Exhibit 99.1

Introduction to HT - KIT an mRNA Frame Shifting Therapeutic Significantly Inhibits Tumor Growth in Mast Cell - Derived Cancers

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H T - KIT HT - KIT is a novel antisense oligonucleotide under development for the treatment of cancers resulting from aberrant KIT signaling . The HT - KIT drug is designed to more specifically target the receptor tyrosine kinase KIT, which is required for the proliferation, survival and differentiation of bone marrow - derived hematopoietic stem cells . Mutations in the KIT pathway have been associated with several human cancers, such as mast cell - derived cancers (aggressive systemic mastocytosis (ASM), systemic mastocytosis with associated hematological neoplasm (SM - AHN), or mast cell leukemia (MCL)), gastrointestinal stromal tumors, and acute myeloid leukemia . HT - KIT is currently in the pre - clinical stage of development .

Targeting KIT by frameshifting mRNA transcripts as a therapeutic strategy for aggressive mast cell neoplasms Douglas B. Snider 1 , Greer K. Arthur 1 , Guido H. Falduto 2 , Ana Olivera 2 , Lauren C. Ehrhardt - Humbert 1 , Emmaline Smith 1 , Cierra Smith 1 , Dean D. Metcalfe 2 and Glenn Cruse 1 1 Department of Molecular Biomedical Sciences, CVM, NC State University 2 Laboratory of Allergic Diseases, NIAID, NIH Fig . 1 . ESO - mediated alternative splicing of exon 4 in c - KIT pre - mRNA . (A) HT - KIT ESO was designed to target the donor splice site of exon 4 , which led to exclusion of exon 4 by the spliceosome . This is predicted to introduce a premature stop codon due to a frameshift in the open reading frame of the mRNA transcript . Yellow boxes represent exons ; thick black bar rep r ese n ts intron s . F L - c - KIT = full - length c - R T - P CR KI T , t - c - KIT = trun c ated c - KI T . (B) demonstrating splice - switching of c - KIT by HT - KIT ESO in comparison to control oligo in HMC - 1. 2 cel l s. Black arrow = ful l - length c - KI T , orange arrow = alternatively spliced truncated c - KIT mRNA . (C) qRT - PCR of KIT transcripts in HMC - 1 . 2 cells demonstrates a significant reduction in KIT mRNA transcripts with HT - KIT relative to control cells after correction against β - acti n . Figure 1

Fi g . 2. H T - KIT ESO reduc e s KIT e x p r e s s i on a n d in d uces apopt o s i s o f neoplas t ic hu m an ma s t cell s . (A) Mean flow cytometry data for total KIT expression calculated from the geometric MFI. (B) Combined data from flow cytomet r y for Annexin V expre s sed a s the ge o metric MF I . (C) C o m b i n e d geome t ric MFI of HMC - 1.2 cells in culture. LIVE/DEAD staining in HMC - 1.2 cells at each time point. (D) Viable cell counts of Data are the mean “ SEM from 3 independent experiments. *p<0.05, **p<0.01, ***p<0.001, ANOVA with Sidak’s post - test. Figure 2

Fig. 4. Systemic delivery of human HT - KIT ESO inhibits tumor growth in a humanized xenograft mast cell neoplasia model . The top schematic representation of the protocol for the xenograft model used . ( A ) Examples of tumors in mice during treatment . The red arrows indicate the tumor and the green arrows show a secondary growth caused by drag of the needle during inoculation . ( B ) Measurements of tumor volume over time during treatment . Arrows indicate days that HT - KIT or vehicle control was administered . ( C ) Photograph of tumors after mice were euthanized at day 14 . Measurements are in centimeters . ( D ) Weight of excised tumors after mice were euthanized on day 14 . ( E ) Spleen weight at the conclusion of the experiment . ( F ) Liver weight at the conclusion of the experiment . ( G ) Mice weight was monitored over the course of the experiment . No significant differences were observed over the course of the experiment . Data are the mean “ SEM from 5 mice per group . *p< 0 . 05 , **p< 0 . 01 , ***p< 0 . 001 . ANOVA with Dunnett’s post - test ( B ), or unpaired t - test ( D & E ) . Figure 3

