Menopause Age Looms Over Women. Efforts to Prevent it Could Extend Fertility.


Photo illustration: Amanda Saviñón; Photo: Amanda Saviñón for Bloomberg Businessweek

A woman’s biological clock is a fact of life, but with new drugs maybe soon it won’t have to be.

When David Pepin dissected the mouse on a dark fall afternoon in 2013, he couldn’t believe what he saw. As he pushed the kidneys aside to get to the ovaries, he noticed something strange. “They looked like neonatal ovaries,” Pepin recalls. They were the size he’d expect to see in a newborn female, not an adult. “They were miniature.”

Pepin, then a postdoc at Massachusetts General Hospital in Boston, had seen enough mouse ovaries to know that something unusual had happened. In a second mouse he found the same thing. The mice had been treated with anti-müllerian hormone, or AMH, a once-overlooked hormone produced by both the testicles and the ovaries that helps regulate the development of eggs in women. Pepin and his mentor, Patricia Donahoe, thought AMH might help treat ovarian cancer, so they’d given immunocompromised mice ovarian tumors and then a gene therapy containing AMH. But Pepin, who has a background in reproductive development, had a hunch the AMH might do something else, too. In prior experiments, researchers had blocked mice’s ability to produce AMH and found their ovaries aged slightly faster. But after removing the tumors from the first mouse, the outcome was clear: The ovaries had shrunk.

A few days later, peering into a microscope at a cross section of the mouse’s ovaries, he discovered why. Follicles, the fluid-filled sacs that contain a developing egg, grow, mature and then die. But this set of ovaries had none of the large, mature follicles you’d expect in an adult mouse. It contained only tiny primordial ones, the kind that remain dormant until they are recruited to mature. The AMH appeared to result in some sort of arrested development; the cycle of growth and death had been halted, leaving the pool of potential future eggs intact and almost returning them to their newborn state.

Immediately, Pepin says, it was clear that this hormone had a powerful sway over the reproductive system, far more so than previously realized. AMH might be able to slow the aging of the reproductive system, extending the window of fertility and staving off menopause. “It was basically Benjamin Button, going backwards,” he says. “I was like, ‘OK, something big is happening.’ ”

David Pepin in his lab at Massachusetts General.

Pepin in his lab at Massachusetts General. Photographer: Philip Keith for Bloomberg Businessweek

Science has given the modern woman incredible tools to control her reproductive destiny. The most obvious is the birth control pill, introduced in 1960 to stop ovulation using hormones. Replacing rudimentary cervical caps and rubber diaphragms, it allowed a woman to modulate her ability to get pregnant with scientific precision. Today’s tools mainly help to turn off the capabilities of the reproductive system. Technologies like in vitro fertilization can help when there are snags in the reproductive machinery, such as blocked fallopian tubes or uterine fibroids. But women are born with all the eggs they’ll ever have, and when they’re gone—at an average age of 51—the time on their biological clock is officially up.

At that point, the production of hormones including estrogen and progesterone drops dramatically, culminating in a massive, sudden biological change. Ovarian hormones regulate not only reproduction, but also things such as bone mass, blood sugar, brain function and cholesterol. The result is often a slew of uncomfortable symptoms—hot flashes, weight gain and mood changes—as well as a marked increase in health risks including heart disease, osteoporosis and dementia. Pregnancy also becomes impossible, though for most women infertility happens years before, when they’re in their mid-40s. This fate befalls anyone with ovaries—cisgender women, as well as nonbinary people and trans men. The ovaries age much faster than the rest of the body, until, one day in middle age, they basically stop functioning altogether. There is no pill that can intervene when they start shutting down. At least not yet.

A surge of interest in both longevity research and women’s health has finally started to change that. “This is the area where there has been no funding and no interest until recently,” says Yousin Suh, a researcher studying ovarian aging at Columbia University Irving Medical Center in New York City. Long-standing gender bias in medicine has left the female reproductive system woefully understudied. (In the US, it’s been a requirement to include women in clinical trials since only 1993, and the study of so-called women’s diseases is historically underfunded.)

Yousin Suh in her lab at Columbia.

Suh in her lab at Columbia. Photographer: Laurel Golio for Bloomberg Businessweek

As Pepin and other scientists finally begin to unravel what makes the reproductive system age so rapidly, they’re also uncovering a tantalizing possibility: There may be ways to slow that aging down. Not only could this extend a woman’s childbearing years, it could dramatically improve women’s health, staving off the ill effects associated with the onset of menopause. Research has shown that women who go through menopause later in life tend to live longer. While women generally outlive men, they also are more likely to spend their later years in poor health, more often suffering from multiple chronic conditions at once. “The ovary has this protective benefit,” says Zev Williams, director of the Columbia University Fertility Center and a collaborator in Suh’s research. “It’s lost when menopause begins.”

