As wireless earbuds continue to get smaller, comfort and awareness of your surroundings can become just as important as compact size. The Zombies Cat B22 takes a different route with an open-ear earclip design that rests around the ear instead of blocking the ear canal. Combined with Bluetooth 6.0 and large 14mm drivers, the B22 is designed for users who want wireless audio while staying more connected to their surroundings during everyday activities and workouts.

That design is paired with Bluetooth 6.0, 14mm dynamic drivers, claimed 720° panoramic sound, a built-in microphone, and a small warm-colored safety light. Instead of trying to compete purely on conventional earbuds specifications, the B22 is designed around the idea of keeping music available while maintaining a more open connection with the surrounding environment.

According to the Banggood listing, the B22 supports Bluetooth 6.0, uses 14mm speakers, offers up to 4.5 hours of playback from the earbuds themselves and up to 20 hours when combined with the charging case.

The B22’s biggest idea is its open-ear design

The most interesting part of the Zombies Cat B22 is not actually Bluetooth 6.0. It is the way the earphones are worn.

Rather than pushing an earbud into the ear canal, the B22 uses an earclip-style open-ear structure. This can be appealing to people who dislike the plugged-in sensation of traditional in-ear headphones or want to remain more aware of their surroundings while listening.

That makes the B22 sports headphones particularly relevant to walking, commuting, cycling and other situations where completely isolating yourself from environmental sound may not be desirable.

It also changes the way the headphones should be evaluated. The goal is not simply maximum isolation. Instead, the B22 is built around a balance between personal audio and environmental awareness.

14mm drivers give the B22 a larger audio foundation

Inside the compact earphones are 14mm dynamic drivers.

A larger driver does not automatically guarantee better sound, but it gives the B22 a substantial hardware foundation for producing bass, vocals and higher-frequency details. For an open-ear design, that can be particularly important because there is no sealed ear canal to create the same acoustic conditions as conventional in-ear headphones.

The product listing describes the 14mm drivers as being designed for a broad soundstage with stronger bass and clear treble.

The stated frequency response is 20Hz–20kHz, covering the commonly specified range for consumer headphones.

What does “720° surround sound” mean here?

The B22 also promotes 720° panoramic sound, which is one of its more unusual specifications.

This should be understood as a spatial-audio presentation rather than literally having sound physically travel in every direction around the listener. The idea is to create a wider and more immersive sense of positioning than conventional stereo playback.

That could make movies, games and music feel more spacious, although the real-world effect will depend on the recording, device and listening environment.

For buyers, the more meaningful takeaway is that Zombies Cat is positioning the B22 as an immersive open-ear headphone, rather than a basic wireless sports earbud.

Bluetooth 6.0 focuses on connection and responsiveness

The B22 uses Bluetooth 6.0 and supports HSP, HFP, A2DP and AVRCP profiles. The listed transmission distance is up to 10 meters.

For everyday users, the important part is less about the Bluetooth version number itself and more about how the headphones fit into daily use.

Bluetooth 6.0 is intended to provide a modern wireless connection, while the supported profiles cover common functions such as music playback, hands-free communication and remote media control.

The listing also highlights low latency for gaming and video. That makes the B22 potentially more versatile than headphones designed exclusively for music listening, although actual latency can vary depending on the connected phone, computer or game system.

The built-in warm light is more than decoration

One of the B22’s most distinctive physical features is its integrated warm safety light.

The light is positioned as a visibility feature for activities such as night running and cycling. Rather than functioning purely as an RGB-style visual effect, the concept is to make the wearer easier to notice in darker surroundings.

This is a clever addition because open-ear headphones are already aimed at active users. A small visibility feature gives the design another practical purpose.

However, the light should be considered an additional visibility aid rather than a replacement for proper cycling or running safety equipment.

Battery life is designed around shorter daily sessions

The B22 uses a 40mAh battery in each earphone and a 300mAh charging case.

Banggood lists approximately 4.5 hours of playback from the earbuds alone and up to 20 hours with the charging case. Charging the case and earbuds is listed at around one hour.

That makes the B22 better suited to several shorter listening sessions than extremely long continuous use.

