
8 Healthy ‘Three-Parent' Babies Born in UK Using Pioneering IVF Technique
Doctors at Newcastle University led the study, which involved around two dozen women with a high risk of passing down harmful mutations of their mitochondria to their children. So far, eight kids have been born using an in vitro fertilization (IVF) technique that replaces a mother's damaged mitochondrial DNA with that of a donor, all of whom appear to be disease-free. The findings seem to validate this new approach to preventing these genetic disorders.
'As parents, all we ever wanted was to give our child a healthy start in life. Mitochondrial donation IVF made that possible,' said the mother of a girl born with the method in a statement from the university. 'After years of uncertainty, this treatment gave us hope—and then it gave us our baby. We look at them now, full of life and possibility, and we're overwhelmed with gratitude. Science gave us a chance.'
Mitochondria are the cell's primary source of energy, but only a tiny slice of our genetic material is responsible for creating them. This mitochondrial DNA (mtDNA) is found outside the nucleus, unlike the rest of our DNA, and the genes for making mitochondria are only inherited from our mothers. Certain mutations of mtDNA are known to cause serious diseases, and women whose eggs carry these variants can pass them down to their children.
The technique pioneered by Newcastle researchers sought to get around this risk in a relatively simple way. They use standard IVF to create a fertilized egg with the mother's and father's DNA, then remove the nucleus. This nucleus is inserted into a donor egg that had its nucleus removed, which is finally transplanted into the mother's uterus for a hopefully successful pregnancy. If all goes well, the resulting child carries all the nuclear DNA of their parents and the healthy mtDNA of the donor.
The researchers enrolled 22 women carrying harmful mtDNA variants to undergo the IVF procedure. These women were compared to a group of women who instead received preimplantation genetic testing (PGT), a common screening technique that can select for healthy mitochondria prior to IVF (for some women, a harmful mtDNA variant will only show up occasionally in their eggs). Eight women who underwent mitochondrial donation had live births, while another woman has an ongoing pregnancy. None of the children—four boys, four girls, and a set of identical twins—have shown signs of mitochondrial disease so far, and all are reaching their developmental goals on schedule. The success rate of the technique (36%) was also similar to PGT (41%). The results were published across two studies in the New England Journal of Medicine.
The findings do point to some current limitations of mitochondrial donation. Some of the children had mitochondria carrying harmful mutations, for instance. Even in these children, however, most of their cells still carried healthy mitochondria, and their levels of mutated mitochondria are likely low enough to prevent disease from emerging. But this result will merit further monitoring of the children, and it suggests the IVF method can be improved to lessen the chance of it happening.
Earlier versions of mitochondrial donation have been developed, though these were eventually banned in countries like the U.S. for being too dangerous. The UK has slowly but steadily been laying the groundwork for this newer and safer technique to be cleared for widespread use (the country officially allowed the first treatment in 2018, now seven years ago). So while there may be important questions left to answer, many women living with this genetic risk may soon have a new option available that will allow them to have children of their own.
