ALDH7A1

A new mouse study has identified a gene-enzyme interaction that appears to play a key role in how the brain forms memories. The findings provide insights into how PDE inhibitor medications may help diseases like Alzheimer's. The process by which memories are formed in the hippocampus region of the brain is complex. It relies on a precise choreography of interactions between neurons, neurotransmitters, receptors and enzymes. A new mouse study led by researchers at the UC Davis School of Medicine has identified an intricate molecular process involving gene expression in the neurons that appears to play a critical role in memory consolidation. The research was published in Science Signaling. "This is an exciting mechanism. It shows that an enzyme like phosphodiesterase is key in controlling gene expression necessary for memory consolidation," said Yang K. Xiang, a professor in the Department of Pharmacology and senior author of the paper. Xiang's research focuses on understanding how dysregulation or impairment of cellular and molecular mechanisms in the heart and brain can lead to diseases like heart failure and Alzheimer's. Multiple steps in neuron appear critical for memory The new study focuses on the central adrenergic system. The ability to pay attention, which is essential in learning and memory, is controlled by the central adrenergic system in the brain. To understand the components critical for memory, the researchers looked at beta-2 adrenergic receptors. The receptors are present in different cell types throughout the body. They are also found on nerve cells in the hippocampal region of the brain. The researchers show that when beta-2 adrenergic receptors are activated -- through a series of molecular steps known as a signaling pathway -- they stimulate the nucleus of the neuron to export an enzyme, phosphodiesterase 4D5 (PDE4D5). Previous studies have identified PDE4D5 as having a role in promoting learning and memory. Lack of phosphorylation leads to poor memory A crucial step to stimulating this memory-related gene expression -- the export of PDE4D5 -- appears to be the attachment of a phosphate group (known as phosphorylation) to the receptor. This is accomplished by an enzyme known as a kinase. The kinase involved in this case is a G-protein receptor kinase. The researchers used genetically altered mice to test whether phosphorylation of the beta-2 adrenergic receptors by G-protein receptor kinase was necessary for gene expression -- the export of the PDE4D5 enzyme. The mice lacked a phosphorylation site on their beta-2 adrenergic receptors, meaning their neurons could not follow the normal signaling pathway when the receptors were activated. The researchers found that, as expected, these genetically altered mice exhibited poor memory related to space and location. This is the same memory pathway that is disrupted during the early stages of Alzheimer's disease. However, when they provided the memory-impaired mice with a drug known as a PDE4 inhibitor (comparable to the PDE4D5 enzyme that would normally be exported), the mice's ability to learn and retain memories was increased. "The gene expression forms the material foundation of the memory in your brain. If you don't have gene expression, you won't have memory," Xiang explained. PDE inhibitors in Alzheimer's have had mixed results The use of PDE inhibitors is being explored for Alzheimer's disease. Studies of the PDE5 inhibitor sildenafil, known as Viagra, have had mixed results. A 2021 NIH study found Viagra was associated with a reduced risk of Alzheimer's disease, but a later study found Viagra was not associated with lower Alzheimer's risk. "We need to understand what is causing impairment in diseases like Alzheimer's so we can find interventions that allow patients to regain ability or slow down the disease progression," said Xiang. "This study highlights the potential of PDE inhibitors in rescuing memory in Alzheimer's patients." Additional authors on the paper are Joseph M. Martinez, Aleksandra Jovanovicand Josephine de Chabotfrom UC Davis; Ao Shen from UC Davis and Guangzhou Medical University; Bing Xufrom UC Davis and VA Northern California Health Care System; and Jin Zhang from, UC San Diego.

