; TGF-beta antisense



Phase III



Hereditary angioedema

Ionis Pharma

Reduce the production of prekallikrein

Donidalorsen sodium; IONIS-PKK-L Rx; ISIS 721744



Phase III



Malignant melanoma; Anti-programmed cell refractory death protein 1 (PD-1) metastatic melanoma

Idera/Bristol Myers Squibb

Immunologic cytotoxicity; Toll-like receptor 9 agonists

IMO-2125; IMO-2125 sodium; Tilsotolimod sodium


Messenger RNA (mRNA)


Phase I



Advanced Melanoma

BioNTech SE

mRNA encoding TAAs: NY-ESO-1, MAGE-A3, tyrosinase, and TPTE




Phase I



Malignant melanoma


mRNA encoding cytokines: IL-12sc, IL-15sushi, IFNa and GM-CSF; BioNTech FixVac platform

BNT-131; SAR-441000



Phase I



Immune Checkpoint Refractory Melanoma, Relapsed/Refractory Solid Tumor Malignancies

Moderna Therapeutics (Collaborator: AstraZeneca)

mRNA encoding OX40L T cell co-stimulator, IL-23, and IL-36γ pro-inflammatory cytokines; immunostimulant

iTu triple combination - Moderna Therapeutics; mRNA intratumoral immuno-oncology therapeutics - Moderna Therapeutics; mRNA 2752; OX40L/IL-23/IL-36γ



Phase I



Malignant melanoma

Immorna Biotherapeutics, Inc.

self-replicating mRNA encoding cytokine IL-12

JCXH 211



Phase I




BioNTech RNA Pharmaceuticals GmbH (BioNTech SE)

mRNA encoding TAAs: RBL001/RBL002

MERIT; RB0001; RB_0001; RBL-001/RBL-002; RBL-002/RBL-001



Phase I



Malignant Melanoma, Unresectable Malignant Melanoma stage IIIA-C and IV

BioNTech RNA Pharmaceuticals GmbH (BioNTech SE)

Poly-neo-epitopic encoding mRNAs specific to patient mutanome with and without the RBL001/RBL002 antigen-encoded mRNA

BNT-121; IVAC MUTANOME; Melanoma RNA vaccine personalised - BioNTech/Ribological/TRON; Personalised melanoma vaccine - BioNTech/TRON



Phase I



Malignant Melanoma

BioNTech US Inc. (Collaborator: Bristol-Myers Squibb)

mRNA encoding neoantigens for a personalized cancer vaccine to patient mutanome; immunoglobulin stimulant

Neo Vax; NEO-PV-01; Neoantigen vaccine; Neoantigen-based vaccine - BioNTech; NeoAntigen-peptides; Personalized-neoantigen-cancer-vaccine-BioNTech; Personalized-neoantigen-vaccine-BioNTech



Phase I



Metastatic Melanoma

BioNTech US Inc. (Collaborator: Apexigen, Inc.)

mRNA encoding neoantigens for a personalized cancer vaccine to patient mutanome; immunoglobulin stimulant




Phase I




Patrick Ott, Md, Dana-Farber Cancer Institute; Oncovir, Inc.

mRNA encoding neoantigens (up to 20 TAAs) for a personalized cancer vaccine to patient mutanome

NeoVax; Hiltonol



Phase I




eTheRNA immunotherapies

mRNA encoding TAAs: tyrosinase, GP100, MAGE-A3, MAGE-C2, and PRAME. Administered with mRNA encoding immunostimulants (TriMix)

ECI 006



Phase I/II



Untreated Advanced Melanoma

Genentech, Inc. (Collaborator: BioNTech SE)

mRNA encoding neoantigens for a personalized cancer vaccine to patient mutanome; BioNTech iNest platform

BNT-122; BNT122/RO7198457; Autogene cevumeran; Individualized Neoantigen Specific immunotherapy; iNeST; IVAC_M_uID; PCV RO7198457; Personalized cancer vaccine RO7198457; RG-6180; RG6180-1; RO-7198457