For example, a commute, workout, walk or evening gaming session can fit comfortably within the stated earbud runtime. Once the earbuds are returned to the case, the additional battery capacity extends the overall listening time.

As always, actual runtime can vary with volume, connection conditions and other usage factors.

The earclip format makes the B22 a sports-oriented headphone

The B22 weighs approximately 43 grams as listed for the product, with dimensions of 60 × 28 × 52mm.

Its physical design is clearly aimed at people who want something different from conventional TWS earbuds.

The earclip structure avoids the need for a traditional silicone ear tip, while the open-ear configuration can make the headphones more suitable for users who prefer a less enclosed listening experience.

That said, fit is highly personal. An earclip that feels secure for one person may not feel identical for another, so the B22’s design should be viewed as an alternative to conventional earbuds rather than a universal replacement.

A microphone makes it useful beyond music

The B22 includes a built-in microphone and supports the standard Bluetooth calling profiles listed by Banggood.

This means the headphones can also be used for calls and voice communication rather than functioning only as a music player.

For people who frequently switch between podcasts, music, phone calls and video content, that makes the B22 a more practical everyday accessory.

Who should consider the Zombies Cat B22?

The B22 makes the most sense for users who specifically want an open-ear Bluetooth headphone rather than a conventional sealed earbud.

It could be particularly interesting for:

• Runners and walkers who prefer an open listening style
• Cyclists looking for headphones with an additional visibility feature
• Commuters who dislike the pressure of in-ear tips
• Users who want larger drivers in an open-ear design
• People interested in Bluetooth 6.0 headphones
• Gamers and video viewers looking for a more spacious audio presentation

It may be less suitable for someone whose first priority is strong passive isolation or deep noise blocking, because the open-ear concept is fundamentally designed around a different listening experience.

Zombies Cat B22 specifications

Feature	Zombies Cat B22
Wearing style	Open-ear earclip
Bluetooth	Bluetooth 6.0
Driver	14mm dynamic driver
Frequency response	20Hz–20kHz
Claimed audio feature	720° panoramic sound
Bluetooth profiles	HSP / HFP / A2DP / AVRCP
Transmission distance	Up to 10m
Earbud battery	40mAh
Charging case	300mAh
Earbud playback	Up to 4.5 hours
Total playback with case	Up to 20 hours
Charging time	About 1 hour
Microphone	Yes
Product weight	About 43g
Product dimensions	60 × 28 × 52mm
Colors	Black, Red, Beige

The specifications above are based on the product information currently published by Banggood.

Final thoughts

Zombies Cat B22 earphone is interesting because it does not try to be another ordinary pair of TWS earbuds.

Its combination of an open-ear earclip structure, 14mm dynamic drivers, Bluetooth 6.0 and built-in warm safety lighting gives it a clearly defined identity. The claimed 720° panoramic sound is another attempt to make the listening experience more immersive without returning to a conventional closed-in design.

The real appeal of the Zombies Cat B22 is not simply its specifications, but the way its open-ear design fits into everyday listening. By leaving the ear canal open, the B22 can be a useful alternative for running, commuting, walking or casual listening when staying aware of nearby sounds is important. For users who prefer a less isolated listening experience than traditional in-ear earbuds provide, the B22 offers a distinctive combination of comfort, situational awareness and wireless convenience.

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Low rainfall and shrinking rivers are causing shipping bottlenecks, and higher prices, around the world.

© Ina Fassbender/Agence France-Presse — Getty Images

Low rainfall and shrinking rivers are causing shipping bottlenecks, and higher prices, around the world.

Idiopathic pulmonary fibrosis, a relentlessly progressive and fatal scarring disease of the lungs, has long frustrated clinicians with only two approved drugs that slow but cannot reverse its course. Now, a team of researchers in Taiwan has identified a surprising new player in the disease’s destructive machinery: doublecortin-like kinase 1, or DCLK1, a kinase better known for its role in cancer stem cells. Their study, published in the Journal of Biomedical Science, demonstrates that DCLK1 drives fibroblast activation in the lung and that blocking it—either genetically or with an oral inhibitor—slows fibrosis and preserves lung function in mice. The findings position DCLK1 as a promising therapeutic target in one of medicine’s most stubborn diseases.