LA JOLLA, Calif., Dec. 06, 2022 (GLOBE NEWSWIRE) -- MediciNova, Inc., a biopharmaceutical company traded on the NASDAQ Global Market (NASDAQ:MNOV) and the JASDAQ Market of the Tokyo Stock Exchange (Code Number: 4875), today announced that MediciNova’s Chief Medical Officer, Kazuko Matsuda, MD PhD MPH, presented positive results from a subgroup analysis of the completed Phase 2 clinical trial which evaluated MN-001 (tipelukast) for the treatment of hypertriglyceridemia at the International Diabetes Federation (IDF) World Diabetes Congress 2022 held online December 5 - 8, 2022. In the completed Phase 2 study, MN-001 (tipelukast) significantly reduced serum triglycerides in participants with non-alcoholic fatty liver disease (NAFLD) and hypertriglyceridemia (HTG). Subsequent in vitro results revealed that MN-001 (tipelukast) downregulated CD36 and upregulated ABCG1 mRNA expression, both of which are highly associated with Type 2 diabetes mellitus (T2DM). Hypothesizing that MN-001 (tipelukast) might be more effective at reducing serum triglycerides in participants with a dual diagnosis of NAFLD and Type 2 diabetes mellitus (T2DM), a subgroup analysis was conducted in participants with and without T2DM. In the presentation entitled, “Improvement of Serum Lipid Panel by Tipelukast (MN-001) in Type 2 Diabetes Mellitus and Non-alcoholic Fatty Liver Disease Patients" (Abstract #LI2022-1192) the following results were announced: Compared to subjects without T2DM, the T2DM group showed a greater reduction in serum triglyceride levels at Week 8 (50.8% reduction for with T2DM versus 17.8% reduction for without T2DM, p=0.098).Mean HDL increase was significantly greater in subjects with T2DM than subjects without T2DM at Week 8 (15.8% versus 1.0%, p<0.0002). In comparison to subjects without T2DM, the T2DM group showed a greater reduction in serum LDL levels at Week 8 (15.4% versus 6.7%). Kazuko Matsuda, M.D. Ph.D., M.P.H., Chief Medical Officer, MediciNova, Inc., commented, “We are very pleased to present this subgroup analysis of the results of our completed Phase 2 trial in individuals diagnosed with NAFLD and hypertriglyceridemia. Those participants with T2DM/prediabetes showed greater improvement in the serum lipid profile than participants without T2DM. These findings suggest that MN-001 is a potential treatment for patients with dyslipidemia and NAFLD due to T2DM. A trial to evaluate the efficacy and safety of MN-001 in patients with T2DM, NAFLD, and HTG is currently ongoing.” About NAFLD, Type 2 Diabetes Mellitus (T2DM), and Hypertriglyceridemia NAFLD is considered the hepatic manifestation of metabolic syndrome; studies have reported that 50% of patients with metabolic syndrome also have NAFLD. There is sufficient clinical and epidemiological evidence supporting the assertion that NAFLD is strongly associated with an increased prevalence and incidence of cardiovascular disease, T2DM, chronic kidney disease, and malignancy. The presence of dyslipidemia (hypercholesterolemia, hypertriglyceridemia, or both) is reported in 20 - 80% of NAFLD cases. About MN-001 MN-001 (tipelukast) is a novel, orally bioavailable, small molecule compound thought to exert its effects through several mechanisms to produce its anti-inflammatory and anti-fibrotic activity in preclinical models, including leukotriene (LT) receptor antagonism, inhibition of phosphodiesterases (PDE) (mainly 3 and 4), and inhibition of 5-lipoxygenase (5-LO). The 5-LO/LT pathway has been postulated as a pathogenic factor in fibrosis development, and MN-001's inhibitory effect on 5-LO and the 5-LO/LT pathway is a novel approach to treat fibrosis. MN-001 has been shown to down-regulate expression of genes that promote fibrosis including LOXL2, Collagen Type 1 and TIMP-1. MN-001 has also been shown to down-regulate expression of genes that promote inflammation including CCR2 and MCP-1. In addition, MN-001 was found to inhibit triglyceride synthesis in hepatocytes by inhibiting arachidonic acid uptake. About MediciNova MediciNova, Inc. is a clinical-stage biopharmaceutical company developing a broad late-stage pipeline of novel small molecule therapies for inflammatory, fibrotic, and neurodegenerative diseases. Based on two compounds, MN-166 (ibudilast) and MN-001 (tipelukast), with multiple mechanisms of action and strong safety profiles, MediciNova has 11 programs in clinical development. MediciNova’s lead asset, MN-166 (ibudilast), is currently in Phase 3 for amyotrophic lateral sclerosis (ALS) and degenerative cervical myelopathy (DCM) and is Phase 3-ready for progressive multiple sclerosis (MS). MN-166 (ibudilast) is also being evaluated in Phase 2 trials in glioblastoma and substance dependence. MN-001 (tipelukast) was