Phase I/II



Malignant Melanoma

University Hospital Tuebingen (Collaborator: German Research Foundation)

mRNA encoding TAAs: melan-A, MAGE-A1, MAGE-A3, survivin, GP100, and tyrosinase

Molgramostim; CSF 39300; GMC 89107; Leucomax; SCH 39300


National Cancer Institute (NCI)-4650

Phase I/II




National Cancer Institute (NCI); Moderna Therapeutics

mRNA encoding neoantigens (up to 15 TAAs) for a personalized cancer vaccine against those expressed by autologous tumor cells

mRNA 4650; NCI 4650; mRNA-based PCV NCI-4650; NC-I4650



Phase II



Melanoma Stage III, Melanoma Stage IV, Unresectable Melanoma, Anti-PD-1-refractory/ relapsed melanoma, malignant melanoma

BioNTech SE (Collaborator: Regeneron Pharmaceuticals)

mRNA encoding TAAs: NY-ESO-1, MAGE-A3, tyrpsinase, TPTE; BioNTech FixVac platform

BNT-111; Lipo-MERIT; RB 0003; RB_0003; RBL 001/RBL 002/RBL 003/RBL 004; RBL001.1/RBL002.2/RBL003.1/RBL004.1; RNA-LPX; RNA(LIP); Tetravalent RNA-lipoplex Cancer Vaccine



Phase II



Malignant Melanoma

Moderna Therapeutics. (Collaborator: Merck Sharp & Dohme LLC)

mRNA encoding neoantigens for a personalized cancer vaccine to patient mutanome; immunostimulant

mRNA 4157; PCV; Personalized Cancer Vaccine - Moderna Therapeutics



Phase II





mRNA encoding single TAA: MAGE-A3

Zastumotide; Astuprotimut-R; D1/3 MAGE-3 fusion protein; D1/3 MAGE-3 fusion protein SB MAGE-3; D1/3 MAGE-3 His; D1/3 MAGE-3 His fusion protein; GSK 1572932A; GSK 2132231A; GSK 249553; GSK1203486A; MAGE-A3; MAGE-A3 antigen specific cancer immunotherapeutic; MAGE-A3 ASCI; NSC 719274; SB 249553; SB MAGE-3; SID 534984


Other RNAs

CV 8102

Phase I



Melanoma, Squamous Cell Carcinoma of the Skin

CureVac AG (Collaborators: Syneos health and Cromos Pharma LLC)

Non-coding, non-capped ssRNA (CV8102) complexed with a cationic peptide to induce an immune response via TLR-7/8 and DDX58/RIG-1; immunostimulant



BO 112

Phase II



Malignant melanoma

Highlight therapeutics

non-coding double stranded synthetic RNA activating TLR3, RIG-1, and MDA5 to sensitize tumor cells to immune response

BO-112; Nanoplexed Poly IC BO-112; Nanoplexed Polyinosinic:Polycytidylic Acid BO-112



Figure 1: The mechanism of action for three RNA-based therapeutics. (left) Schematic depiction of the mechanism of action for multiple siRNAs currently in clinical trials for hypertrophic scars. All three siRNAs aim to reduce fibrosis and scarring by targeting CTGF mRNA to ultimately lower CTGF protein expression. (Center) The wound-healing candidate drug ASO MRG-110 directly targets miR-92a which represses ITGA5 a pro-angiogenic factor. Blocking the actions of miR-92a increases ITGA5 mRNA and protein levels to promote angiogenesis and wound healing. (Right) The mechanism of action depicting a mRNA-based cancer vaccine (e.g., BNT111) where a pool of mRNA encoding tumor-associated antigens (TAAs), linked to a specific cancer (i.e., BNT111 encodes 4 melanoma antigens), is delivered to antigen-presenting cells (APC) via lipid nanoparticles (LNP). The mRNA pool is translated into TAAs and elicits a specific host anti-tumoral immune response against the cancer cells. Created with