Fig . 4 . HT - KIT ESOs redu c e liver of ne o plas t ic mast cells i n a infiltration humanized neoplasia. ( A - D) Example li v er sections from xen o graft m odel o f mast ce l l NSG mice showing neoplastic mast cell infiltrates with H & E (A) and IHC for human KIT (B) in the vehicle control liver and almost no infiltrates in the H T - KIT t r eated livers (C Histopathological assessment neoplastic infiltration in l i v e r . & D ) . (E) o f % of (F) Histopatholo g ical assessm e nt of neop l astic foci size i n liver s . Gr a phic a l re p rese n tati o n of data includes box where middle bar plots and whiskers rep r esent represents median m i ni m um and m a xi m u m . determined by Fisher’s LSD The p - value was test with ordinary on e - w a y A N O VA or uncorrecte d Dunn’ s test with Kruskal - Wallis one - way ANOVA. *p≤0.05, **p≤0.01, ***p≤0.001, ****p≤0.0001 Figure 4

Figure 5 Fi g . 5. H T - KIT E S O reduces tumor g r owth in an isograft model of MC neoplasia. P 815 cells were transduced to make intracellular luciferase . (A) DBA/ 2 J female mice protocol for the isograft model . Vehicle control or HT - KIT ESO was administered every 3 days . (B) Bioluminescence from P 815 neoplastic cells was significantly reduced in intraturmoral (IT) (p= 0 . 0007 ) and intravenous (IV) (p= 0 . 0220 ) HT - KIT ESO treatment groups compared to controls . (C - E) IVIS images overlay primary site tumor where bioluminescent P 815 neopl astic cells were detected . Equal - sized ROIs over the primary tumor site standardized area for photon flux (total counts) detected from all mice on study (representative images shown) . (F - I) Tumor weight (F) , volume (G) , and depth (H) collectively represent decreased primary site tumor burden (F - G) and penetration into underlying structures (H) for IT and IV HT - KIT treatment groups compared to controls. (F) T umor m a ss was r e du c e d for I T (p = 0 .013 2 ) an d IV (p=0.0674) HT - KIT ESO treatment group compared to controls. (G) T umor volume w as reduced for I T (p= 0 .018 8 ) a nd IV (p=0.0530) HT - KIT ESO treatment group compared to controls. (H) Tumor depth was significantly reduced for IT (p <0.0001) a nd I V (p = 0 .000 8 ) H T - KIT ESO tre a tment g ro up compa r ed to controls . (G) Tumor necrosis was increased for IT (p= 0 . 0434 ) and IV (p= 0 . 0588 ) HT - KIT ESO treatment group compared to controls . *p≤ 0 . 05 , **p≤ 0 . 01 , ***p≤ 0 . 001 , ****p≤ 0 . 0001 .

Fig . 6 . HT - KIT ESO reduced cardinal signs of mast cell leukemia in an isograft model of mutant mast cell neoplasia . (A) Percent of m a r r ow i n filtrated by P 8 1 5 ne o pla s tic cell s . bone (B) Re p r e s e n t a t iv e micr o gra p h of bone marrow from vehicle controls (B) compared to IT (C) , and IV (D) HT - KIT ESO . (E) Displacement of hematopoietic bone marrow tissue (myelophthisis) by neoplastic mast cells . (F) Packed red blood cell volume (hematocrit) . (G) Bone marrow hematopoiesis as measured by myeloid progenitor to erythroid progenitor (M : E ratio) . (H) Circulating neoplastic mast cells on differential counts . (I) Blood smear of ne o pla s tic mast cel l s R o m a no w s ky with (representative image shown from vehicle stain cont r ol animal blood). (J) H&E histopathology assessment of ne o pla s tic embo l i an d circu l a t ing neop l a s tic cel l s in or g a ns . ( K - L) E mb o li of neop l astic mast cells in pulmonary vessels from H&E histopathology sections from control (K) and intravenous HT - KIT ESO (L) treatment groups . *p≤ 0 . 05 , **p≤ 0 . 01 , ***p≤ 0 . 001 , ****p≤0.0001. c

