Tauklarify, developed by Lantheus Holdings Inc., is administered intravenously before positron emission tomography (PET) brain scans to detect tau neurofibrillary tangle (NFT) pathology in adults with cognitive impairment who are undergoing evaluation for Alzheimer’s disease, according to FDA documents released in August 2026. The FDA’s approval, announced around August 13–14, 2026, makes Tauklarify the second tau PET imaging agent authorized by the agency, following the 2020 approval of flortaucipir F 18 (Tauvid).

The radiotracer, florquinitau F 18, binds selectively to aggregated tau protein in neurofibrillary tangles, a hallmark of Alzheimer’s pathology that correlates with neuronal degeneration and symptom severity, FDA officials said.

Using fluorine-18 as the radionuclide, which has a half-life of about 110 minutes, Tauklarify can be produced centrally and distributed regionally to imaging centers, similar to other F-18 PET agents. PET scans obtained with Tauklarify are interpreted visually or quantitatively to classify the presence or absence of tau pathology based on standardized criteria established in clinical trials and labeling.

Clinical studies supporting the approval demonstrated that PET images with Tauklarify correlate with post-mortem measures of tau pathology, mirroring the evidentiary framework used for the first approved tau tracer, Tauvid. The FDA’s decision was based on prospective trials involving adults with varying degrees of cognitive impairment, from mild cognitive impairment to dementia, suspected of having Alzheimer’s disease. These trials showed a high likelihood that trained evaluators could accurately identify tau pathology from PET scans compared with neuropathology reference standards, records show.

Tauklarify is intended to be used as an adjunct to other clinical evaluations, including patient history, cognitive testing, and other imaging modalities, rather than as a stand-alone diagnostic tool, according to FDA labeling. Its role parallels that of amyloid PET tracers such as Amyvid (florbetapir F 18), Neuraceq (florbetaben F 18), and Vizamyl (flutemetamol F 18), which are approved for imaging beta-amyloid neuritic plaques. However, Tauklarify specifically targets tau pathology, a distinct hallmark of Alzheimer’s disease, providing complementary information that can aid in differential diagnosis, disease staging, and potentially treatment selection as tau- and amyloid-targeting therapies expand in clinical practice.

The FDA’s approval of Tauklarify follows the agency’s acceptance of a New Drug Application for MK-6240, the investigational tau PET imaging agent developed by Lantheus, with a targeted Prescription Drug User Fee Act (PDUFA) date in August 2026. Lantheus is a radiopharmaceutical company focused on imaging agents for disease identification and management, including Alzheimer’s disease, company records confirm.

The Society of Nuclear Medicine and Molecular Imaging (SNMMI) noted that Tauklarify’s approval “adds a second FDA-approved tau tracer alongside flortaucipir F-18 (Tauvid),” highlighting its significance for nuclear medicine and dementia imaging practice. Regulatory announcements emphasize that tau PET agents like Tauklarify are intended for use exclusively in adults with cognitive impairment undergoing evaluation for Alzheimer’s disease, with labeling designed to ensure appropriate patient selection and interpretation to avoid misuse outside the indicated population.

The approval expands clinicians’ ability to directly visualize tau pathology in vivo, enhancing diagnostic precision for patients presenting with cognitive impairment, according to experts cited by the FDA. The availability of both tau and amyloid PET imaging agents allows for a more comprehensive assessment of Alzheimer’s pathology, supporting refined diagnostic classification and potentially more tailored therapeutic strategies, especially as disease-modifying treatments targeting tau and amyloid proteins emerge in clinical practice.

Amyloid PET tracers have a longer regulatory history, with Amyvid first approved as a radioactive diagnostic agent for brain imaging of amyloid plaques. Its label indicates that a negative scan reduces the likelihood that cognitive impairment is due to Alzheimer’s disease, while a positive scan indicates moderate to frequent amyloid neuritic plaques that may also occur in other conditions. More recently, the FDA approved expanded indications for several amyloid PET agents, including an updated label for Vizamyl in June 2025, reflecting broader acceptance of PET imaging in Alzheimer’s evaluation.

