CKM Syndrome: Staging, Screening, and Treatment

 Today we’re going to discuss a syndrome that you’ve probably been hearing a lot about because it is getting a lot of attention, and that is cardiovascular-kidney-metabolic (CKM) syndrome. It can be a bit challenging to wrap your head around when you first hear about it, so I am going to try to clear that up. This is going to be a brief review of the AHA/ACC/ADA/ASN Guideline for the Prevention, Detection, Evaluation, and Management of Cardiovascular-Kidney-Metabolic Syndrome. When all of these organizations get together and issue a joint statement, it’s something worth paying attention to. 

The term, CKM syndrome, has evolved to describe the close interconnection between cardiovascular disease, kidney disease, and metabolic abnormalities in order to promote a more comprehensive holistic approach to both prevention and treatment of these entities. Today we’re going to first define CKM syndrome, then discuss why it’s important to understand the stages of the syndrome. We’re just going to touch on treatment, but I want us all to be aware of the overlap in treatment between different parts of CKM syndrome.

Let’s start with the definition. CKM syndrome — and I’m going to quote from the guideline here — is “a systemic disorder characterized by pathophysiological interactions among metabolic risk factors, CKD, and the cardiovascular system, leading to multiorgan dysfunction and a high rate of adverse cardiovascular outcomes.” This definition is meant to emphasize the interconnectedness of metabolic risk factors and their outcomes. 

The root cause of CKM syndrome is excess adiposity, particularly visceral adiposity. Visceral adiposity leads to inflammation and insulin resistance, which in turn leads to the development of metabolic abnormalities and progression of CKM syndrome, which in turn leads to multi-organ pathology. When assessing adiposity, both BMI and waist circumference provide complementary prognostic information about the likelihood of progression of CKM syndrome. 

CKM syndrome goes through predictable stages: 

• Stage 1: Excess or dysfunctional adiposity and/or prediabetes.
• Stage 2: The presence of metabolic risk factors, including diabetes and early-to-moderate CKD.
• Stage 3: Subclinical cardiovascular disease, which includes subclinical coronary disease (defined as a coronary calcium score [CAC] > 100) and/or subclinical heart failure (defined as a NT-proBNP ≥ 125 pg/mL with echocardiographic evidence of ventricular dysfunction); very high-risk chronic kidney disease (CKD stage 4 or 5 or by virtue of elevated urine albumin-creatinine ratio by the KDIGO heat map); or high CVD risk with a 10-year predicted risk of > 20% using the PREVENT equation.
• Stage 4: Clinical cardiovascular disease, which can either be coronary artery disease, heart failure, stroke, atrial fibrillation, or peripheral vascular disease.

One of the basic tenets of the guideline is to correctly categorize and identify people in order to institute therapies that slow progression to the next stage of CKM and/or slow progression of organ dysfunction in those who already have end-organ damage. 

To prevent CKM early on, it is all about a healthy diet and adequate physical activity, beginning at a young age — but I suggest it’s never too late. In Stage 1 CKM syndrome, address excess adiposity and periodically check lipids, kidney function, and glucose to identify metabolic abnormalities early on. In Stage 2, treat metabolic risk factors: hypertension, lipids, and glucose. An important element that has been added in this guideline is the recommendation to check a uACR annually to identify early development of CKD. For Stage 3, further risk characterization of subclinical disease can be helpful, particularly when the use of medication is not entirely clear, either by risk prediction or patient preference. 

For example, if a patient with a 5%-10% 10-year risk of atherosclerotic cardiovascular disease (ASCVD) on the PREVENT equation is uncertain about the use of a statin, utilizing additional risk assessment, such as CAC scores, can be helpful. If someone’s heart failure risk is high, consider evaluating for pre-heart failure — a term that not everyone is familiar with, but is worth learning about — using NT-proBNP in order to determine if interventions may be appropriate to prevent progression to clinical heart failure. The identification of subclinical ASCVD or heart failure is important as it helps to determine both the correct medications to use and the intensity of intervention. If someone has a high CAC score, for instance, it argues for a lower LDL goal, which may decrease the likelihood of progression from preclinical to clinical heart disease. Early identification of pre-heart failure with appropriate treatment decreases the risk of developing clinical heart failure by almost half.

