Investigators propose a phase 1b/2a, randomized, double-blind, placebo-controlled, parallel group dose finding and biomarker study to evaluate the safety, tolerability, and biomarker activity of 2-HOBA in 48 MCI/AD participants. Participants will be randomized 1:1:1:1 to receive 250, 500, 750 mg 2-HOBA acetate TID or placebo for 16 weeks. Blood and cerebral spinal fluid (CSF) will be collected to measure markers of protein modification by dicarbonyls (IsoLGs- & MDA), pTau-181, YKL-40, and NF-L.

开始日期2025-09-01

申办/合作机构

MTI Biotech, Inc.

[+1]

NCT06176118

/ Not yet recruiting临床2期IIT

Clinical Trial of 2-HOBA in Pulmonary Arterial Hypertension

Based on existing literature and clinical trials, 2- hydroxbenzylamine (2-HOBA) has clear impact on mechanisms that much of the international field of pulmonary hypertension (PH) research agrees are central to disease progression. The investigator's preliminary data and Phase I studies demonstrate not only a clear positive impact on reducing pulmonary vascular resistances in Group I and II PH, and both cytokine and molecular biomarkers of disease, but also indicated the potential for a substantial positive effect on heart function under load stress. In this Phase II project, investigators will test the safety and efficacy of 2-HOBA in PH patients, improving the function of the right ventricle under stress in a large animal model, and effectiveness in the context of standard-of-care in mouse models and large animals, to establish the remaining data needed to proceed to commercialization.

开始日期2025-12-01

申办/合作机构

Vanderbilt University Medical Center

[+1]

NCT04941599

/ Recruiting临床2期IIT

2-Hydroxybenzylamine (2-HOBA) to Reduce HDL Modification and Improve HDL Function in Familial Hypercholesterolemia (FH)

The Investigators will test the hypothesis that 2-HOBA will reduce modification of HDL and LDL and improve HDL function in humans with heterozygous FH. The Investigators plan to first study subjects with Familial Hypercholesterolemia (FH), treating them with 750 mg of 2-HOBA or placebo every 8 hours for 6 weeks.

开始日期2024-02-14

申办/合作机构

Vanderbilt University Medical Center

[+1]

100 项与 2-羟基苄胺相关的临床结果

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100 项与 2-羟基苄胺相关的转化医学

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100 项与 2-羟基苄胺相关的专利（医药）

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358

项与 2-羟基苄胺相关的文献（医药）

2025-03-04·SYNTHETIC COMMUNICATIONS

Selectfluor-mediated oxidative deamination: A scalable approach to aromatic aldehydes synthesis

作者: Li, Lin ; Pan, Renming ; Zheng, Wenfang ; Gao, Chengkan ; Lin, Xiangyang

The catalyst-free oxidative deamination without over-oxidation constitutes a considerable challenge in the synthesis of aromatic aldehydes.Herein, we introduce a Selectfluor-mediated Lewis acid system that achieves the oxidative deamination of benzylic amines with α-C-H bond activation to yield aromatic aldehydes.Noteworthy features include the direct use of Selectfluor that can activate the α-C-H bond under catalyst- and base-free conditions via the in-situ dehydrofluorination effect.The approach is demonstrated for a broad scope of benzylic amines without over-oxidation and accomplishes 200 mmol scale synthesis.

2025-03-01·Circulation-Arrhythmia and Electrophysiology

Oxidative Stress Causes Mitochondrial and Electrophysiologic Dysfunction to Promote Atrial Fibrillation in Pitx2 ^+/− Mice

Article

作者: Smart, Charles D. ; Amarnath, Venkataraman ; Saffitz, Jeffrey E. ; Murray, Katherine T. ; Agrawal, Vineet ; Van Amburg, Joseph C. ; Christopher, Isis L. ; Dougherty, Owen P. ; Subati, Tuerdi ; Fogo, Agnes B. ; Yang, Zhenjiang ; Barnett, Joey V. ; Woodall, Kaylen K. ; Murphy, Matthew B. ; Johnson, Joyce E. ; Kim, Kyungsoo

BACKGROUND::