What’s not clear is why ovaries age as rapidly as they do. Understanding that could help uncover how and why aging occurs at all. “Normally aging has to be studied over decades to be able to have measurable changes,” Williams says. “The ovary is an ideal model to study aging.” Watching the ovaries age is a little like listening to a podcast at double speed, which is why the ovary could even become a proving ground for longevity drugs, a therapeutics market expected to reach more than $44 billion within the next decade. This could have benefits for everyone, since most of the developed world’s biggest killers for men and women—heart disease, stroke, cancer, dementia—are diseases for which age is the main risk factor.

Scientists and startups are racing to turn these revelations into therapies that could one day advance treatment for menopause and infertility and perhaps eventually intervene in the process of aging itself. Williams and Suh have already begun enrolling women in a clinical trial to test whether rapamycin—an immunosuppresant typically used in organ transplants and cancer treatment that’s also become a popular anti-aging drug—might also slow aging of the ovaries. Researchers at Northwestern University are exploring whether anti-fibrotic drugs could improve the quality of a woman’s eggs as she ages as well as improve reproductive longevity itself. A startup called Gameto has used stem cell science to create a less intensive version of IVF and plans to use the same technology to create better menopause therapies.

Two-and-a-half years ago, Pepin, along with Donahoe and Harvard University Ph.D. Daisy Robinton, founded Oviva Therapeutics Inc. with funding from aging-focused drug development company Cambrian BioPharma Inc. Their goal: to turn AMH into treatments that could improve ovarian function and extend life span. In the universe of aging research, Pepin says, the ovary just might be low-hanging fruit. It’s a far smaller task to intervene in the aging of one organ versus the entire body. “If you’re trying to extend longevity, that’s hard,” Pepin says. “But the ovary is really weird. It starts to degenerate way earlier than anything else. So even if you didn’t touch anything else, you could easily see an effect on the ovary.”

The global fertility market, worth about $35.2 billion last year, is expected to grow to $84 billion by 2028, according to market research firm Imarc Group. Oviva raised $11.5 million in May 2022 for an early-stage treatment that will aim to improve fertility treatments by helping patients increase the number of eggs in each cycle. Eventually, Oviva hopes to pull off a feat that seems almost unimaginable: giving women a drug that will allow them to choose when—and whether—they go through menopause. At a time when politicians are eroding women’s hard-won reproductive choices, Oviva’s founders want to give them even more control. “I see it very much akin to how the contraceptive pill really changed the game for women in the ’70s,” Robinton says.

Human females are the odd ones out in terms of the reproductive life cycle. Most mammals are fertile right up to the end of their lives. The only other mammals that go through menopause are a few species of whales and, depending on whom you ask, some great apes. No one is even quite sure why menopause occurs at all. Perhaps the most popular theory is the “grandmother hypothesis,” which argues there’s an evolutionary benefit: Older women, no longer in their reproductive years, help care for grandchildren, boosting the kids’ chances of survival.

THE LIFE CYCLE OF A FOLLICLE

1 The tiny, dormant follicles women are born with contain a single oocyte (the cell that forms an egg) that’s surrounded by pre-granulosa cells. These eventually provide nutrients and send signals to the oocyte.

2 When a primordial follicle wakes up, it becomes a primary follicle. From before birth until menopause, follicles are recruited to begin growing and developing. The oocyte gets bigger, and pre-granulosa cells activate to become true granulosa cells.

3 The follicle grows. A thick layer develops around the oocyte, and the follicle begins to develop a theca. Akin to a shell, it’s responsible for hormone production, among other things.

4 Growth continues and a fluid-filled cavity called the antrum forms.

5 This is the last stage of a mature follicle before ovulation. Typically, just one dominant follicle is selected to fully mature every month.

6 During ovulation, the now mature egg detaches itself from the rest of the follicle. The follicle releases hormones, such as progesterone, that prepare the body for ovulation, and eventually it ruptures, releasing the egg to begin its journey to the fallopian tube.

7 Ovulation marks the end of what’s known as the follicular phase and the start of the luteal phase, in which remnants of the dominant follicle begin to transform into a new structure called the corpus luteum.