Treatment for CKM varies depending upon the stage and the specific metabolic abnormality or end-organ damage. Some medications address just one particular area, like treatment of hypertension or lipids, for instance. Some medicines, such as GLP-1 receptor agonists and the SGL2 inhibitors, address multiple areas. 

Understanding CKM syndrome allows us to see the interconnectedness between much of the chronic disease that we care for every day. Metabolic abnormalities like hypertension, hyperlipidemia, and diabetes don’t exist in isolation, and end-organ damage including ASCVD, heart failure, metabolic dysfunction-associated steatotic liver disease (MASLD), and CKD have overlapping root causes and treatments.

Neil Skolnik, MD

Professor of Family and Community Medicine, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia; Associate Director, Department of Family Medicine Residency Program, Jefferson Health-Abington, Jenkintown, Pennsylvania 

Disclosure: Neil Skolnik, MD, has disclosed the following relevant financial relationships:
Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AstraZeneca; Teva Pharmaceuticals; Eli Lilly and Company; Sanofi; Sanofi Pasteur; GlaxoSmithKline; Abbott; Novo Nordisk; Boehringer Ingelheim
Serve(d) as a speaker or a member of a speakers bureau for: AstraZeneca; Eli Lilly and Company; GlaxoSmithKline; Teva Pharmaceuticals; Heartland Pharma; Takeda; Astellas Pharma; Novo Nordisk
Received research grant from: AstraZeneca; GlaxoSmithKline; Novo Nordisk; Novartis

https://www.medscape.com/viewarticle/ckm-syndrome-staging-screening-and-treatment-2026a1000oc0

PARP Inhibitors for Prostate Cancer: 5 Things to Know

 Prostate cancer is the second most common cancer in men worldwide, with nearly 1.4 million new cases diagnosed each year. PARP inhibitors have transformed the treatment landscape for biomarker‑selected metastatic disease, moving from experimental agents to a core option for a subset of men with advanced prostate cancer. By exploiting defects in DNA repair — particularly homologous recombination repair (HRR) alterations such as BRCA1 and BRCA2 — these drugs can deliver meaningful survival gains after progression on standard hormone‑directed therapies. But their use is not one size fits all: benefit depends on tumor genomics, indications remain restricted to metastatic settings, and class‑specific toxicities such as anemia demand close monitoring and dose adjustment.

Here are five things to know about currently approved PARP inhibitors for prostate cancer and the next‑generation agents now in clinical trials.

1. The FDA has approved four PARP inhibitors to treat metastatic castration-resistant prostate cancer (mCRPC) or metastatic castration-sensitive prostate cancer (mCSPC) with homologous recombination repair (HRR) gene alterations.

In May 2020, olaparib was approved by the FDA for patients with HRR gene-mutated mCRPC. In May 2023, the FDA approved olaparib with abiraterone and prednisone (or prednisolone) for adult patients with deleterious or suspected deleterious BRCA-mutated (BRCAm) mCRPC. 

In December 2025, the FDA granted regular approval to rucaparib for adults with a deleterious BRCA mutation (BRCAm) (germline and/or somatic)-associated mCRPC previously treated with an androgen receptor-directed therapy. Rucaparib was granted accelerated approval in 2020 for a similar indication. In June 2023, the FDA approved talazoparib with enzalutamide for HRR gene-mutated mCRPC.

In December 2025, the FDA approved niraparib and abiraterone acetate with prednisone for adults with deleterious or suspected deleterious BRCA2-mutated (BRCA2m) mCSPC.

2. PARP inhibitors block the PARP enzyme, which normally repairs single-strand DNA breaks, and the result is synthetic lethality.

When the PARP repair mechanism is blocked in cancer cells that already have faulty DNA repair pathways (such as BRCA1 or BRCA2 mutations), the cancer cells accumulate fatal DNA damage and die. 

Given the importance of PARP to repairing DNA, PARP inhibitors were originally designed to sensitize tumor cells to DNA-damaging agents. Later, single-agent cytotoxicity was demonstrated in cell lines with deleterious germline mutations in DNA repair genes including BRCA1 and BRCA2. This situation, where two genetic defects which by themselves pose little consequence to cell survival are exploited synergistically and pharmacologically to promote cell death, is termed synthetic lethality.

3. Although PARP inhibitors extend progression-free survival and sometimes overall survival in patients with prostate cancer, side effects, especially anemia, are prevalent and can lead to treatment discontinuation. 

