Best Peptides for Muscle Growth: Maximizing Your Anabolic Potential
When researching the best peptides for muscle growth, many individuals discover that building quality muscle mass remains one of the most challenging goals in fitness. Despite consistent training and proper nutrition, plateaus are common, leading people to explore how the best peptides for muscle growth can enhance their results.
The Science Behind Muscle Development
Before exploring specific compounds, it's essential to understand how muscle development occurs. Muscle growth requires adequate protein synthesis, hormone optimization, and proper recovery. Peptides can significantly enhance these natural processes.
Most Effective Peptides for Building Muscle
Among the best peptides for muscle growth, several compounds have shown promising results in research and clinical applications. Growth hormone secretagogues like CJC-1295, Ipamorelin, and BPC-157 have gained attention for their potential to enhance muscle development through various pathways.
How Growth Hormone Affects Muscle Growth
Most of the best peptides for muscle growth work by optimizing growth hormone production. This hormone is crucial in muscle protein synthesis, recovery, and overall anabolic processes. By supporting natural growth hormone release, these peptides may help create an optimal environment for muscle development.
Recovery and Muscle Building
When exploring the best peptides for muscle growth, recovery capabilities cannot be overlooked. Compounds like TB-500 and BPC-157 have shown potential in supporting tissue repair and reducing recovery time between training sessions, allowing for more frequent and effective workouts.
Combining Peptides for Maximum Results
Many experienced users find that combining certain peptides produces superior results. The best peptides for muscle growth often work synergistically, potentially enhancing each other's effects while supporting different aspects of muscle development and recovery.
Strength and Performance Benefits
Beyond pure muscle growth, these compounds may also support improvements in strength and performance. This can lead to more productive training sessions and better progressive overload, a key factor in muscle development.
Natural vs Synthetic Options
Unlike synthetic hormones, these peptides work by supporting the body's natural processes. This approach may lead to more sustainable results and fewer potential side effects compared to more aggressive compounds.
Optimizing Your Training Protocol
When using peptides for muscle enhancement, proper training becomes even more crucial. These compounds may help optimize the body's response to resistance training, potentially leading to enhanced results from each workout session.
Nutrition Requirements for Muscle Growth
The effectiveness of muscle-building peptides depends significantly on proper nutrition and timing. Adequate protein intake, caloric surplus, and strategic nutrient timing all play crucial roles in maximizing results.
Safety and Medical Supervision
While researching peptides for muscle development, safety should remain a top priority. Working with qualified healthcare providers ensures proper dosing, cycling, and monitoring of results while minimizing potential risks.
Anti-Aging Benefits of Peptides
For older individuals, these compounds may help address age-related muscle loss. This becomes increasingly important as natural hormone production typically declines with age.
Recovery Enhancement Strategies
Many athletes incorporate peptides into their recovery protocols. This can be particularly beneficial during intense training phases or when working to overcome plateaus.
Creating a Comprehensive Approach
Using peptides should be part of a comprehensive approach that includes progressive resistance training, optimal nutrition planning, adequate rest and recovery, stress management, and sleep optimization.
Future of Peptide Research
Research into peptides for muscle enhancement continues to evolve. New compounds and combinations are being studied, potentially offering even more effective options for muscle development support.
Working with Healthcare Providers
Success with muscle-building peptides typically requires professional guidance. Healthcare providers can help develop personalized protocols based on individual needs and goals.
Tracking Progress and Results
Regular progress monitoring helps ensure optimal results. This may include tracking body composition, strength gains, and recovery markers.
Conclusion
The best peptides for muscle growth represent an advanced approach to building quality muscle mass. When combined with proper training, nutrition, and recovery strategies, these compounds may help optimize the body's natural muscle-building processes. As research continues and our understanding deepens, peptides will likely play an increasingly important role in performance enhancement and muscle development protocols. Remember to approach peptide use with proper medical supervision and as part of a comprehensive fitness strategy.
Disclosure: The content provided in this article is for informational and educational purposes only and does not constitute medical advice. Always consult with a qualified healthcare professional before making decisions about your health or the use of peptides.
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News24
6 days ago
- News24
SA gets R520m to buy the twice-a-year anti-HIV jab... but there's a snag
SA has accepted an offer of just over $29 million from the Global Fund to Fight Aids, TB and Malaria to buy the twice-a-year anti-HIV jab, lenacapavir. . But there's a snag: the country isn't getting extra money from the fund to buy the medicine. It has to use cash from a grant that it has already been awarded and that was cut by 16% in June. South Africa has accepted an offer of just over $29 million (about R520 million) from the Global Fund to Fight Aids, TB and Malaria to buy the twice-a-year anti-HIV jab, lenacapavir, that research shows could help to end Aids in the country, says health department spokesperson Foster Mohale. But there's a snag. The country isn't getting extra money from the fund to buy the medicine; it has to use cash from a grant that it has already been awarded and that was cut by 16% in June. Moreover, the fund, at this stage, won't tell the health department – or any of the other eight countries it has selected for early roll-out – how much they're paying lenacapavir's maker, Gilead Sciences, for the product. Boitumelo Semete-Makokotlela, the CEO of the country's medicine regulator, the South African Health Products Regulatory Authority (Sahpra), told Bhekisisa it is aiming to have lenacapavir registered in South Africa before the end of the year. According to the national health department's head of procurement, Khadija Jamaloodien, the lenacapavir funds from the Global Fund will become available in October, when the rollout period of South Africa's next grant, known as Grant Cycle 7, kicks in. But rollout – likely in early 2026 – can only start once Sahpra has registered the medicine, the country's essential medicines list committee has reviewed and recommended lenacapavir, procurement processes are in place and health workers and clinics have all they need to hand the drug safely to patients. Two studies released last year showed the medicine completely protects young women from contracting the virus and works almost as well for