The strongest genetic risk factors for atrial fibrillation (AF) are DNA variants on chromosome 4q25 near the transcription factor gene PITX2 (Pitx2:Paired-like homeodomain transcription factor 2). Mice deficient in Pitx2 ( Pitx2+/− ) have increased AF susceptibility, although the molecular mechanism(s) remains controversial. Pitx2 encodes a transcription factor that activates an antioxidant response to promote cardiac repair. Increased reactive oxygen species causing oxidation of polyunsaturated fatty acids generates reactive lipid dicarbonyl moieties that adduct to proteins and other macromolecules to promote cellular injury. We tested the hypothesis that oxidative stress, and specifically isolevuglandins, the most reactive lipid dicarbonyls identified, are increased in the setting of Pitx2 deficiency to promote proarrhythmic remodeling and AF.

METHODS::

Pitx2+/− and Pitx2+/+ wild-type littermate control mice were treated orally with vehicle, the lipid dicarbonyl scavenger 2-hydroxybenzylamine, or an inactive control compound at weaning, until study at age 16 to 18 weeks.

RESULTS::

Pitx2+/− mice demonstrated increased P wave duration indicative of slowed atrial conduction, as well as increased inducible AF burden and sustained AF, compared with wild type, and these abnormalities were prevented by 2-hydroxybenzylamine. Both reactive oxygen species and isolevuglandin protein adducts were elevated in Pitx2+/− atria with reduced expression of reactive oxygen species–protective genes. High-resolution respirometry demonstrated impaired mitochondrial function in Pitx2+/− atria, with disruption of mitochondrial integrity and cell-cell junctions with connexin lateralization, as well as decreased mitochondrial biogenesis gene expression. Proarrhythmic ionic current remodeling in Pitx2+/− atrial myocytes included elevated resting membrane potential, abbreviated action potential duration, and reduced maximum phase 0 upstroke velocity compared with wild type. Most of these abnormalities were ameliorated or prevented by 2-hydroxybenzylamine.

CONCLUSIONS::

These results demonstrate a critical role for lipid dicarbonyl mediators of oxidative stress in the proarrhythmic remodeling and AF susceptibility that occurs with Pitx2 deficiency, implying the possibility of genotype-specific therapy to prevent AF.

2025-02-18·ONCOGENE

Spermine oxidase promotes Helicobacter pylori-mediated gastric carcinogenesis through acrolein production

Article

作者: Carson, Kate S. ; Luis, Paula B. ; Gobert, Alain P. ; Coburn, Lori A ; Gobert, Alain P ; Sierra, Johanna C. ; Coburn, Lori A. ; Williams, Kamery J. ; Latour, Yvonne L ; Choksi, Yash A. ; Latour, Yvonne L. ; Delgado, Alberto G ; Allaman, Margaret M. ; Barry, Daniel P ; Hawkins, Caroline V ; Zagol-Ikapitte, Irene ; McNamara, Kara M. ; Wilson, Keith T ; Sierra, Johanna C ; McNamara, Kara M ; Piazuelo, M Blanca ; Asim, Mohammad ; Tyree, Regina N ; Allaman, Margaret M ; Delgado, Alberto G. ; Wilson, Keith T. ; Hawkins, Caroline V. ; Barry, Daniel P. ; Schneider, Claus ; Williams, Kamery J ; Tyree, Regina N. ; Luis, Paula B ; Piazuelo, M. Blanca ; Carson, Kate S ; Choksi, Yash A

Abstract:

Helicobacter pylori is the primary cause of gastric cancer, and there is a need to discover new molecular targets for therapeutic intervention in H. pylori disease progression. We have previously shown that spermine oxidase (SMOX), the enzyme that catabolizes the back-conversion of the polyamine spermine to spermidine, is upregulated during infection and is associated with increased cancer risk in humans. We sought to determine the direct role of SMOX in gastric carcinogenesis during H. pylori infection. In this study, we demonstrate that transgenic FVB/N insulin-gastrin (INS-GAS) mice that develop gastric carcinoma with H. pylori infection were protected from cancer development with Smox deletion. RNA sequencing revealed that genes associated with the immune system and cancer were downregulated in the infected Smox–/– mice. Furthermore, there was a decrease in cell proliferation and DNA damage in infected Smox–/– animals. There was significant generation of adducts of the highly reactive electrophile acrolein, a byproduct of SMOX activity, in gastric tissues from H. pylori-infected humans and wild-type, but not Smox–/– mice. Genetic deletion of Smox in murine organoids or chemical inhibition of SMOX in human gastric epithelial cells significantly reduced generation of acrolein induced by H. pylori. Additionally, acrolein-induced DNA damage in gastric epithelial cells was ablated with the electrophile scavenger 2-hydroxybenzylamine (2-HOBA). Gastric acrolein adduct levels were attenuated in infected INS-GAS mice treated with 2-HOBA, which exhibit reduced gastric carcinoma. These findings implicate SMOX and acrolein in H. pylori-induced carcinogenesis, thus indicating their potential as therapeutic targets.