For example, in the phase 3 TALAPRO-2 prostate cancer study, the most common severe or life-threatening treatment-emergent side effect during treatment with talazoparib/enzalutamide was anemia at 65.8%. Anemia caused 8.3% of patients to discontinue treatment and 43.2% of patients to receive a dose reduction.

In a review of 14 relevant studies involving 2066 patients with mCRPC treated with PARP inhibitors, the most common hematological toxicity was anemia, reported in 42% of patients. In the same review, the three most common nonhematological toxicities reported were nausea (43%), fatigue (34%), and anorexia (27%).

4. Several investigational PARP inhibitors are being studied. Among these are saruparib and senaparib.

Saruparib is a new-generation PARP inhibitor that selectively inhibits and traps PARP1. It is designed to selectively target cancer cells while sparing normal bone marrow, and thus, may offer a safer toxicity profile compared to earlier generation PARP inhibitors.

Senaparib is a novel, highly selective PARP1/2 inhibitor being studied for the treatment of mCRPC, specifically in patients with HRR gene alterations (such as BRCA1 and BRCA2 mutations). The drug has been reported to demonstrate promising antitumor activity and is well tolerated. 

5. In a study that assessed homologous recombination repair mutation (HRRm) testing patterns in mCRPC in the USA, Europe, and Japan, testing rates were low. 

In an international survey conducted from January to August 2020, three quarters of physicians (oncologists, urologists, specialist surgeons) globally reported access to genetic/genomic testing, but just over half were HRRm testers. Surveyed physicians reported HRRm testing and positivity rates for 1913 patients, which were 18.1% and 33.7%, respectively. Of patients tested (n = 347), the most common HRR genes tested were BRCA (91.6%) and ATM (47.3%).

PARP inhibitors are the first targeted therapies approved for the treatment of advanced prostate cancer, but studies show their use is limited by the low testing rates of tumors. Increased awareness and education are needed to encourage testing but also broader access to somatic genomic profiling to ensure all patients with advanced disease have their tumors tested.

https://www.medscape.com/viewarticle/parp-inhibitors-prostate-cancer-5-things-know-2026a1000ocr

Lipid Levels May ID Postmenopausal Women at Risk for Heart Disease on Hormone Therapy

 Postmenopausal women with elevated low-density lipoprotein (LDL) cholesterol who started conjugated equine estrogens (CEE) plus medroxyprogesterone acetate (MPA) faced increased risk for coronary heart disease (CHD), while those with normal LDL cholesterol showed no increased risk. Women already receiving treatment for hyperlipidemia at baseline experienced no additional CHD risk from hormone therapy.

METHODOLOGY

• Researchers conducted a secondary analysis of two double-blind placebo-controlled randomized trials from the Women's Health Initiative to evaluate how baseline cardiometabolic status modified cardiovascular effects of oral menopausal hormone therapy.
• They analyzed data of postmenopausal women aged 50-79 years between 1993 and 1998 at 40 US centers, including 10,739 women with prior hysterectomy and 16,608 women with an intact uterus.
• Women with prior hysterectomy were randomly assigned to receive CEE (0.625 mg/d) or placebo in one trial, and women with an intact uterus were randomly assigned to receive CEE plus MPA (2.5 mg/d) or placebo in another trial. The mean age of women in both trials was about 63 years.
• Cardiometabolic status was assessed by lipid profile, blood pressure, blood glucose, and presence of metabolic syndrome.
• The primary outcome was CHD, and secondary outcomes were stroke, all-cause mortality, and venous thromboembolism. The CEE trial was stopped at a median follow-up of 6.8 years, and the CEE plus MPA trial at a median follow-up of 5.2 years.

TAKEAWAY

• Among women not already treated for high cholesterol in the CEE plus MPA trial, CHD risk increased progressively with higher levels of baseline LDL cholesterol (P-trend = .002), non-high-density lipoprotein (non-HDL) cholesterol (P-trend = .007), and with a higher LDL/HDL cholesterol ratio (P-trend = .008).
• Participants with HDL cholesterol ≥ 60 mg/dL showed somewhat lower CHD risk on CEE alone compared with those with levels < 50 mg/dL (P-trend = .02).
• Women being treated for high cholesterol, high blood pressure, or diabetes did not show any added CHD risk from hormone therapy. Blood pressure, blood glucose, triglycerides, or presence of metabolic syndrome did not modify CHD risk from hormone therapy.
• The risks for stroke and venous thromboembolism were increased with hormone therapy, and these increases did not vary by baseline cardiometabolic status.