men, transgender and gender-nonbinary people. In fact, a modelling study shows that if between two and four million HIV-negative people in South Africa use the jab every year over the next eight years, the medication could end Aids as a public health threat by 2032. Ending Aids as a public health threat means reaching a stage where fewer people are getting newly infected with HIV than the number of people with HIV who are dying (increasingly for other reasons than HIV, for example old age). According to the latest Joint United Nations Programme on HIV and Aids (UNAids) report, which was released last week, 170 000 people got newly infected with HIV in 2024, while there were 53 000 Aids-related deaths. The Global Fund money for South Africa is, however, not nearly enough to put two to four million people per year in South Africa on the lenacapavir jab (see price explanation below) – and even if it was, the country's health system won't be able to roll the medicine out that fast, scientists and policymakers say. Will the US help to pay for the jab? The fund's offer follows the body's announcement on 9 July, that it has the 'ambition' to finance enough lenacapavir for two million HIV-negative people – in the low- and middle-income countries it supports – over the next three years. But fulfilling this ambition will depend on whether the governments of wealthy countries give enough money to the fund in its next replenishment round. The US government's Aids fund, Pepfar, was originally going to help to pay to roll out lenacapavir in poorer countries. And, although some activists say it's still possible for the US administration to come on board (lenacapavir is mentioned in President Donald Trump's budget proposal for the next financial year, but is understood to be only for pregnant and breastfeeding women), it's not clear at all how this might happen after the Trump administration's drastic cuts to funding for HIV projects in countries like South Africa this year. The Global Fund's offer, however, is a way to get branded, 'bridging' doses from Gilead to South Africa while the world waits for cheaper generics to become available around 2027. 'We now stand at a moment of reckoning and a moment of choice,' Mitchell Warren, the executive director of the international advocacy organisation, Avac, told Bhekisisa at the 13th conference on HIV science in Kigali this week. 'While a lot of the choices over the last six months have been made by an American politician [Donald Trump] who doesn't care about the pandemic or science generally, our choice is to make decisions based on the science that we all now know. Which is that lenacapavir is our most potent opportunity.' Countries have to budget just under R600 per dose Jamaloodien, however, cautions further discussions with the Global Fund and Gilead will be needed about the governance around the pricing of the product. 'We have a transparent pricing system, guided by the Public Finance Management Act. Even if we procure medicine with Global Fund money, we have to follow the same rules that the Treasury requires us to follow with tenders, which includes revealing the price at which the medicine is bought,' Jamaloodien says. In a Global Fund letter sent in early July to the nine early rollout countries – South Africa, Zimbabwe, Eswatini, Lesotho, Zambia, Mozambique, Kenya, Uganda and Nigeria – the fund asked the governments to budget for $60 (about R1 076) per patient per year ($30, or R576, per six-monthly dose), to buy lenacapavir. But in the document, which Bhekisisa has seen, the fund makes it clear that the amount 'reflects the country contribution only, to be used for budgeting purposes, and should not be considered the product price'. Jamaloodien has confirmed to Bhekisisa that the health department did receive such a letter. The letter also states that the gap between the price that the fund pays Gilead per patient per year and the $60 that countries will pay for with their Global Fund grants, will be covered by private sector funding, which Hui Yang, the fund's head of supply operations, confirmed to Bhekisisa will be paid for by a $150-million (about R2.68 billion) donation of the UK-based Children's Investment Fund Foundation to the Global Fund. Furthermore, says Jamaloodien, South Africa's letter instructs the country to submit its first order, for planning purposes, by 30 September under an 'agreed procurement mechanism'. Why does Gilead not want to talk about LEN's price? Lenacapavir, also referred to as LEN for short, was registered for HIV prevention – also called PrEP – by the US medicines regulator, the Food and Drug Administration on 18 June, and is sold in that country for $28 218 (around R505 269) per person per year under the trade name Yeztugo. The US is the only country in which LEN has been registered so far as PrEP. For low- and middle-income countries such as South Africa, Gilead, however, said it will have a 'not-for-profit' price such as the one they negotiated with the Global Fund, but isn't allowing the fund to make it public. Several scientists and activists at the HIV science conference, have, however, told Bhekisisa the rumoured not-for-profit price that Gilead has negotiated with the Global Fund is $100 per person per year, and Avac, confirms it in its analysis of events. But neither Gilead or the Global Fund have confirmed this amount. If South Africa budgets for $60 per person per year, the $29.2 million that Global Fund says we can use to buy lenacapavir, translates to putting and keeping around 400 000 people on the medicine over three years (Global Fund grants run for three years at a time). Gilead argues that because the not-for-profit price is based on the actual cost of making lenacapavir, and shipping it to countries, it can't declare that cost. 'Gilead doesn't publicly disclose manufacturing costs for any of our medications,' Caroline Almeida, Gilead's head of public affairs, told Bhekisisa in Kigali. But activists don't buy this argument. 'Gilead's secrecy will obstruct civil society activism for lower drug prices and keep prices high in middle-income countries [such as South Africa] where Gilead negotiates prices directly,' the Health Justice Initiative and other activist groups said in a press release last week. Avac has identified 16 top lenacapavir markets, of which South Africa is – by far – the largest because of the country's high number of new HIV infections. The country's 170 000 new infections in 2024 is 13% of the 1.3 million new HIV infections around the world in 2024. And research released by Wits RHI on Tuesday in Kigali shows South Africans are open to using the jab: 56% of just over 1 700 participants in a survey in Tshwane, Mthatha and Gqeberha, who were already using public sector HIV prevention services, said they would take a lenacapavir shot. But for LEN to be affordable, activists argue, Gilead needs to be open about its price. 'Such secrecy undermines the power of buyers to negotiate affordable prices and violates the human rights of all people to access information and lifesaving tools,' activists said in last week's press release. Warren concludes: 'Pricing transparency has been a long-standing challenge, as companies try to balance their commercial pricing and marketing strategies with their global public health strategies. We clearly need a new model or compact for pricing that helps break the cycle of small thinking and limited impact.'
