Category: 3. Business

– In the CIRRUS-HCM trial, including interim safety results from Part D, EDG-7500 was generally well tolerated; no clinically meaningful reductions in LVEF or LVEF <50% –

 – On track to deliver full 12-week Part D readout in 2Q 2026 and Phase 3 start in 4Q 2026 –

BOULDER, Colo., Dec. 24, 2025 /PRNewswire/ — Edgewise Therapeutics, Inc., (Nasdaq: EWTX), today announced positive updates from the ongoing CIRRUS-HCM, Phase 2 clinical trial of EDG-7500, a novel oral, selective, cardiac sarcomere modulator, specifically designed to slow early contraction velocity and address impaired cardiac relaxation associated with hypertrophic cardiomyopathy (HCM) without impacting systolic function, two central clinical goals in the current management of HCM.

CIRRUS-HCM is a multi-part, open label trial of EDG-7500 in participants with obstructive and nonobstructive HCM. Earlier this year, the Company reported positive top-line results from the Part B (oHCM, n=17) and Part C (nHCM, n=12) 50 mg and 100 mg fixed dose cohorts, in which EDG-7500 administration led to improvements in key HCM disease markers, including N-terminal pro-B-type natriuretic peptide (NT-proBNP), Kansas City Cardiomyopathy Questionnaire (KCCQ), New York Heart Association (NYHA) class and left ventricular outflow tract gradient (LVOT-G) (in oHCM participants). In both Parts B and C, EDG-7500 administration led to KCCQ score improvements that appeared favorable relative to those reported in other cardiovascular trials, including those with cardiac myosin inhibitors (CMIs). EDG-7500 administration was also associated with measurable improvements in key diastolic parameters, including robust reductions in NT-proBNP, reduced left ventricular filling pressures, and improved relaxation metrics.

In addition to the 50 mg and 100 mg fixed doses previously reported, the Company evaluated a lower 25 mg fixed dose in 4 oHCM and 10 nHCM participants in CIRRUS-HCM Parts B and C, respectively. In these cohorts, evidence of clinical activity was observed across key HCM disease markers, including NT-proBNP, KCCQ, NYHA and LVOT-G (in oHCM participants), while maintaining a favorable safety profile, with no clinically meaningful changes in left ventricular ejection fraction (LVEF) or reductions in LVEF to below <50% and no events of atrial fibrillation (AF). The CIRRUS-HCM Part B and C cohorts have completed dosing, with a total of 43 participants enrolled across all dose groups.

CIRRUS-HCM Part D is designed to explore exposure-response correlations, assess biomarker-guided dose optimization to inform the design of Phase 3 trials, and support regulatory discussions. EDG-7500 is being evaluated over a 12-week active treatment period; participants will be provided the opportunity to continue into a long-term extension study. Dosing is guided by objective measures—LVOT-G in oHCM and NT-proBNP in nHCM—with participants dosed from 25 mg to 150 mg and eligible for further optimization up to 200 mg in the extension phase. With intra-patient dose optimization results from Part D, the Company aims to build on the robust clinical improvements observed in Parts B and C to further support EDG-7500’s best-in-disease potential.

Screening at sites involved in Part D is complete, with more than 40 participants enrolled. As of the December 23, 2025 data cutoff, approximately 70% of participants had reached a dose of 100 mg or higher. Overall, patient demographics in Part D are generally consistent with those reported in Phase 3 studies of CMIs.

In this interim safety update, for the 20 participants who completed 12 weeks of dosing in Part D as of the data cutoff date (8 with oHCM and 12 with nHCM), EDG-7500 generally had a favorable safety profile and was well tolerated. Consistent with previous observations, no clinically significant changes in LVEF or reductions in LVEF to below 50% were observed, with EDG-7500 continuing to demonstrate a differentiated LVEF profile relative to CMIs. The safety profile observed with EDG-7500 to date, across both healthy volunteers and the CIRRUS-HCM trial, supports the potential use of EDG-7500 in diverse HCM patient populations. Unlike CMIs, which have a mechanism of action that has been associated with a risk of systolic dysfunction and an increased risk of heart failure, EDG-7500 administration continues to present no meaningful effect on LVEF. Preservation of systolic function has the potential to avoid the patient safety monitoring burden that could limit CMI adoption outside of HCM centers of excellence, which could expand prescriber reach and patient access, if approved.