evaluated in a Phase 2 trial in idiopathic pulmonary fibrosis (IPF) and a second Phase 2 trial in non-alcoholic fatty liver disease (NAFLD) is ongoing. MediciNova has a strong track record of securing investigator-sponsored clinical trials funded through government grants. Statements in this press release that are not historical in nature constitute forward-looking statements within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, without limitation, statements regarding the future development and efficacy of MN-166, MN-001, MN-221, and MN-029. These forward-looking statements may be preceded by, followed by, or otherwise include the words "believes," "expects," "anticipates," "intends," "estimates," "projects," "can," "could," "may," "will," "would," “considering,” “planning” or similar expressions. These forward-looking statements involve a number of risks and uncertainties that may cause actual results or events to differ materially from those expressed or implied by such forward-looking statements. Factors that may cause actual results or events to differ materially from those expressed or implied by these forward-looking statements include, but are not limited to, risks of obtaining future partner or grant funding for development of MN-166, MN-001, MN-221, and MN-029 and risks of raising sufficient capital when needed to fund MediciNova's operations and contribution to clinical development, risks and uncertainties inherent in clinical trials, including the potential cost, expected timing and risks associated with clinical trials designed to meet FDA guidance and the viability of further development considering these factors, product development and commercialization risks, the uncertainty of whether the results of clinical trials will be predictive of results in later stages of product development, the risk of delays or failure to obtain or maintain regulatory approval, risks associated with the reliance on third parties to sponsor and fund clinical trials, risks regarding intellectual property rights in product candidates and the ability to defend and enforce such intellectual property rights, the risk of failure of the third parties upon whom MediciNova relies to conduct its clinical trials and manufacture its product candidates to perform as expected, the risk of increased cost and delays due to delays in the commencement, enrollment, completion or analysis of clinical trials or significant issues regarding the adequacy of clinical trial designs or the execution of clinical trials, and the timing of expected filings with the regulatory authorities, MediciNova's collaborations with third parties, the availability of funds to complete product development plans and MediciNova's ability to obtain third party funding for programs and raise sufficient capital when needed, and the other risks and uncertainties described in MediciNova's filings with the Securities and Exchange Commission, including its annual report on Form 10-K for the year ended December 31, 2021 and its subsequent periodic reports on Form 10-Q and current reports on Form 8-K. Undue reliance should not be placed on these forward-looking statements, which speak only as of the date hereof. MediciNova disclaims any intent or obligation to revise or update these forward-looking statements. INVESTOR CONTACT: Geoff O'Brien Vice President MediciNova, Inc. info@medicinova.com

ROCKVILLE, Md. and SUZHOU, China, Dec. 4, 2022 /PRNewswire/ -- Innovent Biologics, Inc. ("Innovent") (HKEX: 01801), a world-class biopharmaceutical company that develops, manufactures and commercializes high-quality medicines for the treatment of oncology, autoimmune, metabolic, ophthalmology and other major diseases, and UNION therapeutics A/S (UNION), a privately-held, multi-asset, clinical stage, pharmaceutical development company focused on immunology and infectious diseases, today announced that the first Chinese healthy volunteer has been successfully dosed in the Phase I study of orismilast (Innovent R & D code: IBI353), a potential best-in-class PDE4 inhibitor in global clinical Phase II stage. This study (CTR 20222393) is a multiple dose escalation Phase I study in healthy volunteers aiming to evaluate the pharmacokinetic (PK) profile, safety and tolerability of orismilast in healthy Chinese subjects after multiple doses to support the subsequent clinical development of orismilast in multiple indications such as psoriasis and atopic dermatitis (AD). Orismilast is a next-generation PDE4 inhibitor with high potency for the PDE4 subtypes linked to inflammation. In 2021, Innovent reached a strategic cooperation with UNION to obtain exclusive rights to the research, development and commercialization of orismilast