项与 2-羟基苄胺相关的新闻（医药）

2022-08-03

·PRNewswire

Rigel Pharmaceuticals and Forma Therapeutics Announce Licensing Agreement for Olutasidenib, a Novel Mutant IDH1 Inhibitor for the Potential Treatment of Relapsed or Refractory Acute Myeloid Leukemia

SOUTH SAN FRANCISCO, Calif. and WATERTOWN, Mass., Aug. 2, 2022 /PRNewswire/ -- Rigel Pharmaceuticals, Inc. (Nasdaq: RIGL) and Forma Therapeutics, Inc. (Nasdaq: FMTX) today announced that they have entered into an exclusive, worldwide license agreement to develop, manufacture and commercialize olutasidenib, an oral, small molecule inhibitor of mIDH1 being investigated for the treatment of relapsed/refractory acute myeloid leukemia (R/R AML) and other malignancies. In a Phase 2 registrational study of olutasidenib in patients with mIDH1 R/R AML, olutasidenib demonstrated a robust composite complete remission rate and duration of response and was well-tolerated. The U.S. Food and Drug Administration (FDA) has accepted Forma's New Drug Application (NDA) for olutasidenib. The Prescription Drug User Fee Act (PDUFA) target action date is February 15, 2023. "Olutasidenib is a potential market-leading treatment that we believe, based on the registrational Phase 2 data, can improve outcomes in patients with mIDH1+ relapsed or refractory acute myeloid leukemia, and is a strategic fit for our business," said Raul Rodriguez, Rigel's president and CEO. "This transaction expands our hematology-oncology portfolio and enables us to leverage our strong commercial capabilities to provide a potential new therapy for these patients who remain underserved despite currently available therapies." "The compelling efficacy and safety data generated to date highlight the potential for olutasidenib to transform the treatment of mIDH1+ R/R AML. The development and approval of olutasidenib, pending a favorable FDA decision, would represent an important milestone for Forma that highlights our R&D capabilities," said Frank Lee, Forma's president and CEO. "Given Rigel's focus on hematologic diseases and cancers and the strength of their commercial infrastructure, we believe they are well-positioned to execute on our shared objective of delivering olutasidenib to patients in need." The registrational cohort of the open-label Phase 2 study evaluated olutasidenib as monotherapy in 153 mIDH1+ R/R AML patients. The primary efficacy-evaluable population of the cohort was comprised of 123 R/R AML patients, who received olutasidenib 150 mg twice daily at least six months prior to the interim analysis cutoff date of June 18, 2020 and had a centrally confirmed IDH1 mutation. The primary endpoint was a composite of a complete remission (CR) plus a complete remission with partial hematological recovery (CRh), defined as less than 5% blasts in the bone marrow, no evidence of disease, and partial recovery of peripheral blood counts (platelets >50,000/microliter and ANC >500/microliter). Results from the interim analysis of the trial1 demonstrated a 33% CR+CRh in mIDH1+ R/R AML patients. Among those with CR+CRh, the estimated 18-month survival was 87% and the median duration of CR+CRh was not yet reached, with a more conservative sensitivity analysis indicating a median duration of 13.8 months. Importantly, these data provide compelling evidence of clinical efficacy with a durable response and a favorable tolerability profile, both of which we believe differentiates olutasidenib from other currently available treatment options for mIDH1+ R/R AML patients. Olutasidenib was well-tolerated, with adverse events (AEs) being consistent with the late stage of disease and the heavily pre-treated population. A safety analysis for all 153 patients enrolled in the registrational Phase 2 study found the most common grade 3/4 (≥ 10%) treatment-emergent adverse events (TEAEs) were febrile neutropenia (20%), anemia (19%), thrombocytopenia (16%), and neutropenia (13%). Updated data from the registrational study will be presented at an upcoming medical congress. "The data from the Phase 2 registrational trial of olutasidenib demonstrated encouraging results, particularly on durability and survival, with median duration of response that appears to be longer than currently available treatment options and an 18-month survival rate among those with CR+CRh of 87%," said Jorge E. Cortes, M.D., Director, Georgia Cancer Center, Cecil F. Whitaker Jr., GRA Eminent Scholar Chair in Cancer, and Phase 2 trial investigator. "Given the trial's compelling efficacy data in duration of response, the favorable tolerability profile, and the still limited treatment options of patients with mIDH1+ R/R AML, olutasidenib has the potential to be an important new treatment option for patients." Under the terms of the agreement, Forma will receive an upfront payment of $2.0 million, and is eligible to receive an additional $17.5 million upon the achievement of certain near-term regulatory, approval, and first commercial sale milestones. In addition, Forma is eligible to receive a total of up to an additional $215.5 million in connection with the achievement of certain development and commercial milestones. Forma is also eligible to receive tiered royalties in the low-teens to mid-thirties. Moving forward, Rigel will be responsible for the potential launch and commercialization of olutasidenib in the U.S., and intends to work with potential partners to further develop and commercialize