Furthermore, in Part D, continuous active cardiac monitoring was conducted for four weeks during screening and for two weeks following each dose escalation. More than 300 ambulatory cardiac monitoring devices have been deployed to participants, capturing over 2,600 patient-days of active cardiac monitoring, during which no clinically detectable AF or atrial flutter has been observed. A single adverse event of new onset AF was reported; this event occurred in an oHCM participant who was not on active cardiac monitoring at the time and who had a history of arrhythmias, including supraventricular tachycardia. The investigator deemed the event as not related to study drug.

“I’m excited about the advances we’ve made in Part D of the CIRRUS-HCM trial, where we’ve exceeded our year-end enrollment goal, highlighting continued enthusiasm for the program from patients and physicians” said Kevin Koch, Ph.D., President and Chief Executive Officer. “I’m especially pleased with EDG-7500’s safety profile to date, and the lack of clinically relevant drops in ejection fraction, or any ejection fraction drops below 50%. A major focus of 2026 will be refining our development strategy to deliver the best-in-disease therapeutic profile that EDG-7500 may offer to obstructive and nonobstructive HCM patients.”

The Company remains on track to deliver comprehensive efficacy and safety data from Part D of the CIRRUS-HCM trial in the second quarter of 2026 and is advancing Phase 3 trial design in preparation for trial initiation by the end of 2026.

About Hypertrophic Cardiomyopathy

HCM is the most common form of genetic heart disease, affecting approximately one in 500 people, and is associated with reduced quality of life and an elevated risk of heart failure, abnormal heart rhythms, and sudden cardiac death. Individuals with HCM can become extremely limited in their functional capacity and ability to perform the activities of daily living. Commonly experienced symptoms include breathlessness, irregular heartbeats, chest pain, tiredness, dizziness, or even fainting. These symptoms are caused by excessive contraction and thickening (hypertrophy) of the left ventricular wall of the heart. Over time, the thickened muscle becomes stiff, making it difficult for the heart to relax and fill with blood (diastolic dysfunction). There are two major forms of HCM obstructive and nonobstructive. Despite advancements in treatment options for some patients with HCM, there remains a significant unmet need for additional therapeutic approaches for patients. 

About Edgewise Therapeutics 

Edgewise Therapeutics is a leading muscle disease biopharmaceutical company developing novel therapeutics for muscular dystrophies and serious cardiac conditions. The Company’s deep expertise in muscle physiology is driving a new generation of novel therapeutics. EDG-7500 is a novel cardiac sarcomere modulator for the treatment of hypertrophic cardiomyopathy , currently in Phase 2 clinical development. Sevasemten is an orally administered first-in-class fast skeletal myosin inhibitor in late-stage clinical trials in Becker and Duchenne muscular dystrophies. EDG-15400 is a novel cardiac sarcomere modulator for the treatment of heart failure, currently in Phase 1 clinical development. The entire team at Edgewise is dedicated to our mission: changing the lives of patients and families affected by serious muscle diseases. To learn more, go to: www.edgewisetx.com or follow us on LinkedIn and X.