RNA Interference (RNAi)

The aberrant expression of a protein, a mutated protein, or a non-coding RNA 3,4 can all cause skin disorders, and blocking such elements can be a beneficial therapeutic approach. RNA interference (RNAi) is one method to specifically target and lower the expression of pathological proteins. In RNAi, short double-stranded RNAs of exogenous or endogenous origins are processed by DICER and loaded into the RNA-induced silencing complex (RISC). Loaded RISC complexes recognize targeted mRNAs via perfect (siRNAs) or imperfect (miRNAs) complementarity and inhibit their translation and/or cause their degradation, thereby reducing the level of the encoded protein 5-7. siRNAs are designed to specifically target a single mRNA, whereas miRNAs (naturally occurring or synthetic) often have a broader array of targets 7.

The discovery of RNAi has greatly contributed to our understanding of the role(s) of countless proteins and their potential pathogenicity. More importantly to clinicians, RNAi provided a pathway to target disease-causing proteins that were otherwise impossible to treat. As with other RNA platforms, RNA stability, poor tissue penetration, and off-tissue targeting remain challenges; however, modifications to RNA bases and/or backbones plus the development of a wide variety of delivery systems enabled the FDA-approval of multiple siRNA therapeutics 8. Although several siRNA and miRNA mimics are currently advancing in clinical trials, no RNAi therapies have yet been approved for skin-related diseases.

Currently, at least three siRNAs (BMT101 (OLX101A), LEMS401, and RXI-109) targeting the connective tissue growth factor (CTGF) are in clinical trials (Figure 1, left). High levels of CTGF have been linked to fibrotic disorders, and reducing CTGF levels is thought to be a viable approach for reducing cutaneous fibrosis 8-11. Further, CTGF is also an attractive target for treating keloids or hypertrophic scars, which occur in 40-70% of patients following surgery 12.

Antisense Oligonucleotides (ASOs)

Oligonucleotides are short chains of polymerized nucleotides, and antisense oligonucleotides (ASO) are short (generally 12-30 nucleotides) single-stranded synthetic nucleic acids whose reverse complement sequence allows for the targeting of specific RNA or DNA sequences 13-16. The use of oligonucleotides in clinical trials dates back to the late 1950s and early 1960s when methods to synthesize them were first established 17. Although tested for decades, Fomivirsen, the first-in-class ASO, was only approved by the FDA to treat cytomegalovirus-induced retinitis in 1998 18.

ASOs can reduce or restore protein expression, inhibit 5' cap formation, or alter the splicing of targeted mRNAs. ASOs commonly enter the cell via endocytic pathways and recognize their targeted mRNAs through Watson-Crick base pairing 19,20. ASOs predominantly function via two mechanisms. First, ASOs can employ an occupancy-mediated degradation mechanism by inducing the cell’s RNase H nuclease activity to degrade a targeted mRNA 21. Second, ASOs can use an occupancy-only model and function via steric hindrance. This strategy can up or down-regulate target transcripts by altering their splicing patterns or by masking protein docking sites 22.

ASOs are usually trafficked to late endosomes and lysosomes which accounts for their slow release 23. Notably, the phosphodiester backbones of unmodified ASOs are prone to endonuclease degradation resulting in comparatively short half-lives; however, chemical modifications can overcome these shortcomings 24,25. ASOs are grouped into three generations based on their chemical modifications. (1) First-generation ASOs often replace a non-bridging oxygen atom in the phosphate group with either an amine (phosphoramidites), a methyl group (methyl phosphonates), or a sulfate group (phosphorothioates). When compared to phosphodiester oligonucleotides or unmodified ASOs, first-generation ASOs can resist nucleases and have longer half-lives in plasma 24. However, mRNA targeting affinity is slightly reduced due to the decreased melting temperature of these ASOs 15. (2) Second-generation ASOs usually have alkyl modifications at the 2' position of the ribose which improves binding affinity, tissue uptake, and nuclease resistance, while leading to both longer in vivo half-lives and lower toxicity 26. (3) Third-generation ASOs use chemical modifications to increase their stability, nuclease resistance, and hybridization affinity to the targeted RNA. The most commonly used third-generation ASOs usually incorporate peptide nucleic acids (PNA), locked nucleic acids (LNA), and morpholino phosphoramidite (MF) modifications 27. Notably, many third-generation ASOs function by causing steric hindrance of ribosomal machinery or altering the splicing of its targeted RNA 28,29.