IN PRACTICE

"Measurement of blood lipids could assist with tailoring MHT [menopausal hormone therapy] to the women most likely to benefit," the authors of the study wrote.

SOURCE

The study was led by Jacques E. Rossouw, MD, Division of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle. It was published online on July 24 in Obstetrics and Gynecology.

LIMITATIONS

The subgroup analyses were exploratory and some subgroups had limited data with wide CIs. Researchers tested multiple interactions, raising the possibility of chance findings. Only 2 therapies were studied, limiting applicability of findings to other hormone formulations or routes of delivery.

DISCLOSURES

The Women's Health Initiative program received funding from the National Heart, Lung, and Blood Institute, the National Institutes of Health, and the US Department of Health and Human Services. Wyeth Ayerst donated active and placebo study pills. The authors did not report any conflicts of interest.

https://www.medscape.com/viewarticle/lipid-levels-may-help-identify-postmenopausal-women-risk-2026a1000q0b

Lifestyle Intervention May Slow Brain Aging — Before Age 70

 A structured multidomain lifestyle intervention may help preserve white matter integrity in older adults at risk for cognitive decline, particularly when initiated before age 70.

In a secondary analysis of the US POINTER randomized clinical trial of over 900 adults, a multidomain lifestyle intervention that combined supervised aerobic, resistance, and flexibility exercise; individualized MIND diet counseling; cognitive training; social engagement; and behavioral coaching slowed increases in free water (FW) — a diffusion MRI-derived marker of early white matter changes — in participants aged 60 to younger than 70 years but not in those aged 70 years or older.

Higher baseline FW was associated with faster white matter hyperintensity (WMH) progression and the development of new cerebral microbleeds (CMBs) over time.

“Multidomain lifestyle interventions may have a greater effect on white matter health when initiated earlier in older adulthood, before vascular and structural brain changes become more advanced,” lead investigator Pauline Maillard, PhD, Department of Neurology, UC Davis, told Medscape Medical News.

“However, the age interaction was a secondary finding, and it should not be interpreted as evidence that individuals aged 70 years or older cannot benefit from lifestyle modification.”

The findings were presented on July 13 at the Alzheimer’s Association International Conference (AAIC) 2026 and simultaneously published online in JAMA Network Open.

Early Brain Aging

Multidomain lifestyle interventions that combine physical activity, dietary modification, cognitive training, and management of vascular risk factors have been associated with reduced dementia risk and slower cognitive decline in older adults at risk.

However, their effects on underlying cerebrovascular changes remain unclear. Cerebral small vessel disease contributes to cognitive decline, and diffusion MRI measures such as FW may help identify early white matter changes better than conventional MRI markers, including WMHs and CMBs.

Previously, the US POINTER, a randomized clinical trial conducted across five US sites, found that a structured multidomain lifestyle intervention led to greater improvements in global cognition than a self-guided program.

For the current analysis, the POINTER Imaging study, a prespecified secondary analysis of the US POINTER trial, investigators assessed whether improvements in cognition were accompanied by changes in MRI markers of cerebrovascular injury and whether these effects varied by age.

The cohort included 959 cognitively unimpaired adults (mean age, 68 years; 61.9% women) who were at increased risk for cognitive decline. Overall, 533 participants were younger than 70 years and 426 were aged 70 years or older. Of the participants, 64.5% had hypertension at baseline.

A total of 503 participants were randomly assigned to the structured intervention and 456 to the self-guided program for 2 years. The self-guided group received educational materials covering the same lifestyle domains but without individualized coaching or goal-directed support.

MRI was performed at baseline and repeated at 12 and 24 months. The investigators assessed several imaging markers of cerebrovascular health, including FW, fractional anisotropy, peak width of skeletonized mean diffusivity (PSMD), analysis along the perivascular space (ALPS) index, WMH volume, and incident CMBs.

Analyses comparing participants younger than 70 years with those aged 70 years or older were prespecified.

Impact on White Matter

The investigators observed a significant three-way interaction among time, intervention group, and age for FW (beta-coefficient, 0.050; P = .006).

