As Trump Administration Plans to Burn Contraceptives, Europeans Are Alarmed
When the Trump administration abruptly defunded and dismantled the United States Agency for International Development, or U.S.A.I.D, earlier this year, millions of contraceptives it had purchased were stuck in Geel, Belgium. The pills, intrauterine devices and hormonal implants were destined for clinics in the poorest countries in Africa.
With the contraceptives in limbo, the contractor managing the supply explored selling it to outside organizations, including the United Nations' main sexual and reproductive health agency, the U.N. Population Fund. The nonprofit MSI Reproductive Choices offered to take over the warehousing and redistribute the contraceptives at no cost to the United States.
But last month it emerged that the U.S. government had instead decided to burn the supplies, at a cost to the government of more than $160,000 in transport and incineration fees.
'U.S.A.I.D. was allegedly dismantled to prevent future wastage and to deliver value for money for the American people,' said Sarah Shaw, the associate director of advocacy at MSI Reproductive Choices. 'It's just egregious that they're willing to waste $9 million worth of contraceptives that are so desperately needed.'
She added, 'Women are going to die because they've not had access to those contraceptives.'
Want all of The Times? Subscribe.
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Yahoo
an hour ago
- Yahoo
Sitryx regains rights to SYX-1042 itaconate mimetic for chronic autoimmune and inflammatory diseases from Lilly following portfolio reprioritization
Sitryx regains rights to SYX-1042 itaconate mimetic for chronic autoimmune and inflammatory diseases from Lilly following portfolio reprioritization Novel, oral candidate with first-in-class potential progresses successfully through Lilly's Phase 1 clinical trial in healthy volunteers Sitryx reintegrates SYX-1042 into portfolio of novel small molecule candidates targeting major autoimmune indications with high unmet need Oxford, UK – 8 August 2025 – Sitryx Therapeutics ('the Company'), a clinical-stage biopharmaceutical company developing novel oral therapies to restore immune balance in autoimmune and inflammatory disease, today announces that the Company has regained the rights to its itaconate mimetic, SYX-1042, for the treatment of chronic autoimmune and inflammatory diseases, from Eli Lilly & Company (Lilly), due to strategic considerations and reprioritization of Lilly's pain and inflammation portfolio. In 2024 Lilly commenced a Phase 1 first-in-human study of SYX-1042, a post-translational modification modulator program for chronic autoimmune and inflammatory diseases, following a research collaboration between the two companies. That study has completed successfully. With the return to Sitryx of SYX-1042, its phase 2-ready data package and associated API, Sitryx is assessing how best to prioritize SYX-1042 for continued in-house development or potential further partnering. Iain Kilty, Chief Executive Officer of Sitryx, commented: 'Through our partner Lilly's investment in the clinical development of SYX-1042, this program has progressed significantly, delivering positive first-in-human data. We will be reviewing this clinical data alongside the robust preclinical data package to determine the optimal path forward. We thank Lilly for this collaboration and the advances we made together, progressing important research into a first-in-class candidate which we believe holds exciting potential in multiple chronic autoimmune and inflammatory diseases.' -Ends- For more information about Sitryx please contact: ICR HealthcareMary-Jane Elliott, David Daley +44 (0)20 3709 5700Sitryx@ About SitryxSitryx is a clinical-stage biopharmaceutical company developing novel oral therapies to restore immune balance in autoimmune and inflammatory disease. The Company has a broad pipeline of novel small molecule candidates targeting major autoimmune indications with high unmet need. Its lead candidate, SYX-5219, is a potentially first-in-class PKM2 modulator in development for atopic dermatitis as a once-daily oral therapy with future development potential across multiple autoimmune diseases. Established in 2018 with seed funding from SV Health Investors, Sitryx has raised $85 million to date from an international syndicate of specialist investors including SV Health Investors, Sofinnova Partners, Oxford Science Enterprises, Longwood Fund, Eli Lilly and Company, and GSK. Sitryx is headquartered in Oxford, UK. For more information, please visit in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Medscape
an hour ago
- Medscape
Transplanted Islet Cells Survive Without Immune Suppression