olutasidenib outside the U.S. Conference Call and Webcast Today at 4:30 p.m. Eastern Time, with KOL and Olutasidenib Phase 2 trial investigator, Jorge E. Cortes, M.D. Rigel will host a live conference call and webcast today at 4:30 p.m. Eastern Time (1:30 p.m. Pacific Time) to discuss financial results, provide an update on the business, including the licensing agreement for olutasidenib. The conference call will also feature a presentation of the olutasidenib Phase 2 interim results by Jorge E. Cortes, M.D., Director, Georgia Cancer Center, Cecil F. Whitaker Jr., GRA Eminent Scholar Chair in Cancer, and Phase 2 trial investigator. Participants can access the live conference call by dialing (877) 407-3088 (domestic) or (201) 389-0927 (international). The conference call will also be webcast live and can be accessed from the Investor Relations section of the company's website at www.rigel.com. The webcast will be archived and available for replay after the call via the Rigel website. About Olutasidenib and AML Olutasidenib is an oral, small molecule investigational agent designed to selectively bind to and inhibit mutated IDH1 enzymes. This targeted treatment has the potential to provide therapeutic benefit by reducing 2-HG levels and restoring normal cellular differentiation. IDH1 is a natural enzyme that is part of the normal metabolism of all cells. When mutated, IDH1 activity can promote blood malignancies and solid tumors. IDH1 mutations are present in 6 to 9 percent of patients with AML2. AML is a rapidly progressing cancer of the bone marrow and blood3. AML occurs primarily in adults and accounts for about 1 percent of all adult cancers. The American Cancer Society estimates that about 20,940 new cases, most in adults, arose in 2021 in the United States alone.4 Quality of life declines for patients with each successive line of treatment for AML, and well-tolerated treatments in relapsed or refractory disease remain an unmet need. About Rigel Rigel Pharmaceuticals, Inc., is a biotechnology company dedicated to discovering, developing, and providing novel small molecule drugs that significantly improve the lives of patients with hematologic disorders, cancer, and rare immune diseases. Rigel's pioneering research focuses on signaling pathways that are critical to disease mechanisms. The company's first FDA-approved product is TAVALISSE® (fostamatinib disodium hexahydrate) tablets, the only oral spleen tyrosine kinase (SYK) inhibitor for the treatment of adult patients with chronic immune thrombocytopenia who have had an insufficient response to a previous treatment. The product is also commercially available in Europe (TAVLESSE), the United Kingdom (TAVLESSE) and Canada (TAVALISSE) for the treatment of chronic immune thrombocytopenia in adult patients. Fostamatinib is currently being studied in a Phase 3 clinical trial (NCT03764618) for the treatment of warm autoimmune hemolytic anemia (wAIHA)5; a Phase 3 clinical trial (NCT04629703) for the treatment of hospitalized high-risk patients with COVID-195 and an NIH/NHLBI-sponsored Phase 3 clinical trial (ACTIV-4 Host Tissue Trial, NCT04924660) for the treatment of COVID-19 in hospitalized patients. Rigel's other clinical programs include its interleukin receptor-associated kinase (IRAK) inhibitor program, and a receptor-interacting serine/threonine-protein kinase (RIPK) inhibitor program in clinical development with partner Eli Lilly and Company. In addition, Rigel has product candidates in development with partners BerGenBio ASA and Daiichi Sankyo. For further information, visit www.rigel.com or follow us on Twitter or LinkedIn. Please see www.TAVALISSE.com for full Prescribing Information. About Forma Therapeutics Forma Therapeutics is a clinical-stage biopharmaceutical company focused on the research, development, and commercialization of novel therapeutics to transform the lives of patients with rare hematologic diseases and cancers. Our pipeline is led by etavopivat, an investigational, once-daily, selective pyruvate kinase-R (PKR) activator designed to be a disease-modifying therapy with the potential to improve red blood cell (RBC) health and transform the lives of people living with sickle cell disease, thalassemia, and lower risk MDS. Our R&D engine combines deep biology insight, chemistry expertise and clinical development capabilities to create drug candidates with differentiated mechanisms of action focused on indications with high unmet need. Our work has generated a broad proprietary portfolio of programs with the potential to provide profound patient benefit. For more information, please visit www.FormaTherapeutics.com or follow us on Twitter @FORMAInc and LinkedIn. De Botton, S., et al. Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021) 7006-7006. NCCN Clinical Practice Guidelines in Oncology, Acute Myeloid Leukemia. Version 2.2022 – June 14, 2022. https://www.nccn.org/guidelines/guidelines-detail?category=1&id=1411 Leukemia & Lymphoma Society. Accessed July 25, 2022. https://www.lls.org/leukemia/acute-myeloid-leukemia The American Cancer Society. Key statistics for acute myeloid leukemia (AML). Revised January 12, 2021. Accessed Dec. 2, 2021 at https://www.cancer.org/cancer/acute-myeloid-leukemia/about/key-statistics.html. The product for this use or indication is investigational and has not been proven safe or effective by any regulatory authority.