8 This is a cyst that plays an important role in producing hormones, such as progesterone, that help maintain pregnancy.

9 When pregnancy doesn’t occur, this cyst disappears. The lining of the uterus is shed during menstruation, and the cycle repeats.

1 The tiny, dormant follicles women are born with contain a single oocyte (the cell that forms an egg) that’s surrounded by pre-granulosa cells. These eventually provide nutrients and send signals to the oocyte.

1 The tiny, dormant follicles women are born with contain a single oocyte (the cell that forms an egg) that’s surrounded by pre-granulosa cells. These eventually provide nutrients and send signals to the oocyte.

2 When a primordial follicle wakes up, it becomes a primary follicle. From before birth until menopause, follicles are recruited to begin growing and developing. The oocyte gets bigger, and pre-granulosa cells activate to become true granulosa cells.

3 The follicle grows. A thick layer develops around the oocyte, and the follicle begins to develop a theca. Akin to a shell, it’s responsible for hormone production, among other things.

4 Growth continues and a fluid-filled cavity called the antrum forms.

2 When a primordial follicle wakes up, it becomes a primary follicle. From before birth until menopause, follicles are recruited to begin growing and developing. The oocyte gets bigger, and pre-granulosa cells activate to become true granulosa cells.

3 The follicle grows. A thick layer develops around the oocyte, and the follicle begins to develop a theca. Akin to a shell, it’s responsible for hormone production, among other things.

4 Growth continues and a fluid-filled cavity called the antrum forms.

5 This is the last stage of a mature follicle before ovulation. Typically, just one dominant follicle is selected to fully mature every month.

6 During ovulation, the now mature egg detaches itself from the rest of the follicle. The follicle releases hormones, such as progesterone, that prepare the body for ovulation, and eventually it ruptures, releasing the egg to begin its journey to the fallopian tube.

7 Ovulation marks the end of what’s known as the follicular phase and the start of the luteal phase, in which remnants of the dominant follicle begin to transform into a new structure called the corpus luteum.

5 This is the last stage of a mature follicle before ovulation. Typically, just one dominant follicle is selected to fully mature every month.

6 During ovulation, the now mature egg detaches itself from the rest of the follicle. The follicle releases hormones, such as progesterone, that prepare the body for ovulation, and eventually it ruptures, releasing the egg to begin its journey to the fallopian tube.

7 Ovulation marks the end of what’s known as the follicular phase and the start of the luteal phase, in which remnants of the dominant follicle begin to transform into a new structure called the corpus luteum.

8 This is a cyst that plays an important role in producing hormones, such as progesterone, that help maintain pregnancy.

9 When pregnancy doesn’t occur, this cyst disappears. The lining of the uterus is shed during menstruation, and the cycle repeats.

8 This is a cyst that plays an important role in producing hormones, such as progesterone, that help maintain pregnancy.

9 When pregnancy doesn’t occur, this cyst disappears. The lining of the uterus is shed during menstruation, and the cycle repeats.

For much of modern medical human history, the end of a woman’s reproductive years has been regarded as just that, an oddity. Worse, modern cultural stereotypes portray postmenopausal women as sexually undesirable and fragile. In the movie Sex and the City 2, the character Samantha Jones turns to an assortment of pills, patches and hormone therapies to slow the march toward irrelevance. In the British sitcom Absolutely Fabulous, talking about all of menopause’s terrible symptoms is so loathed by the main characters that they require an anonymous support group. Historically, the postmenopausal woman has often been portrayed as some combination of mystical, monstrous and deadly. In the Victorian era, physicians believed menopause made women insane. Those suffering noticeable symptoms might be locked away in an asylum. Sometimes doctors removed the ovaries altogether, believing that if they were no longer functioning, they were diseased. The operation often only worsened any symptoms.

Eventually, medical science advanced, developing blunt instruments that could bend the female reproductive system to our will. The workings of the endocrine system were discovered, and ovarian hormones including estrogen and progesterone were isolated, leading to the development of the birth control pill as well as hormonal treatments that replace some of the body’s waning hormones to dull menopausal effects. With the development of IVF, the need to understand many of the basics of human reproduction became less urgent.

When it comes to ovarian aging, some of the fundamentals are still elusive. For example, once a woman hits her 30s, the ovaries’ rate of aging seems to accelerate rapidly. Why does it do that? And primordial follicles seem to remain in a sort of sleeper state until it’s their turn to mature. What activates them? “It’s like a black box,” says Jennifer Garrison, a neuroscientist at the Buck Institute for Research on Aging in Marin County, California. “We don’t understand the most basic things about how the system works.”

