Latest news with #JesseRichards
BBC News
31-07-2025
- BBC News
Jesse Richards' mum in 'living nightmare' over missing body
A woman whose son was killed 16 years ago has said she is in a "living nightmare" while his body remains missing. Jesse Richards was killed in Cleeve Prior, Evesham, on 31 July 2009 in an attack over a drugs debt, police at West Mercia Police suspect his body was then taken to Warwickshire and hidden, with the whereabouts of his remains unknown to this day. Five men were jailed over his death in 2012, with three convicted of Richards, whose son would have been 56 this year, said: "Every year I get older, my time shortens and the likelihood of me ever recovering Jesse lessens." She added: "Never having recovered him and my time running out is the living nightmare I face every day."Asking for fresh information, she said: "I make this appeal to anyone with any humanity to put an end to my suffering. If you know anything and have a shred of decency, please, come forward." 'Right thing to do' A spokesperson for West Mercia Police said the force was "still as committed today" as it was 16 years ago to finding the Insp Gareth Evans said: "Despite the time that has passed, the desire to assist in the recovery of Jesse Richards remains strong because it's the right thing to do."All those convicted of involvement in Jesse's death have since been released from their custodial sentences, Jesse's family still live with their loss and inability to put him to rest."While circumstances have changed for them, they could also have changed for others involved or perhaps for their families, yet nothing changes for Lucy Richards. "Someone knows what happened to Jesse and where he is. By not coming forward, you are depriving a family of the closure they so need and desire." Follow BBC Hereford & Worcester on BBC Sounds, Facebook, X and Instagram.
Yahoo
15-05-2025
- Health
- Yahoo
Axovia Therapeutics Unveils New Preclinical Data for AXV-201, for Treatment of Genetic Obesity Caused by MC4R Mutations, at ASGCT
Positive preclinical POC data show that novel gene therapy, AXV-201, prevented obesity and metabolic disease in a monogenic model LONDON, May 15, 2025 (GLOBE NEWSWIRE) -- Axovia Therapeutics Ltd., a biotechnology company developing therapies to address the genetic causes of blindness and obesity, announced that today it will unveil new preclinical proof-of-concept data for novelly designed, AXV-201, to treat individuals with severe obesity and very high BMIs resulting from MC4R mutations, in a poster presentation at the American Society of Gene and Cell Therapy (ASGCT) 28th Annual Meeting, which is being held from May 13-17, 2025 in New Orleans, LA. 'Today's presentation highlights how a new human sequence and AAV9 vector, AXV-201, can rescue the weight gain phenotype and could prove to be a powerful treatment for individuals with severe obesity and very high BMIs resulting from MC4R mutations,' said Dr. Victor Hernandez, Co-Founder and Chief Scientific Officer. 'MC4R is a key regulator of body weight and is the most common cause of genetic early-onset monogenic obesity. A gene replacement therapy could be transformative for those suffering across the globe.' Preclinical proof-of-concept data highlights include: New codon-optimized self-complementary human cMC4R sequence was able to express the MC4R transgene activity greater than five times more efficiently than the wild-type cDNA In vivo administration of AXV-201 in Mc4r-null mice prevented the development of obesity in males and females, restoring a normal weight trajectory comparable to wild-type controls and showed normalization of neurometabolic markers No safety concerns were observed when wild-types cohorts were dosed with AXV-201 'Genetic forms of obesity, such as those linked to MC4R mutations, represent a significant and often overlooked challenge for patients and clinicians alike,' said Dr. Jesse Richards, OU Health. 'Despite advances in obesity research, there remains a critical unmet need for effective therapies that address the underlying genetic causes. These data lay the groundwork for bringing new hope to individuals and families affected by MC4R-related obesity, offering the possibility of a targeted intervention that aims to normalize weight and have a better effect than currently available options.' About Melanocortin 4 Receptor () MutationsMelanocortin 4 receptor (MC4R) mutations are the most common cause of human monogenic obesity. Individuals with MC4R loss of function mutations suffer from hyperphagia, severe obesity and hyperinsulinemia. Impact of the different type of MC4R mutation depends on how they reduce MC4R expression and the impact they have on the production of cyclic AMP (cAMP). Mutations in heterozygosity, with partial MC4R functionality are the most frequent, but homozygous mutations and double heterozygotes account for 25% of MC4R mutations. There are approximately 50,000 patients with complete MC4R loss of function (LoF) and BMI>40 in the United States, European Union and Middle East. About Axovia Therapeutics Therapeutics is leading the development of therapies that address the genetic causes of blindness and obesity syndromes that are driven by cilia dysfunction. Ciliopathies are a group of more than 55 rare inherited genetic diseases linked to more than 950 genes that impact the function of cilia which are critical for protein transport and cellular signaling. The company plans to initiate a clinical study to treat retinal degeneration for its lead program for Bardet-Biedl Syndrome (BBS), AXV-101, in mid-2025, based on robust preclinical efficacy and toxicological data with established scaled GMP manufacturing and patient registries. AXV-101 has achieved U.S. Food and Drug Administration Orphan Drug Designation and Rare Pediatric Disease Designation. The company is developing its second program, AXV-201, for genetic obesity caused by MC4R mutations. Axovia is backed by ALSA Ventures and was formed following decades of work on ciliopathies at University College London by co-founders Professor Phil Beales and Dr. Victor Hernandez. For further information, please visit Contact:Professor Phil BealesChief Executive Officerinvestors@