Business Wire
14-07-2025
- Business Wire
Gilead Presents New Data on Twice-Yearly Lenacapavir (Yeztugo
FOSTER CITY, Calif.--(BUSINESS WIRE)--Gilead Sciences, Inc. (Nasdaq: GILD) today announced that Gilead researchers and collaborators will present new Phase 3 PURPOSE trial data at IAS 2025 showing that twice-yearly lenacapavir (Yeztugo ®) was effective and well tolerated among a broad range of populations who need or want pre-exposure prophylaxis (PrEP) for HIV prevention, including pregnant and lactating women, adolescents and young people, and supports lenacapavir dosing recommendations for people in special situations, such as those taking medication to treat tuberculosis (TB) and other conditions. Researchers will also present new quantitative and qualitative data showing that participants in both Phase 3 PURPOSE trials indicated a preference for twice-yearly PrEP injections over daily oral medication. The new data, from the company's pivotal Phase 3 PURPOSE 1 (NCT04994509) and PURPOSE 2 (NCT04925752) trials that assessed the efficacy and safety of twice-yearly Yeztugo for PrEP, will be presented via poster sessions and during a Yeztugo-dedicated oral session at the International AIDS Society (IAS) 2025, the 13 th IAS Conference on HIV Science in Kigali, Rwanda on Thursday, July 17. The data presentations come less than a month after the U.S. Food and Drug Administration (FDA) approved Yeztugo as the first and only twice-yearly HIV prevention option. The data underscore Gilead's focus on intentional inclusion in the PURPOSE program to ensure broad and robust population data at the trials' primary analyses, as well as spotlight the community and organizational collaborations that guided the trial design and implementation process. 'It's a thrill to be back in Kigali with so many of the community, advocacy and research partners who helped make PURPOSE the most intentionally inclusive HIV prevention trial program ever conducted,' said Moupali Das, Vice President of Clinical Development, HIV Prevention & Pediatrics at Gilead Sciences. 'As the first and only twice-yearly PrEP option, Yeztugo continues to demonstrate efficacy and tolerability among diverse populations, and we're excited to highlight new data on this breakthrough HIV prevention option here at IAS 2025.' Yeztugo was Efficacious and Well Tolerated in Trials Among Pregnant and Lactating Women, Adolescents and Young People, and Can Be Administered in People Receiving Treatment for TB and Other Conditions Pregnant and lactating women—who face a heightened likelihood of acquiring HIV—have historically been excluded from HIV prevention trials. Based on input from community meetings in locations including Kigali, Gilead ensured that pregnant and lactating women were included in the Phase 3 PURPOSE 1 trial, which evaluated twice-yearly Yeztugo in cisgender women and adolescent girls in Sub-Saharan Africa. PURPOSE data presented at IAS 2025 show that Yeztugo was efficacious in pregnant and breastfeeding or lactating women, with no new cases of HIV reported among 184 participants in the Yeztugo group (there were a total of 509 pregnancies among 487 participants in PURPOSE 1). Data also show that Yeztugo was well tolerated by these women, that there were similar safety profiles between pregnant and non-pregnant women, and that there were no clinically significant differences in predicted Yeztugo exposure by pregnancy trimester or postpartum status. Additionally, exposure in breastfed infants was minimal. Young people aged 16-25 years are also at an increased likelihood of experiencing HIV acquisition globally, but, like pregnant women, are often not proactively included in Phase 3 HIV prevention trials. Gilead intentionally included this population in the PURPOSE 1 trial and the PURPOSE 2 trial, which evaluated twice-yearly Yeztugo among a broad and geographically diverse range of cisgender men and gender-diverse people. Data presented at IAS 2025 show that Yeztugo was efficacious in people aged 16-25 years, with zero reported HIV infections in young people receiving Yeztugo in PURPOSE 1 and two HIV infections among young people in PURPOSE 2. Additionally, there were no clinically significant pharmacokinetic differences between the 16-25-year-old group and adults aged over 25 years. Yeztugo was well tolerated across both trials among participants of all ages, with no new safety concerns identified. Globally, those at higher likelihood of HIV acquisition may also be vulnerable to TB, which can be treated by rifamycin-class drugs including rifampin and rifabutin. Yeztugo is a substrate of CYP3A, and strong CYP3A inducers such as rifampin, or moderate inducers such as rifabutin, may potentially lower Yeztugo plasma concentrations. Gilead will present modeling data showing supplemental Yeztugo dosing for strong and moderate CYP3A inducers to allow people receiving Yeztugo to receive rifamycin-containing TB treatment, if necessary. Yeztugo is also a moderate inhibitor of CYP3A and could theoretically increase levels of drugs such as statins for lowering cholesterol or PDE5 inhibitors for treating erectile dysfunction; dosing recommendations for these special situations will also be reviewed. Preference for Twice-Yearly Prevention Option Over Daily Oral PrEP New qualitative and quantitative self-reported data from PURPOSE 1 and PURPOSE 2 show significant preference for twice-yearly injectable PrEP compared with daily oral PrEP among study participants. More than 75% of study participants who were surveyed preferred twice-yearly injectable administration; of these, more than 50% reported a strong preference. Reasons given for favoring twice-yearly injectable PrEP versus daily oral PrEP include feeling more protected from HIV (69%) and feeling more confident about not missing a dose (77%). 'Certain groups—including pregnant and lactating women, adolescents and young people—are disproportionately affected by HIV, yet have long been underrepresented in HIV clinical trials,' said Linda-Gail Bekker, MBChB, DTM&H, DCH, FCP(SA), PhD, Director of the Desmond Tutu HIV Center at the University of Cape Town, South Africa, and former President of the International AIDS Society. 