Cautionary Note Regarding Forward-Looking Statements

This press release contains forward-looking statements as that term is defined in Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Statements in this press release that are not purely historical are forward-looking statements. Such forward-looking statements include, among other things, statements regarding the benefits and potential of, and expectations regarding, EDG-7500; statements regarding the market opportunity for EDG-7500; statements regarding Edgewise’s expectations relating to its clinical trials, including timing of reporting comprehensive efficacy and safety data from Part D of the CIRRUS-HCM trial and timing of the initiation of the Phase 3 trials of EDG-7500 ); clinical outcomes from trials of EDG-7500, which may materially change as more patient data become available; statements regarding the best-in-disease therapeutic profile of EDG-7500; and statements by Edgewise’s President and Chief Executive Officer. Words such as “believes,” “anticipates,” “plans,” “expects,” “intends,” “will,” “goal,” “potential” and similar expressions are intended to identify forward-looking statements. The forward-looking statements contained herein are based upon Edgewise’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. Actual results could differ materially from those projected in any forward-looking statements due to numerous risks and uncertainties, including but not limited to: the potential for the results of the ongoing or any future clinical trial of EDG-7500 to differ from the results of Parts B and C and the interim results of Part D of the ongoing CIRRUS-HCM trial; the risk of delays in completing the ongoing Part D of the CIRRUS-HCM trial or initiating the planned Phase 3 trials of EDG-7500; risks associated with unexpected events during the remainder of Part D of the ongoing CIRRUS-HCM trial, including serious adverse events, toxicities or other undesirable side effects; the risk of difficulties in enrolling or maintaining patients in the clinical trials of EDG-7500; risks associated with Edgewise’s limited operating history, its products being early in development and not having products approved for commercial sale; risks associated with Edgewise not having generated any revenue to date; Edgewise’s ability to achieve objectives relating to the discovery, development and commercialization of its product candidates, if approved; Edgewise’s need for substantial additional capital to finance its operations; Edgewise’s substantial dependence on the success of sevasemten and EDG-7500; Edgewise’s ability to develop and commercialize sevasemten, EDG-7500 and EDG-15400 risks related to Edgewise’s clinical trials of its product candidates not demonstrating safety and efficacy; risks related to Edgewise’s product candidates causing serious adverse events, toxicities or other undesirable side effects; the outcome of preclinical testing and early clinical trials not being predictive of the success of later clinical trials and the risks related to the results of Edgewise’s clinical trials not satisfying the requirements of regulatory authorities; delays or difficulties in the enrollment and/or maintenance of patients in clinical trials; risks related to failure to capitalize on other indications or product candidates; risks related to competition; risks relating to interim, topline and preliminary data from Edgewise’s clinical trials changing as more patient data becomes available; risks related to failure to develop a proprietary drug discovery platform; risks related to exposure to additional risk if we develop sevasemten and potential other programs in connection with other therapies; risks related to production of drugs by Edgewise’s third-party manufacturers; risks related to changes in methods of product candidate manufacturing or formulation; risks related to not achieving adequate market acceptance; risks related to the patient population for our product candidates having a small patient population; risks related to the regulatory approval processes of domestic and foreign authorities being lengthy, time consuming and inherently unpredictable; risks relating to disruptions at the FDA, the SEC and other government agencies; risks relating to Edgewise’s ability to attract and retain highly skilled executive officers and employees; Edgewise’s ability to obtain and maintain intellectual property protection for its product candidates; Edgewise’s reliance on third parties; risks related to future acquisitions or strategic partnerships; risks related to general economic and market conditions; and other risks. Information regarding the foregoing and additional risks may be found in the section entitled “Risk Factors” in documents that Edgewise files from time to time with the U.S. Securities and Exchange Commission. These forward-looking statements are made as of the date of this press release, and Edgewise assumes no obligation to update the forward-looking statements, or to update the reasons why actual results could differ from those projected in the forward-looking statements, except as required by law.

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SOURCE Edgewise Therapeutics

It is known that statins, cholesterol-lowering drugs have been shown to reduce aldosterone levels in humans (Baudrand et al., 2015; Hornik et al., 2020). Moreover, in vitro studies have demonstrated that cholesterol supplementation boosts the production of aldosterone from cultured cells (Simpson et al., 1989; Cherradi et al., 2001; Kopprasch et al., 2009). Given that the adrenal-derived mouse corticosteroids, most notably corticosterone and aldosterone, derive from cholesterol as the common precursor (Figure 1A), we hypothesised that cholesterol binding scavenger receptors could modulate adrenal corticosteroid output by regulating the availability of cholesterol that could feed into the steroid hormone biosynthetic pathway. To test this hypothesis, we measured the concentrations of aldosterone and corticosterone in the plasma of Marco^−/− and wild-type (WT) mice. We found that male Marco^−/− mice had significantly elevated levels of plasma aldosterone relative to WT mice (Figure 1B). In contrast, plasma corticosterone levels were not significantly altered in male mice lacking Marco (Figure 1C). Marco-deficient female mice did not have altered levels of aldosterone relative to WT, but plasma corticosterone was increased relative to WT counterparts (Figure 1D, E). We observed that the adrenal glands from Marco-deficient male mice were significantly lighter than WT controls in male but not female mice (Figure 1F, G). To establish whether cholesterol could explain the elevated plasma aldosterone we observe in Marco-deficient male mice, we measured the levels of total serum cholesterol and intra-adrenal cholesterol in males. We found that Marco^−/− mice had reduced serum cholesterol relative to WT controls (Figure 1H), while the normalised levels of intra-adrenal cholesterol were similar between both mouse strains (Figure 1I). Taken collectively, these findings suggest that, while Marco-deficient male mice have elevated plasma aldosterone concentrations, this is not dependent on systemic or intra-adrenal cholesterol availability. For the purposes of this paper, we focused on the phenotype evident in male mice, namely the increase in plasma aldosterone concentrations.