Post-approval, further data collection on Tauklarify’s clinical use is expected through real-world studies and possibly post-marketing requirements, as the tracer becomes integrated into Alzheimer’s diagnostic and research workflows, FDA sources said. Adoption of tau PET imaging in routine clinical pathways will depend on factors such as reimbursement policies, access to PET imaging facilities, and clinician familiarity with interpreting tau and amyloid PET scans, industry analysts noted.

The approval expands Leqembi’s U.S. labeling to allow initiation of therapy using a subcutaneous injection as an alternative to the original biweekly intravenous (IV) starting regimen, according to the FDA and Eisai officials. The newly approved starting dose regimen for Leqembi Iqlik is 500 milligrams once weekly, delivered as two 250 mg subcutaneous injections administered in approximately 15 seconds each, records show. The subcutaneous autoinjector formulation is designed for at-home administration by patients or their care partners following appropriate training, Eisai representatives said.

In the Phase 3 CLARITY AD trial, lecanemab demonstrated a 27% reduction in clinical decline measured by the Clinical Dementia Rating–Sum of Boxes (CDR-SB) over 18 months compared to placebo.

The FDA granted Priority Review to the supplemental Biologics License Application (sBLA) for the weekly starting dose, with a Prescription Drug User Fee Act (PDUFA) action date of May 24, 2026, before granting approval on July 13, 2026, according to agency records. This approval complements the prior FDA approval of Leqembi Iqlik 360 mg weekly subcutaneous maintenance dosing in August 2025, which allowed patients to continue therapy either by IV infusion every four weeks or weekly subcutaneous injections after an 18-month initiation period, Eisai and Biogen confirmed.

Clinical data supporting the approval include a comprehensive package evaluating subcutaneous administration of lecanemab across multiple studies and dosing regimens, officials said. The overall approval program is based on the Phase 3 CLARITY AD trial, in which lecanemab demonstrated a 27% reduction in clinical decline measured by the Clinical Dementia Rating–Sum of Boxes (CDR-SB) over 18 months compared to placebo. A secondary endpoint, the Alzheimer’s Disease Cooperative Study–Activities of Daily Living Scale for Mild Cognitive Impairment (ADCS-MCI-ADL), showed a 37% statistically significant benefit versus placebo, according to Eisai and Biogen.

Data presented by the companies indicate that transitioning to weekly Leqembi Iqlik after 18 months of IV initiation maintains clinical and biomarker benefits comparable to continued IV dosing. The FDA had previously converted Leqembi’s accelerated approval to traditional approval after confirmation of clinical benefit, establishing the drug’s efficacy for Alzheimer’s disease treatment, agency sources said.

The safety profile of the subcutaneous formulation is similar to intravenous infusion, with no new major safety signals identified, Eisai reported. Injection-related reactions are primarily localized and include erythema, induration, swelling, heat, pain, pruritus, rash, ecchymosis, nodules, and hematoma, most commonly occurring at the first dose. Less frequent systemic reactions such as headache, chills, fever, and fatigue are generally mild to moderate. Prescribers are advised to monitor for recurrent or delayed localized reactions during ongoing weekly administration. Both IV and subcutaneous regimens retain class-typical risks related to amyloid-related imaging abnormalities (ARIA), with specific ARIA data for the subcutaneous starter dose encompassed within the broader clinical safety package referenced in the approval.

Leqembi is indicated in the United States for adults with mild cognitive impairment or mild dementia due to Alzheimer’s disease, collectively referred to as early Alzheimer’s disease in company communications and labeling. Eisai and Biogen emphasized that the drug is intended for adult patients only, with no pediatric use included in the indication or clinical development. The Alzheimer’s Association, based in Chicago, welcomed the FDA’s approval on July 13, 2026, noting that Leqembi Iqlik is the first monoclonal antibody that clears amyloid beta for early Alzheimer’s disease to be approved for subcutaneous administration using an autoinjector, a status now encompassing both maintenance and starter dosing.

Eisai’s partner BioArctic reported that the company plans to launch the Leqembi Iqlik starting dose in the U.S. in late August 2026, following the FDA approval. The maintenance-dose formulation was launched on October 6, 2025, after the August 29, 2025 FDA approval, according to Eisai. Company communications stress that the subcutaneous autoinjector option may increase convenience and flexibility for patients and care partners by providing an at-home weekly injection alternative to infusion-center IV therapy, potentially reducing logistical burdens associated with regular IV infusions.