Much of the research that’s formed the basis of reproductive longevity came out of an effort to preserve the fertility of women diagnosed with cancer. Treatments like chemotherapy often, as a side effect, strip women of their ability to bear children. Egg freezing, in which the eggs are harvested and stored for later, is one way to preserve fertility. But it doesn’t work for every woman, including those who haven’t yet gone through puberty. In 2004, Belgian doctors announced a first: A woman whose reproductive system had been destroyed by cancer treatments gave birth. Doctors had cut out a piece of her ovarian tissue and frozen it, then grafted it back into her body years later. The proof that it had kick-started her reproductive system was the healthy baby girl. Since then, thousands of girls and women have had their ovarian tissue cryopreserved.

To Garrison, this is a sign that the hormone cocktail produced by the female reproductive system might potentially be controlled. She studies what she calls the brain’s Wi-Fi—its ability to send long-range signals, such as those between the brain and the ovaries. She wants to understand how changes with age in that communication might “give us a clue about aging in the rest of the body.” More than that, she wants to create space for work like hers and Pepin’s to flourish. In 2018, Nicole Shanahan, an attorney, philanthropist and (most famously) the former wife of Google co-founder Sergey Brin, approached the Buck Institute. After contemplating IVF, then conceiving naturally, Shanahan’s experience made her realize something was deeply wrong with the medical understanding of fertility. She gave the Buck Institute $6 million to start its Center for Reproductive Longevity and Equality, and the following year she helped create its grant-giving arm for researchers at other institutions to study the topic. “No one has ever funded foundational science in reproductive aging or ovarian function,” Shanahan says. “It is the least funded organ by a significant amount.”

Recasting the problem as one of aging—not just fertility—has finally helped propel the area of study, says Francesca Duncan, a reproductive biologist who studies ovarian aging at Northwestern. “It’s a small field, but at least we’re literally a field now,” she says, noting that the new angle also has helped attract more research dollars. “Yes, it is about fertility, but it’s not just about fertility,” she says. “It’s about endocrine health and general health at the same time.”

At 31, Daisy Robinton suddenly found herself confronted by the incessant, inevitable ticking of her biological clock. It was 2019, and she’d recently finished her postdoc at Boston Children’s Hospital researching the cellular interaction at the root of neurodegenerative diseases. She’d also just ended a five-year relationship and moved to New York City. Her work had received attention, including a popular TedX London talk on the science of aging, but the lab, she realized, wasn’t for her. She didn’t quite know what she wanted to do professionally—she was making a living with a combination of scientific consulting and fashion modeling. She did know that she wanted a family. So she set up an appointment with a reproductive endocrinologist to explore freezing her eggs. She walked away reassured by the state of her own reproductive system but furious at the state of women’s health.

Daisy Robinton photographed in Los Angeles, California

Robinton Photographer: Elizabeth Weinberg for Bloomberg Businessweek

Around this time, she happened to reconnect with stem cell biologist James Peyer, whom she’d once met at an entrepreneurship event and who’d recently started Cambrian Bio. Over coffee, he told her about his company. “All I was thinking about was how our ovaries stop working halfway through our lives and that in any room I had been in that was focused on aging, no one had brought this up,” says Robinton. “It was shocking to me. I just thought it was stupid and rude and horrifying.”

Peyer hired Robinton as a staff scientist to hunt for a way to turn her outrage into a capitalist endeavor. In fall 2020 she organized a virtual summit on reproductive longevity where someone mentioned Pepin’s research. It seemed to mesh with an idea she was already exploring, that slowing the decline of the ovarian reserve could also extend the lifetime of the ovaries. Robinton cold-emailed Pepin, and by the next year Oviva was born. “I was looking to find a way to get this to the clinic, and she was looking for things that she could bring to the clinic,” Pepin says.

To solve the issue of the aging ovaries, three key problems will need to be addressed. The first is that the number of a woman’s eggs decreases, eventually to zero. The general wisdom is that a human female is born with 1 million to 2 million eggs, and more than half are gone by the time she even hits puberty. When she reaches her 30s, not only does she have just a fraction of those eggs left, but the quality of the remaining ones has declined steeply. That’s the second problem: Older eggs are more likely to contain genetic abnormalities, one reason miscarriages become more common with age. Then there’s the third problem, which has to do with the environment of the ovary itself: Over time it becomes fibrotic, stiffening and making it harder for healthy eggs to grow. “If you can solve all these problems, then maybe you can slow down ovarian aging,” Pepin says.