Hashtags

Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Yahoo
an hour ago
- Yahoo
ImCheck's ICT01 Receives FDA Orphan Drug Designation for Treatment of Acute Myeloid Leukemia
ImCheck's ICT01 Receives FDA Orphan Drug Designation for Treatment of Acute Myeloid Leukemia Clinical data showing unprecedented remission rates in newly diagnosed AML patients support advancing ICT01 into pivotal trials Marseille, France, July 18, 2025, 11:00 am CET – ImCheck Therapeutics today announced that the U.S. Food and Drug Administration (FDA) has granted Orphan Drug Designation (ODD) to its lead program, ICT01, a humanized anti-butyrophilin 3A (BTN3A) monoclonal antibody designed to selectively activate γ9δ2 T cells, for the treatment of acute myeloid leukemia (AML). AML remains a significant clinical challenge, particularly for older or unfit patients who are not eligible for intensive chemotherapy. 'Receiving FDA orphan drug designation for ICT01 is a significant recognition of ICT01's innovative therapeutic potential to meet the urgent unmet medical needs of AML patients," said Stephan Braun, MD, PhD, Chief Medical Officer of ImCheck Therapeutics. "This important regulatory milestone reinforces our confidence that ICT01 will become the first immunotherapy for AML patients and supports our goal of rapidly advancing ICT01 into pivotal studies based on the unprecedented results observed in the clinic to date.' In an oral presentation at the 2025 ASCO Annual Meeting, ImCheck reported results from the Phase I/II EVICTION study, evaluating ICT01 in combination with azacitidine and venetoclax (Aza-Ven) in newly diagnosed AML patients unfit for intensive chemotherapy. Remarkably high remission rates and a positive overall survival signal were observed across a broad range of molecular subtypes, in particular those that are typically less responsive to Aza-Ven. The combination demonstrated a clinically well-manageable safety profile, with Grade ≥3 adverse events consistent with the expected hematological toxicity of Aza-Ven and AML itself. 'Orphan drug designation is a catalyst,' added Pierre d'Epenoux, Chief Executive Officer of ImCheck Therapeutics. 'It validates our regulatory strategy, de-risks and supports clinical development acceleration, and sends a strong signal about the unique potential of ICT01 to transform AML treatment as well as other solid tumor indications.' The FDA's orphan drug designation is granted to drugs and biologics intended for the treatment, diagnosis, or prevention of rare diseases affecting fewer than 200,000 people in the United States. The designation is designed to encourage the development of therapies for underserved patient populations and offers benefits including tax credits for clinical trials, exemption from certain FDA fees, and up to seven years of marketing exclusivity upon approval. Additionally, the designation gives access to regulatory assistance for the drug development process. About the medical need in AML Acute myeloid leukemia (AML) remains a significant clinical challenge, particularly for older or unfit patients who cannot tolerate intensive chemotherapy. While the combination of venetoclax and azacitidine has become the standard non-intensive regimen, it is not curative and relapse rates remain high. Most patients are not eligible for stem cell transplantation, often due to age, comorbidities, or insufficient response, and face limited treatment options and poor overall survival. Despite AML's known sensitivity to immune-mediated control, current immunotherapies targeting PD-1, TIM-3, or CD47 have not delivered meaningful clinical benefit. This underscores the urgent need for novel immuno-oncology approaches. Recently, γ9δ2 T cells, with their cytotoxic activity and unique dual role in both innate and adaptive immunity, have emerged as promising immune modulators. Their association with reduced relapse and prolonged survival, particularly in the post-transplant setting, suggests that enhancing their anti-leukemic potential could offer a meaningful new treatment option for high-risk AML patients. About ICT01 ICT01 is a humanized, anti-BTN3A (also known as CD277) monoclonal antibody that selectively activates γ9δ2 T cells, which are responsible for immunosurveillance of malignancy and infections. The three isoforms of BTN3A targeted by ICT01 are overexpressed on many solid tumors (e.g., melanoma, urothelial cell, colorectal, ovarian, pancreatic, and lung cancer) and hematologic malignancies (e.g., leukemia and lymphomas) and also expressed on the surface of innate (e.g., γδ T cells and NK cells) and adaptive immune cells (T cells and B cells). BTN3A is essential for the activation of the anti-tumor immune response of γ9δ2 T cells. As demonstrated by data presented at past AACR, ASCO, ASH, ESMO and SITC conferences, ICT01 selectively activates circulating γ9δ2 T cells leading to migration of γ9δ2 T cells out of the circulation and into the tumor tissue and triggers a downstream immunological cascade through secretion of pro-inflammatory cytokines, including but not limited to IFNγ and TNFα, further augmenting the anti-tumor immune response. Anti-tumor activity and efficacy of ICT01 have been shown in patients across several cancer IMCHECK THERAPEUTICS ImCheck Therapeutics is developing a new generation of immunotherapeutic antibodies targeting butyrophilins, a novel superfamily of immunomodulators. By unlocking the power of γ9δ2 T cells, ImCheck's innovative approach has the potential to transform treatments across oncology, autoimmune, and infectious diseases. The lead clinical-stage program, ICT01, has been advancing to late-stage trials, demonstrating a unique mechanism of action that modulates both innate and adaptive immunity. These 'first-in-class' activating antibodies may deliver superior clinical outcomes compared to first-generation immunotherapy approaches, in particular in rationale combinations with immune checkpoint inhibitors and immunomodulatory anti-cancer drugs. Additionally, ImCheck's pipeline compounds are progressing toward clinical development for autoimmune and infectious diseases. The company benefits from the pioneering research of Prof. Daniel Olive (INSERM, CNRS, Institut Paoli Calmettes, Aix-Marseille University), a global leader in γ9δ2 T cells and butyrophilins, as well as the expertise of a seasoned management team and the commitment of leading U.S. and European investors. For further information: Press contacts: US and EU Trophic CommunicationsGretchen Schweitzer +49 (0) 172 861 8540imcheck@ FranceATCG PARTNERSCéline Voisin+33 (0)6 62 12 53 39imcheck@ Attachment PR in EnglishError while retrieving data Sign in to access your portfolio Error while retrieving data Error while retrieving data Error while retrieving data Error while retrieving data
Yahoo
an hour ago
- Yahoo
How Old-School Lifters Used Paused Reps to Build Serious Strength
When you look at some of the most iconic old-school bodybuilders, legends like Lee Haney, Arnold Schwarzenegger, and Franco Columbu, it's easy to chalk their physiques up to being 'built different.' These guys didn't just turn heads; they stopped traffic. And while genetics certainly played a role (hard work builds muscle, but it doesn't change your muscle insertions), one training technique helped set their physiques apart—even from today's best: paused Pause Reps Build Strength "Old-school lifters swore by paused reps because they eliminate the stretch reflex," says Everett Miner, NASM-CPT. "Instead of bouncing out of the bottom, you pause long enough that your muscles have to generate force purely from a dead stop—no elastic energy to help." Pausing keeps the target muscles under tension longer, which helps expose weak points, increases time under tension, and makes strength gains easier to track over time. By eliminating momentum, it also lowers your risk of injury and shifts the load where it belongs—on your muscles, not your joints, tendons, or connective tissue. "Pausing kills all momentum because you can't use a fast eccentric and/or a 'bounce' to sling the weight back up," Miner says. "Instead, you develop starting strength, the ability to push or pull forcefully from zero at a dead stop. This carries over to your true max lifts, where momentum won't save you."When to Use Pause Reps Realistically, you can use pause reps for just about any exercise, but that doesn't mean you should. Miner says the key is choosing movements with a clear stretched or bottom position. "Use paused reps where they reinforce tightness, control, and tension in the stretched position," Miner says. "That's where you get the biggest payoff for both strength and muscle. For compound lifts like the squat, bench, and deadlift, pausing can help you tighten up your form, clean up sloppy reps, and power through sticking points like the bottom of a squat or just off the floor in a deadlift. "For most big lifts, a good rule of thumb is to use paused variations for about 10 to 30 percent of your total working sets," Miner adds. "This works well for squats, deadlift variations, or Olympic lift progressions. It's a smart way to troubleshoot