For the first time, researchers have transplanted gene-edited donor islet cells that secrete insulin in a person with type 1 diabetes (T1D) without the use of immunosuppression. Twelve-week results from the phase 1, single-participant study were published online on August 4, 2025, as a Brief Report in The New England Journal of Medicine . Six-month data were presented on June 23, 2025, at the American Diabetes Association (ADA) 85th Scientific Sessions in Chicago and announced at the time in a press release from Sana Biotechnology. The study subject, a 42-year-old man with a 37-year history of T1D, has shown no immune response to the gene-edited cells and has maintained ongoing significant circulating C-peptide levels, a measure of insulin secretion, in contrast to zero at baseline. MRI at 12 weeks confirmed persistence of the grafted hypoimmune islets. At 6 months, increased C-peptide levels in response to a mixed-meal tolerance test were seen. He still requires insulin treatment, but that was expected because the protocol for this early safety study involved delivery of only 7% of the number of cells that would be curative, lead author Per-Ola Carlsson, MD, PhD, senior physician and professor at the Clinic for Endocrinology and Diabetology at Uppsala University Hospital, Uppsala, Sweden, told Medscape Medical News . 'Excited,' but 'Many Hurdles to Overcome' Currently, transplantation for treatment of T1D — whether of whole pancreas, cadaveric donor islets, or experimental stem cell-derived islets — is reserved for individuals with frequent severe hypoglycemia or those who are already undergoing another transplant, such as a kidney. In most people with managed T1D, the adverse health risks for immune suppression are viewed as outweighing the benefits of a transplant. In T1D, transplantation provokes two immune system attacks: one against any foreign body, which is common to all organ transplants (allogeneic), and a second to the beta cell-specific autoantibodies that caused the condition in the first place. Thus far, it appears that this novel gene-editing approach overcomes both allogeneic and autoimmune rejection. If upcoming trials using stem cell-derived islets that can be produced in unlimited quantities validate these results, this approach could essentially represent a cure for many people T1D, Carlsson said. 'I have never been so excited in my life. I've been working with the science since the 1990s, and this is the one project that has been so positive and so convincing. I'm really happy to work with it, and since I'm a clinician, it's magic to be able to do something that could turn into a reality for these patients,' he told Medscape Medical News . However, he cautioned, 'This is one subject…we believe it is applicable to all subjects with type 1 diabetes. But of course, there may be subgroups that it does not work for.' Moreover, he noted, 'It will take time before it reaches clinical reality.' Experts in the field contacted by Medscape Medical News expressed cautious optimism. Mark A. Atkinson, PhD, the ADA Eminent Scholar for Diabetes Research and professor in the Department of Pathology at the University of Florida, Gainesville, Florida, said, 'I am very enthusiastic about this study. I think this is a baby step, with the potential for moving forward a full leap. Time will tell. At a minimum, this shows that genetic modification of a stem cell source may prove valuable as a future therapeutic for type 1 diabetes.' However, Atkinson noted that because the treatment is likely to be expensive, 'the cost versus benefit ratio of using such a therapy across the spectrum of type 1 diabetes needs further exploration.' Islet cell transplantation pioneer A.M. James Shapiro, MD, Canada Research Chair in Transplantation Surgery and Regenerative Medicine at the University of Alberta, Edmonton, Alberta, told Medscape Medical News 'This is indeed an exciting development in that human insulin-producing islet cells continued to secrete, albeit small amounts of insulin in the absence of immune suppression. Ongoing research will determine whether this approach can be effectively scaled up and engraftment improved.' David M. Harlan, MD, director of the Breakthrough T1D Barbara D. Cammett Center of Excellence in New England and co-director of the University of Massachusetts (UMass) Diabetes Center of Excellence, Worcester, Massachusetts, said, 'I believe that the genetic modifications of stem cell-derived islets and/or a druggable target within a stem cell-derived islet is likely to represent a practical cure for type 1 diabetes in the next decade or so. I'm excited by this step, but I still see many hurdles to overcome.' Hypoimmune Islets: Breakthrough or Baby Step? Some of the 'hurdles' cited by Harlan, who is also the William and Doris Krupp Professor of Medicine at UMass, relate to the gene-editing procedure itself