合作抗体财报小分子药物

2021-08-10

·GlobeNewswire

Slowing Down the Aging Process Is as Easy as Cel1

AUCKLAND, New Zealand, Aug. 10, 2021 (GLOBE NEWSWIRE) -- It may be the first time in human history we finally have the right tools to age well says Greg Macpherson, a biotechnologist, pharmacist and founder of SRW Laboratories (SRW), who has developed the first full line of targeted cellular health supplements with his team of leading scientists who are the global authorities on aging, cellular structure and function, biochemistry and biotechnology. “Up until now we’ve aged fairly well with basic lifestyle management and a little luck. Today, we have the precise tools to take it to another level – the cellular level,” said Macpherson. “Using the nine hallmarks of aging, or identified causes of aging, we can literally reprogram our cells to function at a much younger biological age than our current chronological age. No other generation has had this technology available to them.” For more than a decade, Macpherson has been working in the biotechnology sector, focusing on the aging process at the cellular level. This work led him to discover ways to target the nine identified, scientific hallmarks of aging, which is the premise of his newly released book, “Harnessing the Nine Hallmarks of Aging.” While writing the book he realized finding the recommended nutrients and compounds needed for optimal cellular stability, nourishment and renewal was not that easy. This led him to the idea of developing a company centered on cellular health supplements to help people succeed at aging well. “No one wants to live a long life if you can’t enjoy it,” said Macpherson. “Humans have the capacity to live up to 120 years, and now we have discovered a way to help get people there, while living a very fulfilled life.” In addition to diet, fasting, exercise, stress reduction and sleep, Macpherson says recent developments on understanding how to support DNA repair mechanisms have opened the door to new nutraceuticals that have a profound impact on slowing the aging process. One of the game changing molecules he is utilizing in SRW’s supplement, Cel1 Stability, is hobamine (2-HOBA), an extract from Himalayan Tartary buckwheat, discovered by Vanderbilt University scientists through the research spearheaded by Dr. Naji Abumrad. It’s so cutting edge, it is hard to find in most supplements; in fact, Macpherson’s company is only the second company in the world to offer it and Abumrad is a part of SRW’s scientific team. 2-HOBA provides new ways to protect DNA and other cellular components from oxidative stress while maintaining healthy levels of free radical signaling. It is vastly different than what is commonly associated with the class of phytochemicals known as antioxidants, in that it can stop the cascading damage in the cell that can ignite inflammation or stress in the body. Research shows that 2-HOBA can help the immune system stabilize to a restful, healthy state, versus being over-stimulated, which can happen over the long term as we age. This is just one of the cutting-edge ingredients found in SRW’s Cellular System Range of nutraceuticals, Cel1Stability, Cel2 Nourishment and Cel3 Renewal, that when taken in combination support the body’s ability to defy the nine identified hallmarks of aging, which are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication. Each Cellular System supplement has a different cellular health focus. A person’s biological age (or cell’s age) can be determined by DNA testing and reveals the actual age cells are acting, which could be vastly different from a person’s chronological age (or number of years lived). SRW’s goal is to curate the very latest in science and research to develop formulations that help people age healthier. The debut of SRW’s Cellular System Range includes Cel1 Stability, Cel2 Nourishment and Cel3 Renewal. Cel1 Stability supports DNA structure and function and is recommended if you experience stress factors that negatively impact DNA, such as lack of sleep, UV and pollution exposure, poor diet or excessive stress. Cel2 Nourishment supports energy levels in the cell by providing a supply of NMN, an energy precursor that is used in the mitochondria, and is recommended if you experience low energy or want extended energy without caffeine. Cel3 Renewal supports the cellular housekeeping processes, which plays an important role in clearing out and recycling cells in the body called senescent cells that are no longer useful and is recommended to support the body’s ability to form proteins and recycle cells. Current studies are pointing to senescent cells as causing the body’s overreaction to coronavirus in older populations, contributing to increased mortality. Another indicator that immune response and the cell’s age have a lot to do with how well we age. Learn more about cellular health at SRW: . Photos accompanying this announcement are available at

2021-03-23

·GlobeNewswire

SRW Founder Unlocks Inner Youthfulness By “Harnessing the Nine Hallmarks of Aging”