The work that could most immediately benefit women primarily focuses on the first problem. When Pepin made his initial discovery, he thought AMH could be the basis of a better birth control therapy. There are receptors for estrogen all over the body, a reason so many women experience a litany of side effects from taking the pill. But AMH receptors are limited to the reproductive system, the nearby adrenal glands and a small part of the brain that modulates reproduction. AMH, Pepin says, also seems to be the only known hormone that can inhibit the growth of primordial follicles, the pool of those waiting to develop.

That’s what made him think a decade ago that it also could help protect the fertility of those undergoing cancer treatment, which he initially demonstrated in mice. But, more recently, Pepin has shown that AMH can be used to create what’s basically a permanent birth control in cats. Working with the Cincinnati Zoo, he tested an AMH gene therapy on cats that halts ovulation. (He envisions it as an alternative to spaying, an invasive surgery in which female cats usually lose not just the ovaries but their uterus, too.) If you could dial that therapy down and turn it into, say, a pill—a difficult feat—then perhaps it could be used to slow the attrition of eggs from women’s resting pool.

Prolonging the depletion of a woman’s eggs could delay the march toward menopause, keeping up the body’s production of critical ovarian hormones for a longer period. In older experiments, when researchers transplanted the ovaries of younger mice into older ones, they lived about 40% longer and also appeared to have healthier hearts. (Mice, of course, do not go through menopause, making them an imperfect model.)

But bringing any drug from benchtop to market is a slog requiring time, uncertainty and millions of dollars. “There is more risk, simply because it just hasn’t been done,” says Cambrian’s Peyer. For Oviva’s AMH-based therapy to make it to market, there’s also the problem of the protein itself to solve. One reason it took so long to figure out that AMH plays such a huge role in reproduction is that it’s difficult to produce in any sort of quantity. Estrogen, the first reproductive hormone isolated, in 1929, is among the least complicated to make. It’s physically small and structurally simple, making it easy to synthesize in a lab. You can plop its synthetic form into a pill, like birth control, and it will work.

A pipette, a lab essential in Dr. Yousin Suh’s study of how cells respond to rapamycin

A pipette, a lab essential in Suh’s study of how cells respond to rapamycin. Photographer: Laurel Golio for Bloomberg Businessweek

A screen in Dr. Yousin Suh’s lab of genetically modified cells that are common in the ovary

A screen in Suh’s lab of genetically modified cells that are common in the ovary. Photographer: Laurel Golio for Bloomberg Businessweek

AMH, in comparison, is massive in size, its structure made up of intricate folds. For it to be activated, AMH has to be cleaved precisely so that its two halves are separated but still in contact. The body does that naturally, but the process is too complex to synthesize. To produce it, you have to program mammalian cells to make AMH for you, creating what’s known as a recombinant protein, a protein produced by a host organism—in Pepin’s case, Chinese hamster ovarian cells. Figuring out how to do this was one of his first big breakthroughs as a postdoc.

Pepin’s cat contraceptive relies on this engineered AMH, a form of the protein close to the original. So will Oviva’s first human therapy, but this drug will amp up reproductive ability, not shut it down. The purpose is to help women going through IVF and egg freezing who are poor responders to traditional ovarian stimulation. The hope is to get them to produce larger quantities of eggs, which could improve the success rates of egg retrieval procedures that are intensive and expensive.

Such a drug, Robinton says, would show that AMH’s ability to influence the reproductive system can translate from mice and cats into humans in an already proven market. From there, Robinton says, Oviva can eventually tackle the bigger goal: delaying menopause. To achieve that, the complicated AMH protein will need to be altered further, turned into a new drug that is less painful than a jab, and virtually side-effect free, which throws novel challenges into the mix. “When I use the gene therapy, I’m using the natural hormone,” Pepin says. “I’ve modified it, but only a little bit. It’s very safe.” Turning that natural hormone into a drug compound, he says, means more unknowns, including side effects.

While major drugmakers have largely avoided AMH drugs, at least in part because of their complexity, the possibilities for the hormone also extend to contraception and treatments for polycystic ovarian syndrome and cancers of the reproductive tract. Celmatix, an early-stage ovarian drug company, also has an AMH-based drug in its pipeline. It’s focused on preserving ovarian function during cancer treatment. As Celmatix founder and chief executive officer Piraye Yurttas Beim says: “The applications for AMH are basically endless.”