Targeting KIT by frameshifting mRNA transcripts as a therapeutic strategy for aggressive mast cell neoplasms Douglas B. Snider 1 , Greer K. Arthur 1 , Guido H. Falduto 2 , Ana Olivera 2 , Lauren C. Ehrhardt - Humbert 1 , Emmaline Smith 1 , Cierra Smith 1 , Dean D. Metcalfe 2 and Glenn Cruse 1 1 Department of Molecular Biomedical Sciences, CVM, NC State University 2 Laboratory of Allergic Diseases, NIAID, NIH Activating mutations in the proto - oncogene c - KIT are associated with the mast cell (MC) clonal disorders cutaneous mastocytosis, systemic mastocytosis and its variants including aggressive systemic mastocytosis and mast cell leukemia, and MC sarcoma . Currently, therapies inhibiting KIT signaling are a leading strategy to treat MC proliferative disorders . However, these approaches may have off - target effects and in some patients, complete remission or improved survival time cannot be achieved . These limitations led us to develop an approach using chemically stable exon skipping oligonucleotides (ESO) that induce exon skipping of pre - mRNA to alter gene splicing and introduce a frameshift into mature KIT mRNA transcripts . Exon - skipping c - KIT to remove exon 4 will force a frameshift in mature mRNA introducing an immediate STOP codon triggering nonsense - mediated mRNA decay . If this pathway is saturated, production of a severely truncated non - functional KIT protein would result . Both of these mechanisms would deplete functional KIT, inhibit proliferation and induce apoptosis of neoplastic MCs . This alternate approach to MC neoplasia results in marked downregulation of KIT expression, diminished KIT signaling, inhibition of MC proliferation and rapid induction of apoptosis in neoplastic HMC - 1 . 2 MCs . This downregulation of KIT expression is achieved by combining two independent mechanisms involving nonsense - mediated mRNA decay and the production of alternatively spliced non - functional proteins . We further demonstrate that in vivo administration of KIT targeting ESOs significantly inhibits tumor growth and systemic organ infiltration using both an allograft mastocytosis model and a humanized xenograft MC tumor model . We propose that our innovative approach, which employs well - tolerated, chemically stable oligonucleotides to target KIT expression through unconventional pathways, has potential as a KIT - targeted therapeutic alone, or in combination with agents that target KIT signaling, in the treatment of KIT - associated malignancies . R a ti ona l e Funding : Department of Molecular Biomedical Sciences, College of Veterinary Medicine, start - up funds (G . C . ), NCSU Center for Human Health and the Environment grant #ES 025128 , NIH T 32 OD 011130 and the Division of Intramural Research of NIAID within the National Institutes of Health . Conflict of Interest disclosure : Dr . Cruse has filed a patent application related to the research reported in this study . Dr . Cruse has research support from Hoth Therapeutics and also serves on their Scientific Advisory Board . The terms of this arrangement have been reviewed and approved by NC State University in accordance with its policy on objectivity in research . Acknowledgements Hy po t he si s Figure 2 Figure 5 Figure 3 Figure 6 Fig . 2 . HT - KIT ESO reduces KIT expression and induces apoptosis of neoplastic human mast cells . (A) Mean flow cytometry data for total KIT expression calculated from the geometric MFI . (B) Combined data from flow cytometry for Annexin V expressed as the geometric MFI . (C) Combined geometric MFI of LIVE/DEAD staining in HMC - 1 . 2 cells at each time point . (D) Viable cell counts of HMC - 1 . 2 cells in culture . Data are the mean “ SEM from 3 independent experiments . *p< 0 . 05 , **p< 0 . 01 , ***p< 0 . 001 , ANOVA with Sidak’s post - test . Fig . 5 . HT - KIT ESO reduces tumor growth in an isograft model of MC neoplasia . P 815 cells were transduced to make intracellular luciferase . (A) DBA/ 2 J pro tocol for the female i so graft HT - KIT mice model. ESO Vehicle control or w a s admi ni ster e d every 3 days. (B) Bioluminescence from P815 neoplastic cells was signi f i c an t ly redu ced in intraturmoral (IT) (p=0.0007) and intravenous (IV) (p=0.0220) HT - KIT ESO treatment groups compared to controls. (C - E) IVIS images overlay prim a ry site bioluminescent t um o r w her e P 81 5 n e op l a stic cells were detected. Equal - sized ROIs over the primary tumor site standardized area for photon flux ( total c o un t s) detected from all mice on study (representative images shown). (F - I) Tumor weight (F) , volume (G) , and depth (H) collectively represent decreased primary site tumor burden (F - G) and penetration into underlying structures (H) for IT and IV HT - KIT treatment groups compared to controls. (F) Tumor mass was reduced for IT (p=0.0132) and IV (p=0.0674) HT - KIT ESO Figure 4 Fig. 6. HT - KIT ESO reduced cardinal signs of mast cell leukemia in an isograft model of mutant mast cell bon e marro w i n fi l trated P815 neopl a stic cel l s. n e o p lasia. (A) Percent of by (B) Representative micrograph of bone marrow from vehicle controls (B) compared to IT (C) , and IV (D) HT - KIT ESO . (E) Dis pla c e ment of hematopoietic bone marrow neopl a stic mast cel l s. tissue (myelop h th i s i s) by (F) Figure 1 Fig . 