and to some of the study methodology. The islets, from a deceased donor with the same blood type as the recipient, were first dissociated into single cells, and the genes encoding human leukocyte antigen (HLA) class I and class II were inactivated using clustered regularly interspaced short palindromic repeat. The cells were reclustered, again dissociated, and transduced with a lentiviral vector containing CD47 complementary DNA. Knocking out HLA class I and II is necessary to protect against adaptive T-cell rejection, while overexpression of CD47 inhibits innate killing via macrophages and natural killer cells, Carlsson explained. According to Harlan, even without HLA class I and II, there would still be other cell surface molecules that would be expected to provoke an antibody response. 'I just don't understand why they don't see any donor-specific antibodies against the gene-modified islets. That doesn't make sense to me. Maybe such antibodies would be benign, but I would still expect them to be picked up.' Carlsson countered, 'Detection of foreign cells is through HLA. Other antigens…are, even if not encoded from the HLA class I or class II genes, presented to the immune system by the HLA molecules.' Atkinson noted that the autoimmune response could take much longer to occur than the allogeneic, and therefore longer follow-up is needed. Carlsson said that the planned follow-up is 15 years, but prior data suggest that the autoimmunity would occur within 1-2 months, and 'we didn't see any attack at all.' Harlan also noted that the patient's high baseline A1c, 10.9%, was unusual and might have adversely affected the findings. Carlsson said that this was per request of the regulatory bodies because such an individual would 'gain most from the development of a curing therapy considering their high risk of complications.' He added that this requirement 'complicated the study since high glucose stresses the beta cells…we were, however, able to improve his metabolic control post-transplantation.' The gene-edited cells were delivered with 17 separate injections — to allow for sufficient oxygen exposure — into the patient's forearm while he was under general anesthesia. Both Harlan and Atkinson questioned the feasibility of that approach going forward. Carlsson said that the forearm was chosen because it was simpler to monitor for safety, but that in future studies abdominal muscles might be used. Sana Biotechnology will not study this product, UP421, further. Instead, they are moving forward with SC451, a stem cell-derived pancreatic gene-edited islet cell product. The next study is still being planned but will involve multiple patients at more than one clinical site, Carlsson told Medscape Medical News . Atkinson commented, 'Over 50 years ago, individuals with type 1 diabetes were told that a cure was on the way, and it was going to occur through islet cell transplantation and understanding of the autoimmune nature of type 1 diabetes. There were animal models of the disease, and there were new classes of drugs that came out, namely cyclosporine. So, people had hopes that a cure for type 1 diabetes was 3-5 years away. Now, six decades later, we're still struggling with that, but there's promise on the horizon.' Carlsson and Shapiro reported having no disclosures. Atkinson is a consultant for Vertex, Sanofi, Diamyd, Novo Nordisk, and Sernova. Harlan is co-founder and chief scientific officer for Stability Health, LLC; a consultant for CG Scientific, Inc.; and chair of the scientific advisory board for TIXiMED.
Health Line
an hour ago
- Health Line
Does Humira Cause Hair Loss?
Is hair loss common Hair loss is a potential but uncommon side effect of Humira (adalimumab). Hair loss wasn't reported during the drug's studies, but has been reported since Humira was approved for use. Humira is a prescription medication used to treat a number of chronic (ongoing) autoimmune and inflammation-related conditions in adults and some children. How common is hair loss with Humira? Hair loss is considered a rare side effect of Humira, since there were no reports of this side effect in the drug's studies. Since Humira came on the market, there have been reports of hair loss, but it's unclear how many people were affected or if Humira was the actual cause. In one small study, there were 62 cases of different types of hair loss reported by people who had taken a TNF blocker. (This is the group of drugs Humira belongs to.) These people typically lost a few small patches of hair during TNF-blocker treatment, but their hair often grew back after the treatment ended. How TNF blockers cause hair loss is uncertain. Hair loss may be an autoimmune response to the condition the drug is being taken to treat, a side effect of the drug itself, or caused by another reason entirely.