AUCKLAND, New Zealand, March 23, 2021 (GLOBE NEWSWIRE) -- Whitening or graying of hair, wrinkling or sagging skin, slowing of thought, memory or thinking, and an overall decrease in energy are often what defines aging. If we wait for these traditional aging markers, it may be too late to do anything about them. It’s the reason why Greg Macpherson, pharmacist and author of the new book, “Harnessing the Nine Hallmarks of Aging,” says understanding aging at a cellular level gives you an advantage. In the absence of a unified theory on aging, about a decade ago, scientists defined the underlying aging process as the nine hallmarks of aging. They developed a consensus model, noting what each hallmark of aging should exhibit during normal aging, and in cell models, if you aggravate it you see accelerated aging and if you make it better it slows the aging process. “Our bodies are dynamic, molecular machines, so what was discovered was the idea that how we age is not predetermined by your literal age,” said Macpherson. “We can easily influence the aging process with specific, healthy lifestyle choices that can make a dramatic difference in how well we age and how long we live.” In Macpherson’s book, he dives deeper into each of the nine hallmarks of aging, which are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication; and how to harness them for better longevity. Macpherson explains how cells are damaged, repaired, and how your DNA plays an important role. He shares how to protect your DNA from damaging disruptors that cause aging, such as, ultraviolet rays from sun, air pollution and smoking. He also describes how to repair DNA during specific decades of your life with cellular supporting nutrients including: hobamine (2-Hoba from Himalayan buckwheat), along with exercising and eating healthier for people in their 30s; and using Nicotinamide Mononucleotide (NMN) to boost the body’s natural levels of NAD+, a key enzyme that supports healthy cell metabolism and energy levels for people in their 40s; and fisetin, a natural compound that can clear out old, defective cells for people in their 50s. The book also covers how the practice of fasting, on a routine basis, can turn back time on a cellular level to help you age more favorably. Beyond theory and concept, Macpherson has used his entrepreneurial spirit to further develop solutions to this new paradigm of aging, described in his book, by launching SRW Laboratories, a science- and research-based company that curates the latest biotechnology research to formulate natural products designed to help slow the onset of aging and disease, and develop evidence based solutions for those who are experiencing age-related health concerns. SRW, which stands for Science, Research and Wellness, is Macpherson’s natural world laboratory that will develop the preventative formulas from nature required to slow down the aging process based on the nine hallmarks of