MRG-110 (Figure 1, center), a third generation LNA ASO developed by miRagen Therapeutics, Inc. (Boulder, CO), is currently in phase 1 clinical trial for wound healing. It blocks miR-92a, which then de-represses the integrin alpha 5 (ITGA5) gene 30. Higher levels of ITGA5 protein promotes angiogenesis which facilitates wound healing 31. Studies have shown significant results for MRG-110 reporting none or very low systemic toxicity and drug accumulation in distal tissues.

Messenger RNA (mRNA)

mRNAs are transient RNAs that encode a protein. Exogenous mRNAs were first used to elicit specific protein expression in vivo over three decades ago 32. Despite that initial success, nearly two decades passed until data were reported for the first clinical trial employing mRNA as a therapeutic 33. The development of mRNA-based therapeutics has seen a renaissance as the COVID-19 global pandemic demonstrated their versatility and power. The mRNA-based therapies currently undergoing clinical trials for dermatologically related diseases are listed in Table 1. Three main mRNA treatment modalities have emerged. First, cancer vaccines use mRNAs encoding tumor-specific antigens to stimulate a protective immune response 1,34. Second, replacement therapies use mRNAs to produce therapeutic proteins or to counteract the phenotypes of a defective gene/protein. Third, cell-based therapies use mRNA transfected into cells ex vivo, with these cells being re-introduced into the patient to modify a specific diseased phenotype/function 1,35. Despite the broad applicability of mRNAs, the constraints of this mini review restrict our discussion to mRNA cancer vaccines.

Therapeutic cancer vaccines generally encode tumor-associated antigens (TAAs), or unique markers expressed in cancerous, but not normal, cells. Targeting several TAAs in a single vaccine reduces the risk of tumor antigen escape as it triggers a broad immune response and it aids in the detection of poorly expressed antigens, thereby increasing the robustness of the vaccine and its antitumor response. BioNTech initially pursued a cancer vaccine targeting four melanoma-associated antigens in their phase 1 Lipo-MERIT monotherapy trial 36. While this clinical trial is still ongoing, BioNTech has used the Lipo-MERIT data to steer the development of BioNTech’s FixVac (BNT111) therapy for melanoma, which shows a promising safety profile and anti-tumor immune response 37. BioNTech’s FixVac mRNA therapeutic platform is a fixed set of mRNA-encoded TAAs known to be expressed in particular cancer types (e.g., melanoma), therefore, prompting a strong and precise immune response against the particular cancer (Figure 1, right). BNT111 was developed to treat patients with anti-PD-1-refractory/relapsed unresectable stage III or IV melanoma and is one of the most promising cancer immunotherapies in development 38-42 .

Cancerous cells are characterized by their rapid proliferation and expansion which often generates somatic mutations, each of which becomes a potentially targetable neoantigen. A patient’s specific tumor neoantigen profile (mutanome) could be analyzed and incorporated into personalized neoantigen-encoding mRNA vaccines. As neoantigen expression is restricted to tumor cells, this feature could easily be exploited to treat melanomas as they have a high mutation burden 43. Recently, Moderna Inc. and Merck & Co. released promising new data regarding their mRNA-based personalized (neoantigen) cancer vaccine, mRNA-4157/V940, for the treatment of melanoma. When the vaccine is administered in concert with Keytruda, a cancer immunotherapy, reports show a 44% reduction in the risk of recurrence or patient death when compared to Keytruda alone over a period of 1 year 39,43,44. These data are a major breakthrough in the field of RNA therapeutics, demonstrating the power of mRNA to “train” a patient’s immune system to recognize and attack their specific tumor mutanome, hopefully, translating into durable remission.