in China (including mainland China, Hong Kong, Macao and Taiwan). Orismilast has generated positive proof of concept (PoC) data in psoriasis (administered orally) and in AD (administered topically) and is being developed as a potential best- or first-in-class oral treatment option in both diseases. Compared to other PDE4 inhibitors, the selectivity of orismilast for PDE4 subtypes B and D and the novel modified release delivery is expected to generate a favorable therapeutic window, potentially resulting in improved efficacy and tolerability. Dr. Lei Qian, Vice President of Clinical Development of Innovent, stated: 'There is currently no cure for psoriasis, and there is a great unmet clinical need in this field. Orismilast is a new target molecule Innovent laid out in the field of autoimmunity by co-development with UNION. It is potentially one of the best candidates in the mid-stage of clinical development at Innovent. The results of ex-China clinical studies have demonstrated that orismilast has good safety profile and biological activity. The ongoing Phase I study will evaluate the safety and tolerability of orismilast in Chinese healthy volunteers and provide the basis for further clinical development. We will accelerate the clinical development of orismilast in Chinese subjects with psoriasis or AD in order to obtain regulatory approval as soon as possible in China and to fulfill the needs of safe, effective and convenient long-term oral treatment for patients, thus significantly reducing the disease burden of patients and their pain. We will truly uphold our mission of "To develop and commercialize high-quality biopharmaceuticals that are affordable to ordinary people".' Kim Kjøller, CEO of UNION therapeutics, stated: 'We are excited by the strong advancement of orismilast by Innovent, which is essential in our joint efforts to provide this novel treatment to patients with dermatological diseases globally. We have seen good progress in our three late-stage clinical trials with orismilast for treatment of psoriasis, atopic dermatitis, and hidradenitis suppurative, respectively. This, together with the now ongoing Phase I study in China, is important steps in the development of orismilast.' About Psoriasis and atopic dermatitis (AD) Psoriasis is a multisystem disease characterized by well-defined erythematous scaly plaques that are often pruritic. Estimates of psoriasis prevalence range from 0.51% to 11.43% in adults and 0% to 1.37% in children[1].Psoriasis is a common disease that occurs more frequently with age. The most common clinical type of psoriasis is psoriasis vulgaris (plaque psoriasis). The involvement of inflammatory cells (e.g., T cells and myeloid dendritic cells) and pro-inflammatory cytokines (e.g., tumor necrosis factor-α, interleukin (IL) -12, and IL-17) in the pathogenesis of psoriasis has been well documented [2]. There is currently no cure for psoriasis. Psoriasis vulgaris can be managed with local therapy, phototherapy, or systemic therapy or any combination of these. It is estimated that around 80% of psoriasis patients have mild to moderate psoriasis[3] [4] , for those patients topical therapy is used first line. About one-third of psoriasis patients experience moderate-to-severe disease, systemic medications (biologic or nonbiologic) or phototherapy are preferred regimens for such patients[5]. However, long term treatment of psoriasis with topical therapies (e.g. TCS), biologic therapies (eg, antibodies) is often limited by safety and tolerability issues, with decreasing efficacy over time, thus resulting in poor patient adherence due to inconvenient routes of administration (eg, injections) [6]. Therefore, there is an unmet need for safe, effective, and convenient long-term oral therapy for patients with psoriasis. Atopic Dermatitis (AD) is a chronic inflammatory disease characterized by eczematous lesions and intense pruritus, affecting up to 20% of children and up to 3% of adults[7].Inflammatory infiltrates in these skin lesions include T lymphocytes, neutrophils, eosinophils, monocytes, macrophages, and mast cells[8].High levels of PDE4 activity have also been identified in leukocytes of these patients[9].AD is usually treated with topical therapies, primarily intermittent prophylactic use of topical corticosteroids and/or topical calcineurin inhibitors, along with daily emollients. Intermittent corticosteroid use poses minimal risk of corticosteroid-related adverse effects such as skin atrophy, striae formation in sensitive or thin skin areas, and systemic effects. However, long-term adherence to topical therapy was low. Off-label use of other conventional systemic oral immunomodulators such as cyclosporine, azathioprine, and