The research, led by Lee-Yuan Lin, Wun-Hao Cheng, Chien-Huang Lin and Bing-Chang Chen of Taipei Medical University, together with collaborators at National Taiwan University Hospital and Universitas Gadjah Mada, began with a question that has lingered in the literature. Gene expression analyses had previously hinted that DCLK1 might be implicated in IPF, and earlier work reported that the kinase is markedly enhanced in the alveolar epithelial cells of patients with pulmonary fibrosis and in mice with bleomycin-induced fibrosis. But its function in fibroblast activation—the cellular engine of fibrosis—had remained unexplained.

To begin untangling that role, the team mined a publicly available single-cell RNA sequencing data set containing more than 312,000 cells from healthy lungs, IPF lungs, and lungs with chronic obstructive pulmonary disease. After stringent quality control filtering, they focused on roughly 240,000 cells from the control and IPF groups and mapped DCLK1 expression across the major lung cell lineages: epithelial, endothelial, lymphoid, myeloid, and stromal cells. The signal was unmistakable. DCLK1 was expressed across many cell populations, but the highest expression appeared in the stromal compartment, particularly in myofibroblasts—the specialized, contractile fibroblasts that churn out the extracellular matrix and stiffen lung tissue in IPF.

Human tissue told the same story. The researchers examined lung samples from eleven patients with IPF, obtained during lung transplantation or surgery, alongside fourteen nonfibrotic control samples. Histological staining with hematoxylin and eosin and Masson trichrome confirmed the expected picture of interstitial consolidation and collagen deposition in the IPF specimens. More importantly, immunohistochemistry revealed that both total DCLK1 and its phosphorylated, activated form were significantly upregulated in the fibrotic lung interstitium compared with control tissue. DCLK1, in other words, was not merely present in scarred lungs—it was switched on.

DCLK1 is an intriguing molecule to find at the center of a fibrotic process. It is a serine/threonine kinase belonging to the calcium/calmodulin-dependent kinase family, distinguished by two microtubule-binding domains. In oncology, DCLK1 overexpression has been documented in colorectal, pancreatic, gastric, renal, and hepatocellular carcinomas, where it correlates with poor prognosis, high recurrence, and metastasis, promoting tumor initiation and the epithelial–mesenchymal transition in cancer stem cells. It has also been linked to inflammatory signaling in SARS-CoV-2 infection, where inhibiting it blocks proinflammatory caspase-1/interleukin-1β signaling. The new study extends this portfolio of mischief to the fibrotic lung.

To test causality rather than mere correlation, the researchers turned to mice. They crossed animals carrying loxP sites flanking exon 3 of the DCLK1 locus with Pgk1-RFP-Cre/ERT2 transgenic mice, generating a system in which tamoxifen administration triggers global deletion of the Dclk1 gene. When these DCLK1 knockout mice and littermate controls were given intratracheal bleomycin, a chemotherapy drug used to induce pulmonary fibrosis in laboratory animals, the difference was striking. Knockout mice showed far less lung infiltration and collagen deposition, reduced numbers of cells staining positive for DCLK1 together with fibroblast surface protein and alpha-smooth muscle actin, and significantly lower levels of the profibrotic proteins fibronectin, α-SMA, and connective tissue growth factor, or CTGF.

The protective effect extended well beyond molecular markers. Using the FlexiVent FX system to measure lung mechanics, the team found that bleomycin treatment significantly reduced respiratory system compliance and pressure–volume performance and increased the normalized work of breathing in control mice—hallmarks of a stiffening, fibrotic lung. In the DCLK1 knockout animals, these functional deficits were substantially attenuated. In vivo microcomputed tomography, acquired at 34.75-micrometer voxel resolution, painted the morphological counterpart: bleomycin caused parenchymal destruction and volume loss in control lungs, while knockout mice retained lung structure and volume. Density histograms shifted toward fibrotic tissue in wild-type animals but stayed largely preserved in the knockouts, and peripheral blood neutrophil percentages, which climbed after bleomycin injury, were significantly reduced in the knockout group.