1 . ESO - mediated alternative splicing of exon 4 in c - KIT pre - mRNA . (A) HT - KIT ESO was designed to target the donor splice site of exon 4 , which led to exclusion of exon 4 by the spliceosome . This is predicted to introduce a premature stop codon due to a frameshift in the open reading frame of the mRNA transcript . Yellow boxes represent exons ; thick black bar represents introns . FL - c - KIT = full - length c - KIT, t - c - KIT = truncated c - KIT . (B) RT - PCR demonstrating splice - switching of c - KIT by HT - KIT ESO in comparison to control oligo in HMC - 1 . 2 cells . Black arrow = full - length c - KIT, orange arrow = alternatively spliced truncated c - KIT mRNA . (C) qRT - PCR of KIT transcripts in HMC - 1 . 2 cells demonstrates a significant reduction in KIT mRNA transcripts with HT - KIT relative to control cells after correction against β - actin . S u mm a r y Fig . 4. S y s t e mic del i ve r y o f hu ma n HT - KIT ESO inhibits tumor growth in a humanized xenograft mast cell neoplasia model. The top schematic representation of the protocol for the xenograft model used. ( A ) Examples of tumors in mice during treatment . The red arrows indicate the tumor and the green arrows show a secondary growth caused by drag of the needle during inoculation . ( B ) Measurements of tumor volume over time during treatment . Arrows indicate days that HT - KIT or vehicle control was administered . ( C ) Photograph of tumors after mice were euthanized at day 14 . Measurements are in centimeters . ( D ) Weight of excised tumors after mice were euthanized on day 14 . ( E ) Spleen weight at the conclusion of the experiment . ( F ) Liver weight at the conclusion of the experiment . ( G ) Mice weight was monitored over the course of the experiment . No significant differences were observed over the course of the experiment. Data are the mean “ SEM from 5 mice per group. *p<0.05, **p<0.01, ***p<0.001. ANOVA with Dunnett’s post - test ( B ), or unpaired t - test ( D & E ). treatment group compared to controls . (G) Tumor volume was reduced for IT (p= 0 . 0188 ) and IV (p= 0 . 0530 ) HT - KIT ESO treatment group compared to controls . (H) Tumor depth was significantly reduced for IT (p < 0 . 0001 ) and IV (p= 0 . 0008 ) HT - KIT ESO treatment group compared to controls . (G) Tumor necrosis was increased for IT (p= 0 . 0434 ) and IV (p= 0 . 0588 ) HT - KIT ESO treatment group compared to controls . *p≤ 0 . 05 , **p≤ 0 . 01 , ***p≤ 0 . 001 , ****p≤ 0 . 0001 . Packed red blood cell volume (hematocrit) . (G) Bone marrow hematopoiesis as measured by myeloid progenitor to erythroid progenitor (M : E ratio) . (H)Circulating neoplastic mast cells on differential counts . (I) Blood smear of neoplastic mast cells with Romanowsky stain (representative image shown from vehicle control animal blood) . (J) H&E histopathology assessment of neoplastic emboli and circulating neoplastic cells in organs . (K - L) Emboli of neoplastic mast cells in pulmonary vessels from H&E histopathology sections from control (K) and intravenous HT - KIT ESO (L) treatment groups . *p≤ 0 . 05 , **p≤ 0 . 01 , ***p≤ 0 . 001 , ****p≤ 0 . 0001 . Fig . 4 . HT - KIT ESOs reduce liver infiltration of neoplastic mast cells in a humanized xenograft model of mast cell neoplasia . (A - D) Example liver sections from NSG mice showing neoplastic mast cell infiltrates with H&E (A) and IHC for human KIT (B) in the vehicle control liver and almost no infiltrates in the HT - KIT treated livers (C & D) . (E) Histopathological assessment of % of neoplastic infiltration in liver . (F) Histopathological assessment of neoplastic foci size in livers . Graphical representation of data includes box plots where middle bar represents median and whiskers represent minimum and maximum . The p - value was determined by Fisher’s LSD test with ordinary one - way ANOVA or uncorrected Dunn’s test with Kruskal - Wallis one - way ANOVA . *p≤ 0 . 05 , **p≤ 0 . 01 , ***p≤ 0 . 001 , ****p≤ 0 . 0001 .