'The PURPOSE program set a new standard for innovative, intentional inclusion by ensuring we would have safety and efficacy data in these populations from the outset. The results not only show that Yeztugo provides strong protection against HIV and was well tolerated in these groups, but also highlight the critical need for PrEP options that reflect people's preferences—reducing barriers to uptake and helping close persistent gaps in prevention.' Continued Global Regulatory Filings for Lenacapavir for PrEP, as Well as Milestone Partnerships On June 18, 2025, Gilead received FDA approval for Yeztugo as PrEP to reduce the risk of sexually acquired HIV in adults and adolescents weighing at least 35kg. Gilead has also submitted a marketing authorization application (MAA) and EU-Medicines for all (EU-M4all) application with the European Medicines Agency (EMA), both of which the EMA has validated and will review under an accelerated assessment timeline. Gilead has also filed for regulatory approval for twice-yearly lenacapavir for PrEP with authorities in Australia, Brazil, Canada, South Africa and Switzerland. Additionally, now that lenacapavir has received FDA approval for PrEP, Gilead is preparing additional filings in countries that rely on stringent regulatory authority approvals for regulatory submission, including Argentina, Mexico and Peru. Gilead will continue to share updates on additional regulatory filings. Lenacapavir for HIV prevention is not approved by any regulatory authority outside of the United States. Last week, Gilead announced a strategic partnership agreement with The Global Fund to Fight AIDS, Tuberculosis and Malaria to supply enough doses of lenacapavir, at no profit to Gilead, to reach up to two million people over three years in countries supported by the Global Fund and that are included in Gilead's voluntary licensing agreements for lenacapavir. There is currently no cure for HIV or AIDS. Please see below for U.S. Indication and Important Safety Information, including Boxed Warning, for Yeztugo. About the PURPOSE Program Gilead's landmark PURPOSE program is the most comprehensive and diverse HIV prevention trial program ever conducted. The program comprises five HIV prevention trials around the world that are focused on innovation in science, trial design, community engagement and health equity. The PURPOSE trials are evaluating the safety and efficacy of the, twice-yearly injectable medicine, lenacapavir, to reduce the chance of getting HIV. The Phase 2 and 3 program, consisting of PURPOSE 1-5, is assessing the potential of lenacapavir to help a diverse range of people around the world who could benefit from PrEP. More information about the PURPOSE program, including individual trial descriptions, populations and locations, can be found at About Lenacapavir Lenacapavir is approved in multiple countries for the treatment of multi-drug-resistant HIV in adults, in combination with other antiretrovirals. Lenacapavir is also approved in the United States to reduce the risk of sexually acquired HIV in adults and adolescents weighing at least 35kg who are at risk of HIV acquisition. The multi-stage mechanism of action of lenacapavir is distinguishable from other currently approved classes of antiviral agents. While most antivirals act on just one stage of viral replication, lenacapavir is designed to inhibit HIV at multiple stages of its lifecycle and has no known cross resistance exhibited in vitro to other existing drug classes. Lenacapavir is being evaluated as a long-acting option in multiple ongoing and planned early and late-stage clinical studies in Gilead's HIV prevention and treatment research program. Lenacapavir is being developed as a foundation for potential future HIV therapies with the goal of offering both long-acting oral and injectable options with several dosing frequencies, in combination or as a mono agent, that help address individual needs and preferences of people and communities affected by HIV. The journal Science named lenacapavir its 2024 'Breakthrough of the Year.' U.S. Indication for Yeztugo Yeztugo (lenacapavir) injection, 463.5 mg/1.5 mL, is indicated for pre‑exposure prophylaxis (PrEP) to reduce the risk of sexually acquired HIV-1 in adults and adolescents (>35kg) who are at risk for HIV-1 acquisition. Individuals must have a negative HIV-1 test prior to initiating Yeztugo. U.S. Important Safety Information for Yeztugo BOXED WARNING: RISK OF DRUG RESISTANCE WITH USE OF YEZTUGO IN UNDIAGNOSED HIV-1 INFECTION Individuals must be tested for HIV-1 infection prior to initiating Yeztugo, and with each subsequent injection of Yeztugo, using a test approved or cleared by the FDA for the diagnosis of acute or primary HIV-1 infection. Drug-resistant HIV-1 variants have been identified with use of Yeztugo by individuals with undiagnosed HIV-1 infection. Do not initiate Yeztugo unless negative infection status is confirmed. Individuals who acquire HIV-1 while receiving Yeztugo must transition to a complete HIV-1 treatment regimen. Contraindications Yeztugo is contraindicated in individuals with unknown or positive HIV-1 status. Warnings and precautions Comprehensive risk management: Use Yeztugo to reduce the risk of HIV-1 acquisition as part of a comprehensive prevention strategy including adherence to the administration schedule and safer sex practices, including condoms, to reduce the risk of sexually transmitted infections (STIs). HIV-1 acquisition risk includes behavioral, biological, or epidemiologic factors including, but not limited to, condomless sex, past or present STIs, self-identified HIV risk, having sexual partners of unknown HIV-1 viremic status, or sexual activity in a high-prevalence area or network. Counsel individuals on the use of other prevention methods to help reduce their risk. Use Yeztugo only in individuals confirmed to be HIV-1 negative. Evaluate for current or recent signs or symptoms consistent with HIV-1 infection. Confirm HIV-1 negative status prior to initiating, prior to each subsequent injection, and as clinically appropriate. Potential risk of resistance: There is a potential risk of developing resistance to Yeztugo if an individual acquires HIV-1 before or when receiving Yeztugo, or following discontinuation. HIV- 1 resistance substitutions may emerge in individuals with undiagnosed HIV-1 infection taking only Yeztugo, because Yeztugo alone is not a complete regimen for HIV-1 treatment. To minimize this risk, it is essential to test before each injection and additionally as clinically appropriate. Individuals confirmed to have HIV-1 must immediately begin a complete HIV-1 treatment regimen. Alternative forms of PrEP should be considered after discontinuation of Yeztugo for those who are at continuing risk of HIV-1 acquisition and should be initiated within 28 weeks of the last Yeztugo