With the new starting-dose approval, Leqembi now supports a fully integrated IV and subcutaneous treatment pathway, enabling initiation and continuation of therapy either by infusion or autoinjector, with the option to switch between routes over time. This integrated approach aims to provide patients with early Alzheimer’s disease greater flexibility in managing their treatment regimen.

The Lumipulse G pTau217/ß-Amyloid 1-42 Plasma Ratio test, developed by Fujirebio Diagnostics with contributions from Johns Hopkins University and Lund University researchers, is the first blood test cleared by the FDA to assist in diagnosing Alzheimer’s disease. The agency announced its clearance on May 16, 2025, authorizing the test for marketing as an in vitro diagnostic device. It is intended for use in adults aged 55 and older who exhibit symptoms of cognitive decline, such as memory loss, confusion, or impaired thinking, according to FDA officials.

According to published data, 91.7% of patients with positive blood test results were confirmed to have amyloid plaques through positron emission tomography (PET) scans or cerebrospinal fluid (CSF) analysis, while 97.3% of those with negative results showed no plaques on follow-up testing.

This blood test measures the plasma ratio of phosphorylated tau 217 (pTau217) to ß-Amyloid 1-42 proteins, biomarkers associated with amyloid plaque formation in the brain, a hallmark of Alzheimer’s disease. The test provides an amyloid range score indicating the likelihood of amyloid pathology but does not offer a definitive diagnosis. Results are to be interpreted alongside other clinical information in specialized care settings, including primary care and specialist clinics, as stated by the FDA. The test uses a routine blood draw, which is then processed in commercial diagnostic laboratories with electronic medical record integration, facilitating broader clinical use, Johns Hopkins’ Abhay Moghekar noted.

Clinical studies reviewed by the FDA demonstrated the test’s high specificity and accuracy. Patients with test results above the high-end cutoff have over a 90% likelihood of having Alzheimer’s amyloid pathology, officials said. This accuracy supports the test’s role as a noninvasive alternative to more costly and less accessible diagnostic tools like PET scans or spinal fluid tests.

The FDA’s Michelle Tarver, M.D., Ph.D., described the clearance as an important step toward making Alzheimer’s diagnosis easier and potentially more accessible. Ken Zaentz, president and CEO of Alzheimer’s New Jersey, called the approval a “giant step forward” in early diagnosis. The Alzheimer’s Association also welcomed the decision on the day of the announcement, highlighting the reduced invasiveness of amyloid detection with the blood test. Yale Medicine’s Sayed Azizi, M.D., Ph.D., characterized the development as a “game changer” for the field.

Nearly 7 million Americans currently live with Alzheimer’s disease, a number expected to rise to 13 million in the coming decades, according to epidemiological data cited by the FDA and Alzheimer’s organizations. The disease affects about 11% of people aged 65 and older. Early detection is considered critical as newly approved drugs such as Leqembi and Kisunla have shown the ability to slow disease progression in early stages. However, existing diagnostic methods like PET scans remain costly and are available only in select centers, limiting access for many patients.

The Lumipulse test is not recommended for general screening of asymptomatic individuals but is aimed at patients already showing signs of cognitive impairment. It is intended to help clinicians determine the need for further confirmatory tests like PET or CSF analysis. Roche’s Elecsys pTau181 plasma test, cleared in October 2025, serves a complementary role by helping primary care providers rule out amyloid pathology. Additionally, Labcorp offers an APOE-4 genetic test to assess late-onset Alzheimer’s risk in individuals over 60 to 65 years old.

The rollout of the Lumipulse test is underway, with diagnostic laboratories acquiring kits to begin processing patient samples. Mayo Clinic specialists note that while the test detects amyloid changes associated with Alzheimer’s, it should be used alongside other diagnostic tools for a comprehensive evaluation. The test’s integration with electronic medical records aims to facilitate its adoption in clinical practice, expanding access to early Alzheimer’s disease detection in symptomatic adults.