Among participants younger than 70 years, those assigned to the structured intervention had a significantly smaller increase in FW over 2 years than those assigned to the self-guided program (beta-coefficient, -0.031; P = .009). No significant between-group difference was observed among participants aged 70 years or older (beta-coefficient, 0.019; P = .18).

The intervention was not associated with significant changes in other MRI measures, including WMH progression, fractional anisotropy, PSMD, the ALPS index, or incident CMBs.

In secondary analyses, the investigators also evaluated whether baseline diffusion MRI markers were associated with later cerebrovascular injury.

Higher baseline FW was associated with a higher likelihood of developing incident CMBs (odds ratio [OR], 1.63; 95% CI, 1.24-2.14; P < .001) and with faster WMH progression over follow-up (beta-coefficient, 0.014; P = .02).

Higher baseline PSMD was also associated with incident CMBs (OR, 1.40; 95% CI, 1.08-1.81; P = .01), whereas lower baseline fractional anisotropy was associated with greater WMH progression (beta-coefficient, -0.018; P = .004).

Beyond Conventional MRI

FW may have been the most sensitive marker for detecting intervention-related changes, said Maillard, because it reflects earlier and potentially reversible biological alterations that occur before more established structural damage develops.

“Free water may capture relatively early and potentially dynamic changes in the extracellular tissue environment, including processes related to vascular dysfunction, inflammation, or blood-brain barrier alterations,” she said.

By contrast, Maillard highlighted that more established MRI markers such as WMHs and CMBs may require longer follow-up before intervention-related changes become apparent.

The link between baseline FW and WMH progression and incident CMBs suggests that elevated FW may identify white matter that is vulnerable to future cerebrovascular injury, Maillard noted.

“These findings support its potential as an early imaging marker of risk, although additional studies are needed to establish its prognostic value, reproducibility, and usefulness at the individual-patient level.”

Maillard cautioned that longer follow-up is needed to determine whether these MRI changes ultimately translate into durable cognitive benefit and to clarify which intervention components and patients are most likely to benefit.

Early Lifestyle Change

The findings add to growing evidence that lifestyle interventions may be most effective when implemented earlier in the course of brain aging, said Zaldy S. Tan, MD, MPH, Carmen and Louis Warschaw Endowed Chair in Neurology, director of the Maxine & Bernard Platzer Lynn Family Memory & Healthy Aging Program, and medical director of the Jona Goldrich Center for Alzheimer’s and Memory Disorders at Cedars-Sinai Medical Center in Los Angeles, who was not involved in the study.

“The age range of participants in this study was 60-79 years, so starting interventions in one’s early sixties — if not earlier — will likely be more beneficial than starting them later in life,” Tan told Medscape Medical News.

FW is an emerging marker of early white matter injury that may be detectable before other changes, such as WMHs and CMBs, become apparent on MRI, Tan noted.

“An increasing white matter free water may indicate several underlying processes, including disruption of the blood-brain barrier and impairment of clearance mechanisms,” he said.

“The attenuation of white matter free water increase over time in the structured multidomain lifestyle intervention group may indicate a lessening of the age-related changes that lead to more permanent signs of white matter injury,” Tan added.

The findings reinforce recommendations for early multidomain lifestyle intervention in older adults at increased risk for cognitive decline, Tan said.

“The earlier people start these interventions, the greater the likelihood of benefit as processes that lead to white matter damage may still be reversible in their early stages.”

Disclosure information for study authors is available in the original study publication. Tan reported no relevant financial disclosures. The study was supported by the Alzheimer’s Association, the National Institute on Aging, and additional public and private partners supporting the US POINTER trial.

https://www.medscape.com/viewarticle/lifestyle-intervention-may-slow-brain-aging-only-before-age-2026a1000pyf

US Intel Chiefs Back Trump's Claim China Interfered In American Elections

  by Tom Ozimek via The Epoch Times,

The heads of four U.S. intelligence and national security agencies have backed key elements of President Donald Trump’s claim that China engaged in election interference by targeting American voter-registration data.

A fact sheet released July 30 by the White House Government Transparency Task Force says China and its proxies bought, stole, or hacked voter data belonging to as many as 220 million Americans, including some information that was not publicly available.

The fact sheet pairs that finding with the intelligence community’s official definition of election interference, which includes a foreign power’s targeting of voter data.

It notes that, for a foreign country’s actions to amount to “election interference,” they do not have to change the actual results.