injection. Long-acting properties and potential associated risks: Residual concentrations of Yeztugo may remain in systemic circulation for up to 12 months or longer after the last injection. Select individuals who agree to the required injection dosing schedule because nonadherence or missed doses could lead to HIV-1 acquisition and development of resistance. Serious injection site reactions: Improper administration (intradermal injection) has been associated with serious injection site reactions, including necrosis and ulcer. Only administer Yeztugo subcutaneously. Adverse reactions Most common adverse reactions (≥5%) in Yeztugo clinical trials were injection site reactions, headache, and nausea. Drug interactions Strong or moderate CYP3A inducers may significantly decrease Yeztugo concentrations. Dosage modifications are recommended when initiating these inducers. It is not recommended to use Yeztugo with combined P-gp, UGT1A1, and strong CYP3A inhibitors. Coadministration of Yeztugo with sensitive substrates of CYP3A or P-gp may increase their concentrations and result in the increased risk of their adverse events. Yeztugo may increase the exposure of drugs primarily metabolized by CYP3A initiated within 9 months after the last injection of Yeztugo. Dosage and administration HIV screening: Test for HIV-1 infection prior to initiating, prior to each subsequent injection, and as clinically appropriate using an approved or cleared test for the diagnosis of acute or primary HIV-1 infection. Dosage: Initiation dosing (injections and tablets) followed by once-every-6-months continuation injection dosing. Tablets may be taken with or without food. Initiation: Day 1: 927 mg by subcutaneous injection (2 x 1.5-mL injections) and 600 mg orally (2 x 300-mg tablets). Day 2: 600 mg orally. Continuation: 927 mg by subcutaneous injection every 6 months (26 weeks) from date of last injection ±2 weeks. Anticipated delayed injections: If scheduled 6-month injection is anticipated to be delayed by more than 2 weeks, Yeztugo tablets may be taken on an interim basis (for up to 6 months) until injections resume. Dosage is 300 mg orally (1 x 300-mg tablet) once every 7 days. Resume continuation injections within 7 days of the last oral dose. Missed injections: If more than 28 weeks have elapsed since the last injection and Yeztugo tablets have not been taken, restart with initiation dosing if clinically appropriate. Dosage modifications of Yeztugo are recommended when initiating with strong or moderate CYP3A inducers. Consult the full Prescribing Information for recommendations. About Gilead HIV For more than 35 years, Gilead has been a leading innovator in the field of HIV, driving advances in treatment, prevention and cure research. Gilead researchers have developed 13 HIV medications, including the first single-tablet regimen to treat HIV, the first antiretroviral for pre-exposure prophylaxis (PrEP) to help reduce new HIV infections, and the first long-acting injectable HIV treatment medication administered twice-yearly. Our advances in medical research have helped to transform HIV into a treatable, preventable, chronic condition for millions of people. Gilead is committed to continued scientific innovation to provide solutions for the evolving needs of people affected by HIV around the world. Through partnerships, collaborations and charitable giving, the company also aims to improve education, expand access and address barriers to care, with the goal of ending the HIV epidemic for everyone, everywhere. Gilead has been recognized as one of the leading philanthropic funders of HIV-related programs in a report released by Funders Concerned About AIDS. About Gilead Sciences Gilead Sciences, Inc. is a biopharmaceutical company that has pursued and achieved breakthroughs in medicine for more than three decades, with the goal of creating a healthier world for all people. The company is committed to advancing innovative medicines to prevent and treat life-threatening diseases, including HIV, viral hepatitis, COVID-19, cancer and inflammation. Gilead operates in more than 35 countries worldwide, with headquarters in Foster City, California. Forward-Looking Statements This press release includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks, uncertainties and other factors, including Gilead's ability to realize the anticipated benefits from the collaboration; difficulties or unanticipated expenses in connection with the collaboration and the potential effects on Gilead's earnings; Gilead's ability to initiate, progress and complete clinical trials in the anticipated timelines or at all, and the possibility of unfavorable results from ongoing and additional clinical trials, including those involving Yeztugo (lenacapavir) (such as PURPOSE 1 and PURPOSE 2); uncertainties relating to regulatory applications and related filing and approval timelines, including regulatory applications for lenacapavir for PrEP, and the risk that any regulatory approvals, if granted, may be subject to significant limitations on use or subject to withdrawal or other adverse actions by the applicable regulatory authority; the possibility that Gilead may make a strategic decision to discontinue development of lenacapavir for indications currently under evaluation and, as a result, lenacapavir may never be successfully commercialized for such indications; the risk that physicians may not see the benefits of prescribing Yeztugo; Gilead's ability to effectively manage the access strategy relating to lenacapavir, subject to necessary regulatory approvals; and any assumptions underlying any of the foregoing. These and other risks, uncertainties and factors are described in detail in Gilead's Quarterly Report on Form 10-Q for the quarter ended March 31, 2025, as filed with the U.S. Securities and Exchange Commission. These risks, uncertainties and other factors could cause actual results to differ materially from those referred to in the forward-looking statements. All statements other than statements of historical fact are statements that could be deemed forward-looking statements. The reader is cautioned that any such forward-looking statements are not guarantees of future performance and involve risks and uncertainties and is cautioned not to place undue reliance on these forward-looking statements. All forward-looking statements are based on information currently available to Gilead, and Gilead assumes no obligation and disclaims any intent to update any such forward-looking statements.