methotrexate may be effective in adult AD patients, but patients discontinue treatment due to adverse events or lack of efficacy. Use of these agents has known safety limitations and requires regular laboratory monitoring. Therefore, better systemic treatment options are needed, particularly for AD patients who do not respond well to topical treatment. Dupilumab, a subcutaneous biologic therapy targeting IL-4 and IL-13 receptors, is approved by the US Food and Drug Administration for the treatment of moderate to severe AD in adults. The need for oral treatment options remains imperative in this disease state. About Orismilast IBI353 (Orismilast) is a next-generation PDE4 inhibitor with high potency for the PDE4 subtypes linked to inflammation currently under development as an oral treatment for psoriasis, AD and HS. PDE4 is a cyclic adenosine monophosphate (cAMP)-specific PDE that is expressed by immune and inflammatory cells, including T lymphocytes, neutrophils, eosinophils, monocytes, dendritic cells, and macrophages[10]. In these cells PDE4 is the predominant PDE form and PDE4 inhibitors increase cAMP levels. High cAMP levels tend to reduce proliferation and cytokine production, whereas low concentrations of cAMP have the opposite effects. PDE4 inhibition has previously been shown to downregulate production of a range of proinflammatory cytokines[11]-[13]. Consistent with previously published work, orismilast demonstrates a potent and broad anti-inflammatory effect by inhibiting the secretion of Th1 (TNFα and IFNg, Th17 (IL-22 and IL-23), and Th2 (IL-4, IL-5 and IL-13) effector cytokines in human PBMCs. In addition, potent inhibition of innate cytokines (IL-1α and IL-1b ) was also observed. These results support further development of orismilast as a potential best-in-class or first-in-class PDE4 inhibitor for the treatment of chronic inflammatory skin diseases including psoriasis, HS and AD. About Innovent Inspired by the spirit of "Start with Integrity, Succeed through Action," Innovent's mission is to develop, manufacture and commercialize high-quality biopharmaceutical products that are affordable to ordinary people. Established in 2011, Innovent is committed to developing, manufacturing and commercializing high-quality innovative medicines in the fields of oncology, metabolic, autoimmune, ophthalmology and other major diseases. On October 31, 2018, Innovent was listed on the Main Board of the Stock Exchange of Hong Kong Limited with the stock code: 01801.HK. Since its inception, Innovent has developed a fully integrated multi-functional platform which includes R&D, CMC (Chemistry, Manufacturing, and Controls), clinical development and commercialization capabilities. Leveraging the platform, the company has built a robust pipeline of 35 valuable assets in the fields of cancer, metabolic disorder, autoimmune disease and other major therapeutic areas, with 8 approved products on the market. These include: TYVYT (sintilimab injection), BYVASDA (bevacizumab biosimilar injection), SULINNO (adalimumab biosimilar injection), HALPRYZA (rituximab biosimilar injection), Pemazyre (pemigatinib oral inhibitor), olverembatinib （BCRABLTKI, Cyramza (ramucirumab) and selpercatinib. An additional 2 assets are under NMPA NDA review, 5 assets are in Phase 3 or pivotal clinical trials, and 20 more molecules are in clinical studies. Innovent has built an international team with advanced talent in high-end biological drug development and commercialization, including many global experts. The company has also entered into strategic collaborations with Eli Lilly and Company, Sanofi, Adimab, Incyte, MD Anderson Cancer Center and other international partners. Innovent strives to work with many collaborators to help advance China's biopharmaceutical industry, improve drug availability and enhance the quality of the patients' lives. For more information, please visit: . and . Note: TYVYT® (sintilimab injection) is not an approved product in the United States. BYVASDA® (bevacizumab biosimilar injection), SULINNO®, and HALPRYZA® (rituximab biosimilar injection) are not approved products in the United States. TYVYT® (sintilimab injection, Innovent) BYVASDA® (bevacizumab biosimilar injection, Innovent) HALPRYZA® (rituximab biosimilar injection, Innovent) SULINNO® (adalimumab biosimilar injection, Innovent) Pemazyre® (pemigatinib oral inhibitor, Incyte Corporation). Pemazyre® was discovered by Incyte Corporation and licensed to Innovent for development and commercialization in Mainland China, Hong Kong, Macau and Taiwan. CYRAMZA® (ramucirumab, Eli Lilly). Cyramza® was discovered by Eli Lilly and licensed to Innovent for commercialization in Mainland China. Selpercatinib (Eli Lilly). Selpercatinib was discovered by Eli Lilly and licensed to Innovent for commercialization in Mainland China. Disclaimer: 1. This indication is still under clinical study, which hasn't been approved in China. 