The Johns Hopkins University research team found that cystathionine γ-lyase (CSE) prevents harmful phosphorylation of the Tau protein by sulfhydrating the enzyme glycogen synthase kinase 3 beta (GSK3β), a process that becomes disrupted with aging and in Alzheimer’s disease patients. This sulfhydration occurs at the Cys218 residue on GSK3β, located near the enzyme’s active site, according to the research.

The study showed that hydrogen sulfide (H2S) produced by CSE inhibits phosphorylation of Tau at the Ser396 site, which is associated with cognitive decline.

CSE, an enzyme previously thought to be mostly active in peripheral tissues such as the liver and kidney, was found to play a significant neuroprotective role in the brain. The enzyme catalyzes the production of H2S and cysteine from cystathionine, which itself is synthesized from homocysteine by cystathionine β-synthase (CBS). While CBS has been considered the primary source of H2S in the brain, the Johns Hopkins team’s findings challenge this assumption by demonstrating CSE’s involvement in cognitive functions and its decline in Alzheimer’s disease, according to co-first author Sunil Jamuna Tripathi.

In 2021, the researchers reported that mice lacking CSE exhibited Alzheimer’s-like symptoms, including cognitive deficits and increased DNA damage in the hippocampus. These CSE-deficient mice also showed deterioration of the blood-brain barrier, which is linked to neurodegeneration and cognitive impairment. The study employed genetic, proteomic, biochemical, and behavioral analyses to elucidate CSE’s role in brain health, officials said.

The team’s earlier experiments involved administering small doses of hydrogen sulfide to Alzheimer’s disease mouse models, which alleviated symptoms associated with CSE malfunction. For example, treatment with H2S donors such as AP39, administered at 100 nanomoles per kilogram in APP/PS1 mice, resulted in improved cognition, reduced brain atrophy, and decreased amyloid plaque levels. Similarly, intracerebroventricular injections of NaHS, another H2S donor, reduced hippocampal cell death in mouse models exposed to amyloid beta protein. GYY4137, a slow-releasing H2S donor, was shown to increase CSE activity and lower homocysteine levels in plaque models, according to the published data.

Plasma levels of hydrogen sulfide were found to be significantly reduced in patients with Alzheimer’s disease, vascular dementia, and cerebrovascular disease compared with healthy controls. A study analyzing postmortem brain tissue from 13 Alzheimer’s patients and six controls confirmed lower H2S concentrations in the diseased brains. Moreover, plasma H2S levels negatively correlated with disease severity in Alzheimer’s patients, suggesting a potential biomarker role. In contrast, CBS enzyme levels in Alzheimer’s brains did not differ significantly from those in normal brains, indicating that CSE’s decline may be more critical in disease progression, researchers noted.

Endogenous hydrogen sulfide is generated through four enzymatic pathways, including CBS, CSE, 3-mercaptopyruvate sulfurtransferase, and cysteine aminotransferase. While CBS is expressed in the brain, liver, and kidney and is regulated by molecules such as S-adenosyl-L-methionine, nitric oxide, and carbon monoxide, CSE is predominantly found in peripheral tissues but now recognized to have functional expression in the brain, according to biochemical analyses.

The study further identified that depletion of CSE in mice perturbed pathways related to neurodegeneration and reactive oxygen species, reinforcing the enzyme’s role in maintaining neuronal health. Immunostaining and transmission electron microscopy revealed that CSE contributes to blood-brain barrier integrity, which is essential for protecting the brain from toxic substances and maintaining homeostasis, according to the Johns Hopkins team.

Hydrogen sulfide signaling participates in various cellular processes through sulfhydration or persulfidation of target proteins, which modulates their activity. The research highlighted that H2S protects nerve function by influencing amyloid precursor protein metabolism and exerting anti-apoptotic, anti-inflammatory, and antioxidant effects. These mechanisms further support the therapeutic potential of targeting CSE and its H2S production in Alzheimer’s disease.

The findings challenge the long-standing view that CBS is the principal H2S-producing enzyme in the brain and instead position CSE as a critical regulator of cognitive function and neuroprotection. The research, conducted by Johns Hopkins University School of Medicine and published recently, advances the understanding of hydrogen sulfide’s role in brain health and identifies CSE as a promising target for therapeutic intervention in Alzheimer’s disease.