We next hypothesised that adrenal gland-derived Marco could play a role in modulating aldosterone output. Analysis of publicly available single-cell sequencing data from murine adrenal glands shows that adrenals do contain a substantial population of macrophages expressing Ptprc (CD45), Adgre1 (F4/80), and Cd68 (CD68). However, we did not detect Marco expression in this cluster of cells, nor any other cluster identified in our analyses (Figure 2A). This finding was corroborated by immunostaining of male murine adrenal glands, which showed CD68⁺ macrophages in the adrenal zona fasciculata and zona glomerulosa that did not stain positively for MARCO (Figure 2B). Given that the lung is another site in the RAAS axis, we postulated that Marco-expressing cells in the lung could be involved in mediating the aldosterone phenotype we observed in Figure 1B. Indeed, single-cell RNA-seq analysis of the murine lung shows that Ptprc (CD45), Adgre1 (F4/80), and Cd68 (CD68) expressing cells (alveolar macrophages) also express Marco (Figure 2C), a finding corroborated by immunostaining in the lung (Figure 2C). To further validate our single-cell sequencing and immunofluorescence data, we carried out qPCR for Marco in the lungs and adrenal glands from male WT and Marco^−/− mice, which further demonstrated that the lung is the primary site of Marco expression in the RAAS (Figure 2E).

Aldosterone is a potent blood pressure-regulating hormone, the dysregulation of which can cause severe hypertension and increased cardiovascular risk. It therefore follows that its production is tightly regulated. Aldosterone biosynthesis is fundamentally regulated intra-adrenally by cytochrome P450 family members in the corticosteroid biosynthetic pathway (Figure 1A). We therefore tested whether altered expression of enzymes in this pathway could explain the hyperaldosteronism observed in Marco-deficient mice. Marco^−/− male and female mice showed similar expression of aldosterone biosynthetic enzymes (Star, Cyp11a1, Hsd3b1, Cyp11b1, and Cyp11b2) as WT mice (Figure 3A, B). While Cyp11b2 (aldosterone synthase) is only expressed in the adrenal zona glomerulosa, other biosynthetic enzymes essential for aldosterone production are expressed in the zona fasciculata.

CYP11B1 catalyses the conversion of 11-deoxycorticosterone to corticosterone. Corticosterone can be catalysed to aldosterone by CYP11B2. In this sense, the route via CYP11B1 is a bona fide route for the generation of aldosterone, as evidenced by the fact that Cyp11b1 deletion in mice results in a significant reduction in aldosterone production (Mullins et al., 2009). This route is one that is suppressible via the suppressive action of dexamethasone on ACTH and Cyp11b1 expression. Moreover, ACTH is a known stimulator of aldosterone (Seely et al., 1989; Daidoh et al., 1995). Dexamethasone-mediated suppression of the zona fasciculata (Figure 3C; Finco et al., 2018) was used to test whether the elevated aldosterone phenotype was zona fasciculata-dependent. Marco-deficient mice fed dexamethasone-supplemented drinking water had plasma aldosterone concentrations comparable to vehicle-treated mice (Figure 3D), indicating zona fasciculata activity does not contribute to elevated aldosterone levels in Marco^−/− mice. Taken collectively, these findings indicate that elevated aldosterone observed in Marco-deficient mice arises extra-adrenally and can therefore be considered a form of secondary hyperaldosteronism. Kidney-derived renin is the initiating hormone in the enzymatic cascade that generates Angiotensin II, a potent stimulator of adrenal aldosterone production. We therefore compared plasma renin activity between male WT and Marco^−/− mice, finding no significant differences between the two strains (Figure 3E).