2. Innovent does not recommend any off-label usage. About UNION therapeutics UNION therapeutics is a privately-held, multi-asset, clinical stage, pharmaceutical development company focused on immunology and infectious diseases. The company is currently working with two complementary chemistry classes, spanning immunology and microbiology with multiple candidates in clinical development. UNION is headquartered in Hellerup, Denmark, and led by an international team consisting of biotech entrepreneurs and senior pharma executives, with a collective track record of developing and launching more than fifteen marketed drugs. Read more at Innovent's Forward-Looking Statements This news release may contain certain forward-looking statements that are, by their nature, subject to significant risks and uncertainties. The words "anticipate", "believe", "estimate", "expect", "intend" and similar expressions, as they relate to Innovent Biologics ("Innovent"), are intended to identify certain of such forward-looking statements. Innovent does not intend to update these forward-looking statements regularly. These forward-looking statements are based on the existing beliefs, assumptions, expectations, estimates, projections and understandings of the management of Innovent with respect to future events at the time these statements are made. These statements are not a guarantee of future developments and are subject to risks, uncertainties and other factors, some of which are beyond Innovent's control and are difficult to predict. Consequently, actual results may differ materially from information contained in the forward-looking statements as a result of future changes or developments in our business, Innovent's competitive environment and political, economic, legal and social conditions. Innovent, the Directors and the employees of Innovent assume (a) no obligation to correct or update the forward-looking statements contained in this site; and (b) no liability in the event that any of the forward-looking statements does not materialise or turn out to be incorrect. Reference: [1]. Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol. 2017 Feb;31(2):205-212. doi: 10.1111/jdv.13854. Epub 2016 Aug 30. [2]. Quaglino P, Bergallo M, Ponti R, Barberio E, Cicchelli S, Buffa E, et al. Th1, Th2, Th17 and regulatory T cell pattern in psoriatic patients: modulation of cytokines and gene targets induced by etanercept treatment and correlation with clinical response. Dermatology. 2011;223(1):57-67. [3]. Stern RS, Nijsten T, Feldman SR, Margolis DJ, Rolstad T. Psoriasis is common, carries a substantial burden even when not extensive, and is associated with widespread treatment dissatisfaction. J Investig Dermatol Symp Proc 2004;9:136-9 [4]. Menter A, Gottlieb A, Feldman SR, Van Voorhees AS, Leonardi C, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol 2008;58:826-50 [5]. Menter A, Korman NJ, Elmets CA, Feldman SR, Gelfand JM, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 5. Guidelines of care for the management and treatment of psoriasis with phototherapy and photochemotherapy. J Am Acad Dermatol. 2010;62:114-135. [6]. Ravindran V, Scott DL, Choy EH. A systemic review and meta-analysis of efficacy and toxicity of disease modifying anti-rheumatic drugs and biological agents for psoriatic arthritis. Ann Rheum Dis. 2008;67:855-859. [7]. Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr Metab. 2015;66 Suppl 1:8-16. [8]. Cooper KD: Atopic dermatitis: recent trends in pathogenesis and therapy. J Invest Dermatol 1994, 102:128–137. [9]. Butler JM, Chan SC, Stevens S, Hanifin JM: Increased leukocyte histamine release with elevated cyclic AMP-phosphodiesterase activity in atopic dermatitis. J Allergy Clin Immunol 1983, 71:490–497. [10]. Spina D. PDE4 inhibitors: current status. Br J Pharmacol. 2008;155(3):308-315. [11]. Brideau C, Van Staden C, Styhler A, Rodger IW, Chan C-C. The effects of phosphodiesterase type 4 inhibitors on tumour necrosis factor-α and leukotriene B4 in a novel human whole blood assay. Br J Pharmacol 1999;126(4):979-88. [12]. Manning CD, Burman M, Christensen SB, Cieslinski LB, Essayan DM, Grous M, et al. Suppression of human inflammatory cell function by subtype-selective PDE4 inhibitors correlates with inhibition of PDE4A and PDE4B. Br J Pharmacol 1999;128(7):1393-8. [13]. Samrao A, Berry TM, Goreshi R, Simpson EL. A pilot study of an oral phosphodiesterase inhibitor (apremilast) for atopic dermatitis in adults. Arch Dermatol 2012;148(8):890-7.. SOURCE Innovent Biologics