aging. With aging being the single biggest risk factor for developing disease, Macpherson’s mission to slow the aging process at a cellular level could help millions of people delay the onset of diseases associated with advanced aging like Alzheimer’s and heart disease. “We have brought together the world’s leading scientists on aging to SRW and synthesized their work to curate an array of cutting edge nutrients that uniquely combat the nine hallmarks of aging,” said Macpherson. “I’m most excited about this project because it is a culmination of my life’s work.” A proud New Zealander, Macpherson grew up in Ōtaki, a small town on the Kāpiti Coast of the North Island. He earned his bachelor of pharmacy degree at the University of Otago Medical School in 1992. Macpherson then got involved with a number of technology-driven startups including founding a pharmacy that specialized in providing health care to older adults in residential care facilities, bringing the first robotic dispensing machines into New Zealand and achieving the first license to provide wholesale packing services to the pharmacy sector. In 1997, he established , one of the first online pharmacies in New Zealand with a focus on client wellness, making it the No. 1 online pharmacy for more than two decades. Since that time he has been building other companies with the aging endgame in mind. SRW is his first company that will aggressively address aging at the cellular level with the only cell-focused nutrient line called Cel Range designed to specifically slow down the aging process based on the nine hallmarks of aging. More on SRW at: ; order, “Harnessing the Nine Hallmarks of Aging” at: . Photos accompanying this announcement are available at:

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100 项与 2-羟基苄胺相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
阿尔茨海默病引起的痴呆症	临床2期	美国	Vanderbilt University Medical Center	2025-09-01
轻度认知障碍	临床2期	美国	Vanderbilt University Medical Center	2025-09-01
II型高脂蛋白血症	临床2期	美国	Vanderbilt University Medical Center	2024-02-14
动脉粥样硬化	临床2期	美国	Vanderbilt University Medical Center	2022-09-30
高血压	临床2期	美国	Vanderbilt University Medical Center	2022-09-30
炎症	临床2期	美国	Vanderbilt University Medical Center	2022-09-30
类风湿关节炎	临床2期	美国	Vanderbilt University Medical Center	2022-08-09
高胆固醇血症	临床2期	美国	National Institute for Materials Science IAI	2021-08-15
II a型高脂蛋白血症	临床2期	美国	National Institute for Materials Science IAI	2021-08-15
心房颤动	临床2期	美国	Vanderbilt University Medical Center	2020-05-15

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04433091 (CTgov)	临床2期	心房颤动	95	2-Hydroxybenzylamine (2-HOBA)	醖鏇壓蓋積網廠鏇顧鹽 = 蓋糧顧膚壓簾積範夢鏇壓範衊廠鏇壓選繭顧製 (鏇獵願衊窪糧廠廠衊獵, 鏇鏇襯網夢糧製壓繭憲 ~ 糧選繭鑰積淵鬱醖膚構) 更多	-	2024-11-21
NCT04433091 (CTgov)	临床2期	心房颤动	95	Placebo (Placebo)	醖鏇壓蓋積網廠鏇顧鹽 = 簾餘鏇繭壓壓蓋網醖鹽壓範衊廠鏇壓選繭顧製 (鏇獵願衊窪糧廠廠衊獵, 醖廠艱製艱選廠餘齋憲 ~ 鬱餘鏇鏇膚鏇積網憲鹽) 更多	-	2024-11-21
ATS2023	N/A	肺性高血压	-	2-HOBA	簾蓋鹹觸繭積醖選廠窪(餘蓋積夢鏇鹽築鹹築製) = 顧築獵選餘廠鏇憲獵廠願鏇襯範顧構鏇憲遞餘 (願製淵壓構衊網鏇願網 )	-	2023-05-21