Next, we investigated whether lung-derived angiotensin-converting enzyme (Ace) could explain the elevated aldosterone levels observed in Marco^−/− mice. ACE in the lung catalyses the conversion of Angiotensin I to the aldosterone-stimulating peptide Angiotensin II. We carried out a qPCR test for Ace in the lungs of WT and Marco^−/− mice in both sexes, finding that Marco-deficient male animals had elevated levels of lung Ace relative to WT controls in male mice only (Figure 4A). Immunofluorescent staining of WT and Marco^−/− lungs revealed a substantially higher level of ACE protein in Marco-deficient male mice, while myeloid presence, as measured by CD68 staining, remained unchanged (Figure 4B). While low levels of ACE expression could be detected in CD68⁺ cells (data not shown), the vast majority of ACE was outside of monocytes and macrophages. We used image analysis software to quantify these changes, finding that ACE median fluorescence intensity (MFI) was significantly increased in male Marco-deficient lungs, while CD68⁺ myeloid cells were present in WT and knock-out animals at similar levels (Figure 4C, D). Myeloid cell numbers and lung ACE expression were similar in WT and Marco-deficient female lungs (Figure 4E, F). We also measured the levels of plasma potassium and sodium levels in male and female WT and Marco-deficient animals, but observed no differences between the genotypes (Figure 4G–J). Since aldosterone is a known regulator of blood pressure via regulation of blood fluid balance, we also measured blood pressure using the tail-cuff method. We observed that Marco-deficient male mice had marginally reduced diastolic blood pressures, but systolic and mean blood pressure were no different between the two strains (Figure 4K–M).

We then turned back to analysis of single-cell RNA-seq data to identify the cells in the lung that could be mediating this effect. In the lung, unsupervised cluster analysis revealed a total of 12 cell clusters with distinct gene expression signatures (Figure 5A). We determined the identity of each cell cluster based on the expression of established cell type-specific marker genes, aided by the marker genes identified and outlined in Figure 5B. We next used dot plots to visualise expression of Marco and Ace across the different cell clusters. We observed notable Marco expression only in alveolar macrophages amongst the different cell clusters (Figure 5C). Ace was shown to be primarily expressed by lung endothelial clusters 1 and 2 (Figure 5C), in agreement with what is known about lung Ace expression. To test whether alveolar macrophages are capable of suppressing endothelial cell Ace expression, we co-cultured the MPI alveolar macrophage cell line (Fejer et al., 2013), with or without deletion of Marco, with HUVECs endothelial cells for 24 hr, and measured Ace expression via qPCR. We observed an increase in Ace expression in the Marco-deficient MPI co-cocultures but not WT, though this did not reach statistical significance. Taken collectively, these data suggest a model whereby Marco-expressing alveolar macrophages may, in responses to an as-of-yet unidentified factor, inhibit Ace expression at the gene and protein level, and thereby negatively regulate the cleavage of Angiotensin I to form Angiotensin II, and thereby aldosterone production (Figure 5E).

In conclusion, we hereby demonstrate that Marco is a negative regulator of aldosterone production, associated with a suppression of angiotensin-converting enzyme expression in the lungs of male mice. We propose a model in which extra-adrenal Marco expressing alveolar macrophages, through tissue crosstalk with lung endothelial cells, actively inhibit Ace expression and thereby inhibit the production of aldosterone from the adrenal glands.

Global law firm White & Case LLP has advised Maticmind S.p.A. (Zenita Group), a European company active in the Italian ICT sector, on the issuance of a €375 million senior secured bond due 2032 at a floating rate equal to three-month EURIBOR plus 5.25% per annum, reset quarterly.

The proceeds from the offering will be used by the company for general corporate purposes and to support its growth and operational needs. The notes, offered and sold pursuant to Rule 144A and Regulation S under the US Securities Act, have been admitted to listing on the Euro MTF market organised and managed by the Luxembourg Stock Exchange.

Italy-headquartered Zenita Group is a leading system integrator and ICT service provider, offering advanced technological solutions including networking, cybersecurity, cloud services, data centers, enterprise applications and IoT. It serves both public and private clients and provides integrated, innovative solutions to support digital transformation initiatives.