mRNA cancer vaccines have many advantages. First, mRNA-based modalities elicit a potent yet reliable immune response to selected antigens in vivo and are customizable to a patient’s particular neoantigen profile. Second, mRNA therapies are safe compared to viral vector vaccines as they do not incorporate into the host genome, thus avoiding the risk of insertional mutagenesis. Lastly, mRNA vaccines are relatively inexpensive and rapid to synthesize 34. Altogether, mRNA therapeutics hold great promise for the treatment of various dermatological diseases.


As mentioned above, RNA therapeutics are a rapidly evolving class of therapies that have the potential to change the face of personalized medicine and revolutionize healthcare1. A number of RNA therapeutics have been approved by FDA and many more are in clinical trials for a broad array of indications. In this review, we focused exclusively on RNA therapeutics in clinical trials for dermatological disorders, such as those used to treat melanoma, psoriasis, hypertrophic scars, wound healing, alopecia, epidermolysis bullosa, keloids, etc. Our research uncovered 35 different RNA therapeutics currently undergoing clinical trials and dozens more are in the discovery or preclinical stages of development for skin conditions as well. In closing, many RNA therapies are rapidly progressing through clinical trials and this evolving and growing class of drug candidates offers much promise to improve existing treatment regimens or to become standalone treatments themselves.

Acknowledgments and Funding

REK, SK, and NB contributed equally to this work and all authors acknowledge that all three authors can list themselves first on career materials such as curriculum vitae. REK, SK, NB, and DLK all performed the literature searches and wrote and revised sections of the manuscript. REK, SK, and NB constructed and edited the table and figure. DLK reviewed and edited the entire manuscript incorporating revisions from all authors. All authors approved the final manuscript. All authors apologize for primary works that were not cited due to citation limits for minireviews. This work was supported by a Houston Methodist Research Institution (HMRI) Career Cornerstone Award, an award from the Houston Methodist Foundation (both to DLK) and Cancer Prevention and Research Institute of Texas (RP150611 and RP200619) grants to the RNA Core at the HMRI. DLK is supported in part by an R35 grant from the NIH (R35GM137819). REK is supported by an NIH postdoctoral supplement (R35GM137819-03S3). The content presented here is solely the responsibility of the authors and does not represent the official views of the HMRI, CPRIT, or the NIH.

Conflict of Interest

Dr. Kiss runs an externally funded laboratory (American Heart Association [20CDA35310329], and NIH [R35GM137819-03, -03S1, -03S2, -03S3], plus two subcontracts to NIH Contract #: 75N93019C00045) that is actively designing and testing different candidate RNA therapeutics. All authors anticipate seeking appropriate intellectual property protection for promising candidates that emerge from the lab's work. Dr. Kiss and Dr. Bejar are named inventors on a recently filed patent for a novel RNA therapy platform. Dr. Kiss also has patents planned for several additional RNA therapeutics and an inducible stable HUVEC cell line. Dr. Bejar is named as a co-inventor on a patent filing for a candidate RNA therapeutic (no.17969496). Further, Dr. Kiss serves as an ad hoc consultant for multiple different for-profit companies and to the RNA Core at the Houston Methodist Research Institute. Dr. Kiss also reports private stock for BioLife Solutions Inc.


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Article Info

Article Notes

  • Published on: March 09, 2023


  • RNA therapeutics
  • Skin
  • mRNA therapeutics
  • siRNA therapeutics
  • Antisense oligonucleotide therapeutics
  • ASO
  • Melanoma
  • Hypertrophic scars
  • Wound healing
  • Dermatology


Dr. Daniel L. Kiss,
Houston Methodist Academic Institute, Houston Methodist Research Institute, 6670 Bertner Ave, R10‑113, Houston 77030, TX, USA;

Copyright: ©2023 Kiss DL. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.