Ludwig Maximilian University of Munich

WEDNESDAY, July 10, 2024 -- Adherence to a Mediterranean diet incorporating eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) reduces skin lesions and improves quality of life in patients with acne, according to a study published online July 10 in the Journal of Cosmetic Dermatology . Anne Guertler, M.D., from Ludwig Maximilian University in Munich, and colleagues examined the clinical effects associated with increasing EPA/DHA levels in patients with acne. Sixty participants without prescription medication (23 with acne comedonica [AC] and 37 with acne papulopustulosa [AP]) adhered to a Mediterranean diet, incorporating omega-3 fatty acid supplementation. Blood EPA/DHA levels were tracked at four visits (V1 to V4) using the HS-omega 3 index (EPA/DHA [percent] of total identified fatty acids in erythrocytes: target, 8 to 11 percent; deficit, <8 percent; severe deficit, <4 percent). The researchers found that 98.3 percent of patients had an EPA/DHA deficit at baseline, with the mean HS-omega 3 index increasing from 4.9 to 8.3 percent at V1 to V4. At V4, significantly higher indices were seen for AC than AP. In both inflammatory and noninflammatory lesions, there were objective improvements observed. Four patients self-reported worsened appearance, but overall quality of life improved, especially in AP. Compared with beneficial foods, dietary triggers were more clearly defined. Cow's milk and dairy product intake was reduced. A high rate of compliance was observed, and there were no reports of adverse events. "Lifestyle interventions, including dietary recommendations, should not be considered in opposition to prescription medications, but rather as a valuable adjunct to any modern acne treatment plan," Guertler said in a statement. Omegametrix® GmbH performed the analysis of the HS-omega-3 Index® free of charge. Queisser Pharma GmbH & Co. KG offered omega-3 supplements free of charge.

MARLBOROUGH, Mass., March 21, 2024 (GLOBE NEWSWIRE) --Phio Pharmaceuticals Corp. (Nasdaq: PHIO), a clinical stage biotechnology company whose proprietary INTASYL™ siRNA gene silencing technology is designed to make immune cells more effective in killing tumor cells, today announced it is presenting new data about INTASYL on March 21st. The event is scheduled to take place at the 10th Immunotherapy of Cancer Conference (ITOC10), which will be held in Munich, Germany from March 21-23, 2024. The poster, Enhancing NK cell cytotoxicity against tumor cells with a novel self-delivering RNAi compound targeting Cbl-b, reveals new preclinical data demonstrating the potential of treatment with INTASYL self-delivering siRNA Compound PH-905, formerly known as Compound 27547, to improve function of natural killer (NK) cells. The data reveals a consistent silencing of Cbl-b mRNA, which has been shown to limit NK cell activation. Cytotoxic activity of NK cells against K562 (Chronic Myelogenous Leukemia) cancer cells was also increased. By reducing the expression of Cbl-b, INTASYL promotes NK cell activation and proliferation. These preclinical data demonstrate the potential of INTASYL Compound PH-905 to improve Adoptive Cell Therapy (ACT) by targeting and silencing Cbl-b. This may result in a more effective cell therapy for hematological malignancies. “These data underscore the versatility and potential of Phio’s INTASYL siRNA technology,” said Phio’s President & CEO Robert Bitterman. “It offers a strategy to enhance the effectiveness of ACT therapies in hematological malignancies.” The preclinical data demonstrate the following: INTASYL self-delivering RNAi compound PH-905 effectively targets and silences Cbl-b in primary NK cells without negative impact on their viability. Silencing of Cbl-b results in increased proliferation of primary NK cells. INTASYL silencing of Cbl-b in primary NK cells enhanced their functional cytotoxicity towards tumor cells. Silencing of Cbl-b leads to enhanced fitness of NK cells through increased expression of CD98 and CD25, potentially improving NK metabolism and promoting activation in response to IL-2. INTASYL compound PH-905 may be used to improve the anti-tumor response of NK cells to provide a more effective cell therapy for cancer treatment. Presentation Details are as follows: Title: Enhancing NK cell cytotoxicity against tumor cells with a novel self-delivering RNAi compound targeting Cbl-b Poster Number: P01.03 Topic: 01.Emerging concepts / New Agents Presenting Author: Melissa Maxwell Date and Time: 18:00 hrs Thursday, March 21, 2024 18:00-19:00 hrs Friday, March 22, 2024 Location: Ludwig Maximilian University Campus Großhadern, Lecture Room 3, Marchioninistrasse 15 81377 Munich, Germany About Phio Pharmaceuticals Corp. Phio Pharmaceuticals Corp. (Nasdaq: PHIO) is a clinical stage biotechnology company whose proprietary INTASYL™ siRNA gene silencing technology is designed to make immune cells more effective in killing tumor cells. INTASYL is the only self-delivering RNAi technology focused on immuno-oncology therapeutics. INTASYL drugs precisely target specific proteins that reduce the body’s ability to fight cancer, without the need for specialized formulations or drug delivery systems. For additional information, visit the Company’s website, . Forward Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements can be identified by words such as "intends," "believes," "anticipates," "indicates," "plans," "expects," "suggests," "may," "would," "should," "potential," "designed to," "will," "ongoing," "estimate," "forecast," "target," "predict," "could" and similar references, although not all forward-looking statements contain these words. These statements are based only on our current beliefs, expectations and assumptions and are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Examples of forward-looking statements include statements regarding the combination of an INTASYL compound targeting Cbl-b to demonstrate improved NK cell activity and to result in a more effective therapy for hematological malignancies. Our actual results may differ materially from those indicated in the forward-looking statements as a result of a number of important factors, including, but not limited to, the impact to our business and operations by inflationary pressures, rising interest rates, recession fears, the development of our product candidates, results from our preclinical and clinical activities, our ability to execute on business strategies, our ability to develop our product candidates with collaboration partners, and the success of any such collaborations, the timeline and duration for advancing our product candidates into clinical development, the timing or likelihood of regulatory filings and approvals, the success of our efforts to commercialize our product candidates if approved, our ability to manufacture and supply our product candidates for clinical activities, and for commercial use if approved, the scope of protection we are able to establish and maintain for intellectual property rights covering our technology platform, our ability to obtain future financing, market and other conditions and those identified in our Annual Report on Form 10-K and subsequent Quarterly Reports on Form 10-Q under the caption "Risk Factors" and in other filings the Company periodically makes with the SEC. Readers are urged to review these risk factors and to not act in reliance on any forward-looking statements, as actual results may differ from those contemplated by our forward-looking statements. Phio does not undertake to update forward-looking statements to reflect a change in its views, events or circumstances that occur after the date of this release, except as required by law. Contact: Phio Pharmaceuticals Corp. ir@phiopharma.com PR Contact Michael Adams Bridge View Media adams@bridgeviewmedia.com