With the in vivo evidence established, the investigators dissected the molecular wiring in cultured normal human lung fibroblasts. Transforming growth factor beta, the master profibrotic cytokine, induced DCLK1 phosphorylation within 30 minutes and DCLK1 expression within 8 hours. Chromatin immunoprecipitation assays showed that after TGF-β stimulation, both Smad3—the canonical transcriptional mediator of TGF-β signaling—and the nuclear factor kappa B subunit p65 enriched at the DCLK1 promoter, indicating that TGF-β switches on DCLK1 through both Smad-dependent and noncanonical NF-κB pathways. Silencing DCLK1 with small interfering RNA then blunted the fibroblast’s profibrotic response, reducing TGF-β-induced expression of fibronectin, collagen 1A1, α-SMA, and CTGF.

The pathway, however, does not stop there. The team found that TGF-β also phosphorylated Akt, and that transfecting fibroblasts with a dominant-negative Akt construct reduced TGF-β-induced DCLK1 phosphorylation and the expression of fibronectin and CTGF—placing Akt upstream of DCLK1. Downstream, DCLK1 knockdown reduced Smad3 phosphorylation while DCLK1 overexpression enhanced it. Coimmunoprecipitation revealed a physical association between DCLK1 and Smad3, and immunofluorescence microscopy showed the two proteins colocalizing in the nucleus within 30 minutes of TGF-β treatment. A ChIP assay using a DCLK1 antibody pulled down DNA from the Smad3-binding region of the CTGF promoter, and pretreatment with the selective DCLK1 inhibitor DCLK1-IN-1 reduced TGF-β-induced CTGF expression. Together, the results sketch an Akt/DCLK1/Smad3 axis through which TGF-β drives the production of connective tissue growth factor, a potent profibrotic mediator.

The clinical payoff came in the pharmacological arm of the study. Mice receiving oral DCLK1-IN-1 at 10 milligrams per kilogram daily, beginning on day 7 after bleomycin instillation and continuing until day 28, showed visibly reduced fibrotic progression on histology, lower expression of fibronectin, α-SMA, and CTGF in lung tissue and lysates, preserved pulmonary compliance, improved pressure–volume loops, and reduced work of breathing. Serial microCT scans on days 7, 17, and 27 documented less severe fibrotic remodeling in the treated animals, with lung attenuation histograms showing a smaller fraction of dense, nonaerated voxels. Blood neutrophil counts were also lower. In short, a pill-like oral inhibitor measurably slowed the disease in a model that mirrors the human condition.

The implications are significant because the current therapeutic landscape for IPF is so thin. Only nintedanib, a tyrosine kinase inhibitor targeting growth factor receptors, and pirfenidone, which suppresses TGF-β production and activity, are approved by the US Food and Drug Administration, and both merely slow progression. The recent failure of pamrevlumab, a monoclonal antibody against CTGF, in the phase 3 ZEPHYRUS-1 trial suggested that targeting downstream fibrotic end products alone may be insufficient—pointing to the value of upstream signaling regulators such as DCLK1. Adding to the appeal, a DCLK1 inhibitor has already been shown to prevent inflammatory responses in acute lung injury, hinting at dual anti-fibrotic and anti-inflammatory potential.

The authors are careful to note limitations. DCLK1 is expressed across multiple lung cell types, and the tamoxifen-inducible knockout used here was global rather than cell-type-specific, so the contributions of fibroblasts versus epithelial, endothelial, and immune cells could not be fully separated. Human control tissue, as in most fibrosis studies, came from heterogeneous sources, including tumor-adjacent lung. The precise subcellular mechanics of the DCLK1–Smad3 interaction, whether DCLK1 inhibition can promote fibrosis resolution rather than merely slow progression, and the systemic safety of long-term DCLK1 blockade—all relevant given the kinase’s role in cancer and other processes—remain open questions.

Even so, the convergence of evidence is striking: DCLK1 is upregulated in human IPF, amplified in experimental fibrosis, mechanistically coupled to the TGF-β–Smad3 engine of fibroblast activation, and its suppression by both genetics and a small molecule preserves lung structure and function. What began as a cancer stem cell marker has now emerged, unexpectedly, as a central node in the scarring of the lung—offering fresh hope that a disease long considered irreversible may one day be stopped at its molecular source.