The White & Case team which advised on the transaction’s capital markets aspects was led by partners Michael Immordino (London & Milan), James Greene (London) and Evgeny Scirtò Ostrovskiy (Milan & London) and included associates Pietro Bancalari (London & Milan) and Diala Kakish (London) and lawyers Noemi Stimamiglio and Aurora Zamagni (both Milan). The team which advised on the transaction’s debt finance aspects included partner Martin Forbes (London) and associates Ben Morrison and Vic Sohal (both London). Counsel Tommaso Tosi (Milan) advised on FDI matters and partner Neil Clausen (Houston) and associate Avery Lewis (Houston) advised on US tax matters.

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NEW YORK – New York Attorney General Letitia James today issued a consumer alert urging New Yorkers planning to fly during the holiday season to know their rights when faced with cancellations, severe delays, or other issues with airlines. Attorney General James urges all New Yorkers to file complaints online to potentially receive compensation if their travel plans are disrupted. 

“As New Yorkers head to the airport for the busiest travel days of the year, my office is going the extra mile to make sure they are treated fairly,” said Attorney General James. “I urge all New York travelers to know their rights and file complaints with my office if they experience significant delays, flight cancellations, or are denied boarding after purchasing a ticket.”

The U.S. Department of Transportation (DOT) has recently announced rollbacks of policies put in place during the prior administration that would ensure travelers receive compensation for certain delayed or canceled flights. However, travelers are still entitled to compensation in some cases of disrupted travel. Attorney General James urges all New Yorkers with air travel plans to know their rights and take the following steps to protect themselves during holiday travel:

• If a flight is significantly delayed, cancelled, or if a traveler is denied boarding despite purchasing a ticket, they may be entitled to compensation. Travelers can submit complaints online and should have the following documents and materials available to provide with their complaint:
  • Booking details, such as their ticket, itinerary, and invoice;
  • Flight details, such as dates, flight numbers, and city pairs; and
  • Any supporting documentation, such as a copy of the complaint filed with the airline or ticket agent, if available.
     
• Travelers are eligible to receive a full refund on their ticket within 24 hours of purchasing it, if the ticket is purchased more than seven days before the flight. However, most discount fares are non-refundable.
   
• Travelers are entitled to a refund if an airline cancels a flight, regardless of the reason, and the consumer chooses not to travel or accept travel credits, vouchers, or other forms of compensation offered by the airline.
   
• Airlines are required to adhere to the promises that they make in their customer service plan, including commitments to care for travelers in the event of controllable delays or cancellations. Travelers should consult the DOT’s airline cancellation and delay dashboard to see what amenities and compensation airlines have committed to provide passengers in the event of a controllable delay or cancellation.
   
• If a flight is scheduled to depart within seven days, airlines are required to provide status updates within 30 minutes of the airline becoming aware of a change. The flight status information must, at a minimum, be provided on the airline’s website and telephone reservation system. The airline must also update all flight status displays and other sources of flight information at U.S. airports that are under the airline’s control within 30 minutes of the airline becoming aware of the problem.
   
• If an airline has overbooked a flight and not enough passengers have volunteered to give up their seats to fly on a different flight, they may select passengers to bump off the flight. Passengers who are bumped may be entitled to compensation and must receive a written statement describing their rights and explaining how the airline decides who gets bumped.
   
• Travelers are entitled to refunds of their checked bag fees if their baggage:
  • Has been declared lost by the airline;
  • Is not delivered within 12 hours after the flight has arrived if it is on a domestic flight;
  • Is not delivered within 15 hours after the flight has arrived if the flight is international and shorter than 12 hours; or
  • Is not delivered within 30 hours after the flight has arrived if the flight is international and longer than 12 hours. 

New Yorkers who wish to file a complaint concerning air travel can do so online or by calling the Office of the Attorney General (OAG) at 1-800-771-7755.

Attorney General James has consistently taken action to protect New York travelers from being taken advantage of. In May 2023, Attorney General James supported new DOT rules requiring airlines to compensate passengers for cancellations or significant delays. These came after Attorney General James called on DOT in August 2022 to take specific actions to crack down on airlines and prevent future delays and cancellations. In March 2022, Attorney General James secured $2.6 million from an online travel agency, Fareportal Inc., for misleading consumers with false information about airline tickets and hotel rooms. In September 2021, Attorney General James urged DOT to take action to end airline “slot-squatting,” which is when airlines occupy flight slots at airports but under-utilize them, holding on to slots simply to prevent them from being used by their competitors, which inconveniences travelers.