Immune cells must learn not to attack the body itself. A team of researchers has discovered a previously unknown mechanism behind this: other immune cells, the B cells, contribute to the 'training' of the T cells in the thymus gland. If this process fails, autoimmune diseases can develop. The study confirms this for Neuromyelitis optica, a disease similar to Multiple Sclerosis. Other autoimmune diseases may be linked to the failure of this new mechanism as well. Immune cells must learn not to attack the body itself. A team of researchers from the Technical University of Munich (TUM) and the Ludwig Maximilian University of Munich (LMU) has discovered a previously unknown mechanism behind this: other immune cells, the B cells, contribute to the "training" of the T cells in the thymus gland. If this process fails, autoimmune diseases can develop. The study confirms this for Neuromyelitis optica, a disease similar to Multiple Sclerosis. Other autoimmune diseases may be linked to the failure of this new mechanism as well. In children and adolescents, the thymus gland functions as a "school for T cells." The organ in our chest is where the precursors of those T cells that would later attack the body's own cells are discarded. Epithelial cells in the thymus present a large number of molecules that occur in the body to the future T cells. If any of them reacts to one of these molecules, a self-destruction program is triggered. T cells that attack the body's own molecules remaining intact and multiplying, on the other hand, can cause autoimmune diseases. New mechanism discovered In Nature, the team led by Thomas Korn, Professor of Experimental Neuroimmunology at TUM and a Principal Investigator in the SyNergy Cluster of Excellence, and Ludger Klein, Professor of Immunology at LMU's Biomedical Center (BMC), describe another previously unknown mechanism behind this. In addition to the precursors of T cells, the thymus gland also contains other immune cells, the B cells. They develop in the bone marrow but migrate to the thymus in early childhood. "The function of B cells in the thymus gland has been a mystery that has puzzled immunologists for many years," says Thomas Korn. The researchers have now been able to show for the first time that B cells play an active role in teaching T cells which targets not to attack. MS-like disease due to malfunction in tolerance formation Neuromyelitis optica is an autoimmune disease similar to multiple sclerosis (MS). While it is not yet known which molecules are attacked in MS, it is well-established that T cells respond to the protein AQP4 in neuromyelitis optica. AQP4 is most prominently expressed in cells of the nervous tissue, which then becomes the target of the autoimmune reaction. Frequently, the optic nerve is affected. The researchers were able to show that in the thymus gland of humans and mice not only the epithelial cells but also B cells express and present AQP4 to the T cell precursors. If the B cells were prevented from doing so in animal experiments, AQP4-reactive T cell precursors were not eliminated and the autoimmune disease developed. This was also the case when the epithelial cells still presented the molecule. The team concludes from this that B cells in the thymus are a necessary condition for immune tolerance regarding AQP4. Protection against subsequent interactions between T cells and B cells "We suspect that this previously unknown process has evolved particularly to prevent dangerous interactions between autoreactive T and B cells in the lymph nodes and spleen, the so-called peripheral immune compartment," says Ludger Klein. Once the immune system is developed, B and T cells can communicate and thus trigger highly effective immune reactions. This is useful when it comes to fighting pathogens quickly. On occasion, however, B cells may accidentally present the body's own proteins, such as AQP4. If the T cells that react to AQP4 had not been sorted out in the thymus, this could lead to a sudden and violent large-scale attack on the body. Possible cause of other immune disorders "We assume that problems with the training of T cells by the B cells in the thymus can cause other autoimmune diseases as well," says Thomas Korn. "After all, the B cells in the thymus present a whole range of the body's own proteins. The corresponding interactions must be investigated in further studies." According to the researchers, likely suspects include antiphospholipid syndrome (APS) and certain forms of cerebral amyloid angiopathy. "Looking further into the future, this interaction in the thymus might be exploited to treat existing autoimmune diseases in a very targeted manner," says Thomas Korn.