News24
11-07-2025
- News24
TB's tight grip: Why this curable disease is so hard to treat
TB is a tough and ancient adversary and keeps adapting. It can be cured, but ridding the body of the bug often takes many months and usually requires different medicines. In this special briefing, Spotlight zooms in on what makes the TB bacterium so hard to beat. There are many things we've learned from studying the ancient Egyptians. One especially fascinating discovery was evidence of skeletal deformities in mummies, which serves as silent markers of a tenacious bug still stalking us today: tuberculosis (TB). With about 10.8 million people around the world getting sick with TB in 2023, it remains the leading infectious disease on the planet, according to the World Health Organisation (WHO). Just in South Africa, it claims more than 50 000 lives per year. In this Spotlight special briefing, we take a closer look at the bacterium that causes TB and why, even now in an era where TB is curable, beating it still requires months of treatment with multiple different medicines. Adapted for survival The mystery of TB's staying power starts with the bug itself. As explained by Dr Jennifer Furin, Mycobacterium tuberculosis is well adapted to survive on multiple fronts. Furin is an infectious diseases clinician and medical anthropologist who specialises in TB. Firstly, she explains, there's it's size. TB is spread through the air when someone who has the bacterium in their lungs coughs it up. It's then contained in small amounts of fluid called droplet nuclei. This droplet is precisely the right size to hang in the air, allowing TB to survive for hours and even days. These droplets can then be inhaled by other people and are just the right size to travel to their lungs. 'It is really amazing from an evolutionary point of view and would be absolutely fascinating if it did not lead to such a horrible disease,' says Furin. Secondly, the bacteria itself are well adapted to avoid being killed, sporting a thick, slimy coating called mycolic acid. This coating makes it difficult for drugs or immune system cells to get into the organism to kill it. The bacteria also have some clever ways of getting around the human immune system, which allows it to 'persist in the body for years and years'. Furin says one way it's able to stay in the body for so long is the bacterium's ability to go into a 'metabolically quiet state' when the immune system starts coming after it. In this state, it stops multiplying until the pressure from the immune system quiets down. It is this combination of being able to pass from person to person and lay dormant in the body when challenged by the immune system that enables TB to thrive in humans. How the body fights back Though hard to estimate with great accuracy, it is thought that only in the region of one in 10 people who inhale the TB bacterium and become infected actually fall ill with TB disease. In fact, some people's immune response is so good that even though they've been exposed to TB, there's no evidence it was ever able to establish an infection in the lungs. For everyone else exposed to TB, one of two things happens. Either the body mounts an immune response that contains and may eventually kill the bug, or the bacteria gets past the immune system and causes illness. To make people ill, the bug needs to get past the first line of defence and get a foothold in the lungs. Unfortunately, the antibodies relied on to kill other bacteria or viruses don't work against TB. Instead, Furin explains, special pulmonary macrophages recognise TB as a threat and 'gobbles it inside them'. Macrophages work by 'swallowing' bugs and then neutralising them by 'digesting' them. But the bacterium's thick, slimy mycolic acid layer prevents the macrophages from killing it. The macrophages with the TB inside, along with other essential immune system cells called CD4 and CD8 cells, then signal more macrophages to help out. These cells then work together to build a wall around the bacteria to keep it contained. Furin compares the CD4 and CD8 cells to foremen who oversee the building of a wall called a granuloma, while the macrophages are like the bricks and cement that form the actual structure. This wall around the TB bacteria needs to constantly be maintained by the immune system. If the immune system is weakened, Furin says the walls break down and the bacterium escapes, coming out of its dormant state and starts multiplying again. If this happens, TB could spread beyond the lungs to other parts of the body. If the walls are built right and maintained, eventually the bacterium is starved to death. Yet, this process can take a long time, sometimes years, because of the bacterium's ability to go dormant. 'Double-edged sword' The 'interaction between TB and the immune system is a double-edged sword', says Professor Graeme Meintjes, an infectious diseases specialist with a research interest in HIV and TB at the University of Cape Town. 'The immune system is trying to contain and kill TB. But at the same time, TB is using the immune system to perpetuate infection from one person to the other,' he says. Meintjes explains that TB has evolved alongside people and developed special proteins and molecules that cause the immune system to react to it. It needs this reaction to cause damage in the lungs, leading to it being released during coughing or even breathing, which helps spread it to other people. 'The TB excites the immune response that causes damage [to the lungs] and that allows it to be released into the airway and either coughed or breathed out. So, there's some evidence that TB has evolved to elicit the immune response in order to achieve that,' he says. Adding to this, for some people cured of TB, Furin says that a condition known as post-TB lung disease can, in part, be caused by the granulomas grouping together, which causes cavities to form in the lungs. This can lead to scarring and sometimes surgery is required to remove these areas of destroyed lung tissue. The immune system can also start 'over functioning' if it senses the bacterium has escaped from the granulomas and is spreading. This causes the immune system to send out special chemicals called cytokines that can cause indiscriminate killing of the lung cells around it. She says this is like the immune system going after one target with the intention to kill it but then blowing up the whole neighbourhood. TB works differently in different people The complex interplay between the immune system and TB makes it difficult to predict which individuals will become sick with TB and who won't, although there are some clear trends. Meintjes says factors like malnutrition, poverty, overcrowded living or working conditions and multiple exposures to TB are some of the biggest drivers of infection and disease. Factors like genetics, the amount of TB someone is exposed to, or a person's initial immune response are also thought to play a role. 