AMH is only one potential way into manipulating the ovary. At Columbia, Suh and Williams are enrolling about 50 women for a pilot study to see how the decades-old organ transplant drug rapamycin affects ovarian aging. Rapamycin acts on the body’s mTOR pathway, a buzzword in longevity circles: Activation of the mTOR pathway seems to be associated with aging, suggesting that intervening in it could slow the process. But it also seems to play a role in the activation of primordial follicles, which raises the question of whether targeting the mTOR pathway could reduce the rate at which those follicles mature. Kara Goldman, Northwestern’s medical director of fertility preservation and an associate professor, has explored how mTOR-inhibiting drugs could protect mice from the rapid depletion of eggs caused by cancer treatments. Now Suh and Williams are applying that work to humans. “We are really confident that rapamycin can help women to delay aging in the ovary, thereby improving aging in the body,” Suh says.

When you compare older ovaries to younger ones, she says, the signaling of the mTOR pathway is “screaming high.” At a molecular level, she says, the cells of the ovaries resembled cells from other tissues in people twice as old. With intervention, Williams says, “in a regular month, instead of losing, let’s say, 15 eggs, you lose, let’s say, eight. So you’ve slowed down the rate at which you’re using up eggs.”

But only slowing the depleting of the pool won’t necessarily extend a woman’s fertile years. To do that, you probably need to solve the other two problems: egg quality and the quality of the ovarian environment. “If your nest is crappy, your eggs are going to be crappy,” says Northwestern’s Duncan. She says ovarian stiffness affects how the follicles grow, the caliber of the eggs inside of them and the chances for ovulation to occur. So far, Duncan has shown how low doses of anti-fibrotic drugs in mice could successfully intervene. But scientists like her are just beginning to untangle all the complex signaling involved in reproductive function, from understanding the pathway responsible for fibrosis of the ovary to whether a bigger pool of eggs also helps improve egg quality and deter ovarian stiffness.

Garrison, the Buck Institute neuroscientist, says she hopes that studying the signals between the brain and the ovaries themselves can finally bring an understanding of what’s in the black box. “If we could increase the number of healthy eggs the woman has by 1% or 2% when she’s at age 40, that would maybe on average push out the age of menopause by five or 10 years. That would be profound,” she says. “We could give women the ability to make choices about their life in the same way that men do.”

Of course, because we don’t know why menopause occurs, we don’t know what would happen if it didn’t. Stephanie Faubion, the medical director for the North American Menopause Society, says she’s not sure delaying menopause would make a difference in women’s overall health. The association of some health problems with menopause, she says, may simply be correlation, not causation. “We’ve already tried using hormone therapy, and it didn’t prevent heart disease,” she says, noting that it could even have a negative effect.

Getting to the bottom of these reproductive aging questions requires money, another challenge for an industry where there isn’t always obvious intellectual property. Take rapamycin. Since it’s a generic drug, finding out that it can slow human ovarian aging would be a huge scientific discovery without a windfall. Bigger trials will require bigger funding, and it’s unclear where that money will come from. “The challenge with the medication being generic and low-cost is that there isn’t industry funding for the work,” Williams says. “The support would likely need to come from philanthropy or [the National Institutes of Health].” The more ovarian aging research is recast as the first step in studying aging more generally, the more potential it has for backers.

In the meantime, startups such as Oviva are working to make the leap from testing in animals to humans. Robinton expects its AMH fertility drug could be in human trials within a few years. And from where Oviva is at, she says, a small molecule drug like the one they’re developing could typically be in clinical trials in as quickly as four years. Robinton envisions a not-too-distant future—maybe before she reaches menopause herself—in which women will have therapeutic interventions that allow their ovaries to keep working for longer, helping maintain the skin and hair and mood and health and maybe even the sex life of their younger years. “For me, the pie in the sky is really choosing when to have the sun set on your ovaries,” she says.

Pepin is more reserved. There are still major safety questions to answer, such as whether the ovary would continue to perform all of its other critical functions if you slowed down aging. He’s less bullish on the probability of one magic anti-aging pill for reproductive function, but he thinks a solution might more likely combine findings from all the different corners of the field. Who knows whether we’ll be able to slow ovarian aging completely, he says, or merely intervene in certain facets of it. “What I do know,” he says, “is we have a very good contraceptive for cats.”

Read next: There’s a Black Market on Social Media for Pricey Fertility Drugs

More On Bloomberg



Source link

Rate this post

Leave a Comment