“That definition includes a foreign power’s targeting of voter registration infrastructure or data,” the task force states, citing declassified documents produced by the U.S. intelligence community.

The fact sheet was approved by the heads of the Office of the Director of National Intelligence (ODNI), the National Security Agency, the Central Intelligence Agency (CIA), and the Department of Homeland Security, according to the White House.

Representatives from those agencies—as well as the Federal Bureau of Investigation—also coordinated with the White House before Trump’s July 16 address and “approved the factual statements” drawn from intelligence documents used in the speech, the task force states.

Election Interference Defined

In his speech, Trump said China has long been meddling in U.S. elections, including that it was “working to influence” the results of the 2020 presidential election, in which President Joe Biden was ultimately declared the winner.

Trump did not explicitly claim that China managed to change the 2020 result, and neither did the heads of U.S. intelligence agencies.

The spy chiefs did say in the fact sheet that voter-registration data is itself part of election infrastructure and could be manipulated in ways that affect election results, for instance by preventing groups of voters from casting their ballots.

“Adversaries could alter data to potentially prevent individual voters or groups of voters from voting, causing delays on election day or forcing voters to use provisional ballots,” the task force states, citing intelligence community documents.

A voter walks to a polling place in Milwaukee, Wis., on July 28, 2026. Nam Y. Huh/AP

“Adversaries could also use the registration data which in some cases is also available publicly or for purchase—to tailor other interference or influence efforts,” it adds.

Election interference “is a subset of election influence targeted at the technical aspects of the election, including voter registration, casting and counting of ballots, and reporting of results,” according to the task force.

The release of the fact sheet marks the clearest institutional backing yet for central parts of Trump’s allegations, which were challenged by some Democrats who cited an earlier intelligence assessment that China did not interfere in the 2020 election.

Trump Orders Investigation

During his July 16 address, Trump described China’s acquisition of the voter data as “the largest compromise of election data in history” and an “unprecedented election security nightmare.”

Trump said U.S. intelligence had found that “China was working to influence the results of the U.S. midterm elections, and later the results of the 2020 presidential election itself.”

He also said U.S. intelligence agencies began learning in 2020 that China had bought, stolen, or hacked tens of millions of voter records across 18 states but that some officials withheld or downplayed the information.

Trump directed the Department of Justice, CIA, FBI, and ODNI to investigate why the intelligence was withheld and, where appropriate, to seek criminal charges.

Sen. Mark Warner (D-Va.), the ranking member of the Senate Intelligence Committee, accused Trump of using the disclosures to influence the approaching midterm elections. Warner cited the intelligence community’s previous assessment that China did not attempt to interfere in the 2020 election.

“China is a serious strategic competitor, and it absolutely seeks to advance its interests at America’s expense,” Warner said.

“The Intelligence Community … concluded that China considered—but ultimately did not deploy—an influence campaign intended to affect the outcome of the 2020 election, and that no foreign government altered vote totals, hacked voting machines, or compromised the integrity of our election infrastructure,” he added.

Trump, in his speech, called the U.S. election system “so broken and so vulnerable that no one can possibly defend it.”

“It is not defensible,” Trump said.

The president also said that many previously classified documents spanning from January 2020 to June 2026 that support his claims would be declassified and released to the public.

“This is a cyber threat aimed at the very heart of our democracy,” he said.

https://www.zerohedge.com/geopolitical/us-intel-chiefs-back-trumps-claim-china-interfered-american-elections

'US sees Iran as likely behind Minnesota water cyberattack - NYT'

 

US investigators believe Iran was likely behind a cyberattack targeting water systems in Minnesota, though the assessment remains preliminary, The New York Times reported on Thursday.

According to the report, officials cautioned that the investigation is ongoing and that the attribution has not been finalized.

https://www.iranintl.com/en/202607300309

US sanctions networks supporting Iran's Mahan Air

 

The United States on Thursday imposed new sanctions targeting individuals and entities in China, India, Russia and Iran accused of supporting Mahan Air, an Iranian airline Washington says has transported Islamic Revolutionary Guard Corps personnel, weapons and drones.

The US Treasury Department designated six entities and individuals for allegedly acting as sales agents and support networks for Mahan Air, which is already under US and European Union sanctions, according to a statement cited by Reuters.

https://www.iranintl.com/en/202607305151