'But still, in a given setting where you have two people living in a household, one of them might go on to develop TB disease with the same exposure and the other not. And there are factors that are not fully explained about why some people will develop TB and others won't,' he says. Probably the most important risk factor for TB in South Africa over the last three decades has been untreated HIV. Because HIV targets specifically CD4 cells, it's the worst thing that could have happened in a world with TB, Furin says. HIV infiltrates and kills a person's CD4 cells, which means the immune system then has fewer of the cells ready to fight TB. In 2024, more than half (58%) of all adults receiving TB treatment in South Africa were also living with HIV, according to estimates from Thembisa, the leading mathematical model of HIV and TB in the country. READ | IN THE SPOTLIGHT: SA has started a TB revolution – can we see it through? Another group that is at high risk of TB disease is children, particularly those younger than two. The good news is that there is a vaccine that reduces this risk. As Furin explains, the BCG (Bacillus Calmette-Guérin) vaccine works by showing the CD4 and CD8 cells how to build the 'protective wall' against TB, because the immune systems of children are still too 'immature' to know how to do it without help. 'It [the BCG vaccine] only works for a little bit of time, but it works great to protect kids against those very severe forms of disease, while their own immune systems are learning [how to fight TB],' says Furin. Because the vaccine only protects children for a short time, the WHO recommends one dose be given at birth for children in countries with a high TB burden. Despite much research efforts to find another vaccine, and a promising candidate being studied in a Phase 3 trial, BCG remains the only TB vaccine in use for now. A brief history of TB treatment Though TB has been making humans sick for many centuries, the bug that causes the illness was only identified in 1882, by German physician and microbiologist Robert Koch. It would be roughly another 60 years before the first effective treatments would become available. Until the 1940s, TB treatment mainly involved staying in a sanatorium. The first drugs to treat TB with any success were the antibiotics streptomycin and para-aminosalicylic acid. These two drugs had significant side effects and using only two drugs often lead to TB becoming resistant to the treatment. As described in this excellent overview, what followed was a 'great flurry of drug discovery research' that lasted from the 1940s to the 1960s. The four drugs used to treat most cases of TB today – isoniazid, rifampicin, pyrazinamide, and ethambutol – were all first used to treat TB in this period. After the 1960s, there was a lull in investment in TB research for several decades, likely because TB rates in wealthy countries had declined and what cases there were could generally be cured with the new treatments. 'The Global North was very much of the perspective that it's a disease that's waning and 'it's no longer our problem',' Meintjes says. 'It was seen as a disease of poverty; a disease of other countries and money was put into diseases that are common in the Global North.' This all changed around the turn of the century with the HIV epidemic and a resurgence of TB, particularly drug-resistant TB (DR-TB) in Europe and North America, says Meintjes. By definition, DR-TB means that some of the standard drugs used to treat TB no longer work. READ MORE | 'We were the first ones to do it': Innovative SA study takes TB testing to people's homes The renewed interest in TB resulted in a new flurry of TB drug discovery. Maybe most notably in the 2010s, a drug called bedaquiline replaced older DR-TB drugs that were associated with hearing loss. A slightly older antibiotic called linezolid also became a cornerstone of DR-TB treatment. Today, in South Africa 'normal' drug susceptible TB (DS-TB) in adults is treated with a six-month treatment course – consisting of four drugs for two months and then two drugs for the next four months. A four-month treatment course has been shown to work in a clinical trial but is not yet routinely provided in the country. Kids are typically treated for four or six months. DR-TB is treated with anything from three to six drugs, for any time from six to 24 months. How someone's TB is classified is largely determined by which drugs their particular strain of TB is resistant to. Lindsay McKenna, co-director of the TB Project at the Treatment Action Group, suggests thinking of it as a ladder. If the standard four drugs all work for your TB, then you don't have to climb any rungs. If rifampicin doesn't work for you, you have rifampicin-resistant TB (RR-TB) and must climb to the first rung to find drugs that work. If both rifampicin and isoniazid no longer work, you have multi-drug-resistant TB (MDR-TB) and must climb another rung. If you have resistance to even more drugs and you have pre-extensively drug-resistant TB and after that extensively drug-resistant TB. (In practice, TB programmes often classify RR-TB and MDR-TB together since the same medicines are used to treat it.) All of the above treatments are for people who are ill with TB disease. There is also so-called TB preventive therapy, which aims to kill the TB bacteria in the lungs of someone who is infected, but who hasn't yet become ill with TB disease. These preventive treatments typically involve taking one or two medicines for one to six months, depending on the specific treatment regimen. It is possible that new long-acting formulations could allow for an entire course of preventive therapy to be administered as a single injection, though that research is still at an early stage. How the treatments work One reason for the complexity of TB treatment is the bacterium's large and complex genome. Meintjes says that HIV has nine genes, while TB has around 4 000. Having so many genes means the bug has lots of potential to bypass the effect of drugs targeting certain molecules or pathways and still survive. On the other hand, the many genes, at least in theory, provides many potential targets for antibiotics to attack. As noted, to cure TB one typically has to attack the bug with at least three or four different drugs. Meintjes says it is like a group of lions taking down a large buffalo - each one targeting a different part of the buffalo. Along these lines, TB drugs can broadly fit into different categories based on which part of the bacterium they target. Some drugs attack the way the bacterium builds its cell wall, others disrupt how the bug makes its protein, yet others interfere with the way in which the bacterium produces or gets energy, and finally, some sabotages the way TB replicates. As Meintjes explains, isoniazid targets the cell wall of the bacteria, by affecting the formation of molecules within the wall, ultimately causing it to leak and die. Rifampicin targets the genetic mechanisms of the TB bacteria, which prevent it from replicating. Bedaquiline, works by targeting the mechanisms that allow the bug to metabolise energy, essentially starving it of fuel. ALSO READ | Casual encounter: New research challenges thinking on the places where TB is transmitted A class of antibiotics called fluoroquinolones, specifically levofloxacin and moxifloxacin, target the TB bacteria's DNA while it's trying to copy itself and stops that process, explains Furin. Another drug, linezolid, interferes with how the bacteria make proteins, which it needs to survive. It is not entirely clear how some other drugs, like clofazimine and pyrazinamide, work, says Furin. Even when attacking TB with several drugs and from multiple angles like this, it can still take months for all the bacteria in someone's body to be killed and for them to be cured. This is because, according to Furin, sometimes the protective wall formed by the immune system to contain the TB becomes too thick for the drugs to get through. And the environment inside the wall is often very acidic and deactivates some of the drugs that do manage to get in. How treatment could get better Novelist George Orwell, who was diagnosed with TB in 1947, was one of the first people to be treated with streptomycin. 