sticking points, refine technique, and add an extra stimulus during specific training blocks." Programming Pause Reps According to Miner, a good pause rep is long enough to eliminate the stretch reflex, but not so long that you lose tightness or rack up unnecessary fatigue. For most lifters, that sweet spot falls between half a second and three seconds, depending on the lift and your goals. One-Half to One Second Half a second to one second is a great cue for beginners who are trying to perfect their form, but can also be used "to kill momentum and increase control of the lift for most general strength and hypertrophy training while minimizing extra fatigue," Miner says. Two to Three Seconds "Two to three seconds is the likely optimal pause time for most pure strength-training focused lifts like squat and bench," Miner says. "It demands even more control and strength and can be used in intermediate-advanced trainees. Longer pauses are great for troubleshooting, increasing the challenge and stimulus, but can increase fatigue." Try the following exercises with a pause, focusing on these instructions from Jonathon Sullivan, M.D., Ph.D., SSC. Pause Squat How to Do It Set up with a barbell in a squat rack. Standing with the weight across your back, take a big breath and brace your core. Push your hips back, knees slightly out, keeping your chest up throughout. Descend at a normal, controlled speed, not too slow, not a dive-bomb. Balance midfoot, keeping your heels down as you move through the movement. Pause for one to three seconds at the bottom. Drive up powerfully, no bouncing out. Why It Works Pause squats require you to use just your quads, hamstrings, and glutes to lift up out of the squat, instead of momentum, leading to more muscle recruitment and positive stress. Pause Bench How to Do It Set up with a barbell over a bench. Lift the weight off the rack. As you lower the weight down to your chest, take a deep breath into your upper thoracic region and pin your shoulder blades down—don't relax into the chest. The pause can be short—about a half a second to two seconds—just enough to eliminate momentum. Push the weight back up. Expect your paused bench to be roughly 10 to 30 percent lighter than your touch-and-go. That's normal. Why It Works Paused benching locks in tightness, standardizes your bar path, and builds big pec strength and powerful triceps. How Old-School Lifters Used Paused Reps to Build Serious Strength first appeared on Men's Journal on Jul 17, 2025
Yahoo
an hour ago
- Yahoo
ImCheck's ICT01 Receives FDA Orphan Drug Designation for Treatment of Acute Myeloid Leukemia
ImCheck's ICT01 Receives FDA Orphan Drug Designation for Treatment of Acute Myeloid Leukemia Clinical data showing unprecedented remission rates in newly diagnosed AML patients support advancing ICT01 into pivotal trials Marseille, France, July 18, 2025, 11:00 am CET – ImCheck Therapeutics today announced that the U.S. Food and Drug Administration (FDA) has granted Orphan Drug Designation (ODD) to its lead program, ICT01, a humanized anti-butyrophilin 3A (BTN3A) monoclonal antibody designed to selectively activate γ9δ2 T cells, for the treatment of acute myeloid leukemia (AML). AML remains a significant clinical challenge, particularly for older or unfit patients who are not eligible for intensive chemotherapy. 'Receiving FDA orphan drug designation for ICT01 is a significant recognition of ICT01's innovative therapeutic potential to meet the urgent unmet medical needs of AML patients," said Stephan Braun, MD, PhD, Chief Medical Officer of ImCheck Therapeutics. "This important regulatory milestone reinforces our confidence that ICT01 will become the first immunotherapy for AML patients and supports our goal of rapidly advancing ICT01 into pivotal studies based on the unprecedented results observed in the clinic to date.' In an oral presentation at the 2025 ASCO Annual Meeting, ImCheck reported results from the Phase I/II EVICTION study, evaluating ICT01 in combination with azacitidine and venetoclax (Aza-Ven) in newly diagnosed AML patients unfit for intensive chemotherapy. Remarkably high remission rates and a positive overall survival signal were observed across a broad range of molecular subtypes, in particular those that are typically less responsive to Aza-Ven. The combination demonstrated a clinically well-manageable safety profile, with Grade ≥3 adverse events consistent with the expected hematological toxicity of Aza-Ven and AML itself. 'Orphan drug designation is a catalyst,' added Pierre d'Epenoux, Chief Executive Officer of ImCheck Therapeutics. 'It validates our regulatory strategy, de-risks and supports clinical development acceleration, and sends a strong signal about the unique potential of ICT01 to transform AML treatment as well as other solid tumor indications.' The FDA's orphan drug designation is granted to drugs and biologics intended for the treatment, diagnosis, or prevention of rare diseases affecting fewer than 200,000 people in the United States. The designation is designed to encourage the development of therapies for underserved patient populations and offers benefits including tax credits for clinical trials, exemption from certain FDA fees, and up to seven years of marketing exclusivity upon approval. Additionally, the designation gives access to regulatory assistance for the drug development process. About the medical need in AML Acute myeloid leukemia (AML) remains a significant clinical challenge, particularly for older or unfit patients who cannot tolerate intensive chemotherapy. While the combination of venetoclax and azacitidine has become the standard non-intensive regimen, it is not curative and relapse rates remain high. Most patients are not eligible for stem cell transplantation, often due to age, comorbidities, or insufficient response, and face limited treatment options and poor overall survival. Despite AML's known sensitivity to immune-mediated control, current immunotherapies targeting PD-1, TIM-3, or CD47 have not delivered meaningful clinical benefit. This underscores the urgent need for novel immuno-oncology approaches. Recently, γ9δ2 T cells, with their cytotoxic activity and unique dual role in both innate and adaptive immunity, have emerged as promising immune modulators. Their association with reduced relapse and prolonged survival, particularly in the post-transplant setting, suggests that enhancing their anti-leukemic potential could offer a meaningful new treatment option for high-risk AML patients. About ICT01 ICT01 is a humanized, anti-BTN3A (also known as CD277) monoclonal antibody that selectively activates γ9δ2 T cells, which are responsible for immunosurveillance of malignancy and infections. The three isoforms of BTN3A targeted by ICT01 are overexpressed on many solid tumors (e.g., melanoma, urothelial cell, colorectal, ovarian, pancreatic, and lung cancer) and hematologic malignancies (e.g., leukemia and lymphomas) and also expressed on the surface of innate (e.g., γδ T cells and NK cells) and adaptive immune cells (T cells and B cells). BTN3A is essential for the activation of the anti-tumor immune response of γ9δ2 T cells. As demonstrated by data presented at past AACR, ASCO, ASH, ESMO and SITC conferences, ICT01 selectively activates circulating γ9δ2 T cells leading to migration of γ9δ2 T cells out of the circulation and into the tumor tissue and triggers a downstream immunological cascade through secretion of pro-inflammatory cytokines, including but not limited to IFNγ and TNFα, further augmenting the anti-tumor immune response. Anti-tumor activity and efficacy of ICT01 have been shown in patients across several cancer IMCHECK THERAPEUTICS ImCheck Therapeutics is developing a new generation of immunotherapeutic antibodies targeting butyrophilins, a novel superfamily of immunomodulators. By unlocking the power of γ9δ2 T cells, ImCheck's innovative approach has the potential to transform treatments across oncology, autoimmune, and infectious diseases. The lead clinical-stage program, ICT01, has been advancing to late-stage trials, demonstrating a unique mechanism of action that modulates both innate and adaptive immunity. These 'first-in-class' activating antibodies may deliver superior clinical outcomes compared to first-generation immunotherapy approaches, in particular in rationale combinations with immune checkpoint inhibitors and immunomodulatory anti-cancer drugs. Additionally, ImCheck's pipeline compounds are progressing toward clinical development for autoimmune and infectious diseases. The company benefits from the pioneering research of Prof. Daniel Olive (INSERM, CNRS, Institut Paoli Calmettes, Aix-Marseille University), a global leader in γ9δ2 T cells and butyrophilins, as well as the expertise of a seasoned management team and the commitment of leading U.S. and European investors. For further information: Press contacts: US and EU Trophic CommunicationsGretchen Schweitzer +49 (0) 172 861 8540imcheck@ FranceATCG PARTNERSCéline Voisin+33 (0)6 62 12 53 39imcheck@ Attachment PR in EnglishError 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