'I am a lot better, but I had a bad fortnight with the secondary effects of the streptomycin. I suppose with all these drugs it's rather a case of sinking the ship to get rid of the rats,' he wrote in a letter at the time. More than 75 years later, TB treatments have improved massively, but drug side effects remain a real problem, especially when treating DR-TB. Some older treatments for TB involved injections of toxic drugs and had horrible side effects, including hearing loss and kidney damage. While newer drugs are better, there are still issues. Linezolid, for example, can cause peripheral neuropathy (painful tingling in the hands and feet) and anaemia. McKenna says none of the TB drugs are 'necessarily a walk in the park' and all come with side effects. This is because of the drugs themselves, the dosages required to kill the TB bacterium, and how long the drugs need to be taken. Because of this, much of the focus in TB research has been on finding drug combinations that can reduce the duration of treatment and the severity of side effects. For Furin, an ideal future regimen includes 'fewer pills' – she's hoping for one pill once a day for no more than 8 weeks, 'fewer side effects', and doing away with the one-size-fits-all approach. Her reference to the 'one size fits all approach' points to one of the central tensions in TB treatment programmes. People with TB often do not get optimal treatment based on the specific characteristics of their own illness. For example, in countries with limited testing for drug resistance, people might be treated with medicines that their specific strain of TB is resistant to. They might thus suffer the side effects of that medicine without any of its benefits. This is less of an issue in South Africa than elsewhere, since the country's health system provides routine testing for resistance against several of the most important TB drugs. There are also questions as to whether everyone really needs to be treated for six months to be cured. A landmark study called TRUNCATE has shown that many people can be cured in two months. The difficulty is that we can't currently predict who will be cured after two months and who will need the full six months, or even longer. Figuring this out, as McKenna points out, would enable more personalised care that would mean fewer people are over or under-treated. Some in the TB world have argued for the development a pan-TB regimen – a combination of three or so drugs that nobody is resistant to and that accordingly could be given to everyone with TB, no matter what strain of TB they have. The benefit of such a pan-TB regimen would be that it would dramatically simplify the treatment of TB if it worked. But the experts interviewed by Spotlight agree that resistance is likely to develop against the drugs in such a regimen, and as such, testing people for drug resistance will remain necessary, as will alternative treatment regimens. Furin also points out that, pharmaceutical companies have a greater incentive to invest in a pan-TB regimen since its potential market share is bigger than for drugs in a more fragmented treatment model. A hard task getting harder One of the biggest obstacles in the way of finding new TB treatments is that there really aren't any reliable shortcuts when it comes to doing the research. With HIV, one can get a good idea as to whether a treatment is working by looking at biomarkers, such as a person's viral load and CD4 count. TB, by contrast, doesn't have any similarly clear biomarkers that tell us whether a treatment is working or not. Arguably, the most promising biomarker for TB is bacterial load - essentially how many bacteria is left in someone's sputum a while after treatment has started. Having a high TB bacterial load is associated with a poor treatment outcome, but the problem is that it is difficult to measure reliably. Without a good biomarker, the only way to measure how well treatment is working is to follow patients for a long time and see if they are cured, and if they are, whether they suffer a relapse. Because of this, TB treatment trials often take several years to complete. Despite these challenges, there has been a good deal of activity in recent years. 'There are about 20 different new drugs in clinical trials at the moment - either early or later phase,' says Meintjes. But much of that momentum might now be lost because of the United States' abrupt slashing of research funding, including much TB research. The US government has, until now, been the largest funder of TB research by some distance. It spent $476 million or more than R8.7 billion through its agencies on TB research in 2023, according to a report by TAG. Many ongoing US-funded TB clinical trials have already been affected, according to McKenna, although there have recently been indications that some research funding might be restored. Where does this leave us? That most people with TB can be cured is something worth celebrating. That treatment for DR-TB has gotten a lot better and shorter over the last two decades is also something to be grateful for. But as we have shown in this Spotlight special briefing, TB is a tough and ancient adversary and keeps adapting. The treatments at our disposal today are far from as good as we'd like them to be. The treatment side effects are often horrible, and many people find it very hard to take these drugs for month after month. We didn't linger on it, but many people who are cured struggle with post-TB lung disease for the rest of their lives - meaning the bug might be gone, but that person's lungs are never the same again. The scientific search for better TB treatments is not a matter of convenience. It is critical to reducing the suffering that several million people will endure just this year. It is also vital for reducing the number of lives that are still being claimed by this age-old disease. And of course, TB will keep mutating, and we will likely see more and more resistance developing against the drugs that we are depending on today. That is why it is imperative that governments, donors, and pharmaceutical companies all maintain and increase their investment in the search for better TB treatments. After all, TB claims more lives than any other single infectious agent on the planet. If that alone doesn't warrant more investment, what does? But there is also a case to be made that we should change the way we conduct TB research. Ideally, more research should be driven, and informed by, what actually matters to people with TB and to people in the communities where TB is rampant. After all, when given the choice, who wouldn't opt for more personalised and more respectful treatment and care? 'The TB community keeps making the same mistakes over and over and then acts mystified when things do not turn out the way they want,' says Furin. 'All the new drugs and new regimens in the world will never be enough if we do not listen to what impacted communities need and follow their lead.' - Additional reporting by Marcus Low. .
