Choroid Diseases

Oral gildeuretinol demonstrated a statistically significant reduction in the geographic atrophy (GA) lesion growth rate of 15.3% from 6 to 24 months (p=0.047) in a pre-specified analysis. Gildeuretinol is the first investigational oral therapy to demonstrate a functional benefit in low luminance visual acuity (LLVA) over 24 months (p=0.031), a key secondary endpoint. Gildeuretinol showed a clinically meaningful reduction in GA lesion growth rate of 13.4% from baseline to 24 months (p=0.075), the study’s primary endpoint. Results indicate that slowing the formation of toxic vitamin A dimers could help address the high unmet need for oral therapies in multiple retinal diseases. Gildeuretinol demonstrated a favorable safety and tolerability profile. Among participants at risk of developing Choroidal Neovascularization (CNV) or wet AMD, only 11% in the gildeuretinol group experienced these adverse events compared to 44% in the placebo group, as reported by clinical investigators. CAMBRIDGE, Mass., Oct. 23, 2024 (GLOBE NEWSWIRE) -- Alkeus Pharmaceuticals, Inc., a biopharmaceutical company dedicated to preserving the sight of individuals impacted by retinal diseases, today announced that patients with geographic atrophy (GA) secondary to age-related macular degeneration (AMD) treated with investigational oral therapy gildeuretinol (ALK-001) showed a statistically significant reduction in the GA lesion growth rate of 15.3% vs. placebo from 6 to 24 months (p=0.047). Gildeuretinol also demonstrated a statistically significant visual function improvement, showing 4.4 fewer letters lost (p=0.031) in low luminance visual acuity (LLVA) over 24 months. Gildeuretinol showed a clinically meaningful trend in slowing GA growth rate of 13.4% from baseline to 24 months (p=0.075), the study’s primary endpoint. A trend toward functional benefit in best corrected visual acuity (BCVA) was demonstrated with 3.3 fewer letters lost (p=0.099). Topline results of the SAGA study of gildeuretinol for the treatment of GA secondary to AMD were presented by Alexander Melamud, M.D., M.A., retina specialist and vitreoretinal surgeon with the Retina Group of Washington and a principal investigator in the SAGA study during the 128th Annual Meeting of the American Academy of Ophthalmology (AAO) held in Chicago October 18-21, 2024. “These data indicate a significant slowing of the growth rate of GA lesions, as well as reducing visual function decline,” said Seemi Khan, M.D., M.P.H., M.B.A., Chief Medical Officer of Alkeus Pharmaceuticals. “It takes a couple of months for gildeuretinol to replace vitamin A and achieve a therapeutic effect. Therefore, we are encouraged by the sensitivity analysis measuring the effect starting at six months of treatment. These data represent the first clinical demonstration that slowing vitamin A dimerization could be a target in the treatment of GA secondary to AMD. By slowing dimerization with gildeuretinol’s unique mechanism, we could reduce further damage to the retina at more advanced stages and possibly delay or prevent the onset of GA. We are excited by the potential of gildeuretinol as an oral therapy with functional benefits in GA, in addition to its potential to be the first therapy for Stargardt disease. We would like to thank the patients, investigators and trial sites for their participation in this study, as well as the National Institutes of Health National Eye Institute for providing funding for this study.” SAGA was a 24-month, double-masked, randomized, placebo-controlled trial to investigate the safety, pharmacokinetics, tolerability and efficacy in patients with GA secondary to AMD. The study enrolled 198 patients. The primary efficacy endpoint was the growth rate of GA lesions from baseline to 24 months as assessed by Fundus Autofluorescence (FAF). The first key secondary endpoint was the change in LLVA from baseline to 24 months. A favorable safety and tolerability pro demonstrated by gildeuretinol, consistent with prior clinical studies of gildeuretinol in Stargardt disease. Additionally, among participants at risk of developing Choroidal Neovascularization (CNV) or wet AMD, only 11% in the gildeuretinol group experienced these adverse events compared to 44% in the placebo group, as reported by the retina specialist investigators. “These data are meaningful and changing the conversation in the space about what might be possible with next generation treatments for patients with GA and earlier stages of AMD,” said Charles Wykoff, M.D., Ph.D., retina specialist and Director of Research at Retina Consultants of Texas. “While the primary endpoint was not met, the anatomic efficacy signal appears real, and most interestingly there appears to be a consistent signal of functional preservation with treatment. This patient population could benefit tremendously from a safe and effective systemic treatment option.” GA is a serious, progressive condition that causes irreversible loss of central vision. It is estimated that the median time of progression to severe visual impairment is slightly over six years. There is no oral therapy approved by the FDA to treat GA. The prevalence of GA in the United States is estimated to be over 1 million people, with 160,000 new cases occurring each year. “One of the most exciting aspects of these results is that gildeuretinol is the first oral medication to show a meaningful positive effect on low luminance visual acuity in macular degeneration,” Dr. Melamud said. “One of the first things patients lose in macular degeneration is low light vision, which can have a dramatic impact on daily living. The positive effect demonstrated on LLVA is significant. Based on these results, this therapy would definitely have a place in the overall strategy of treating AMD and slowing the decline observed in our patients. The favorable safety pro warrant treatment as early as possible.” About Gildeuretinol Acetate (ALK-001) Oral gildeuretinol acetate (ALK-001) is a new chemical entity designed to reduce the dimerization of vitamin A without modulating the visual cycle. In preclinical studies, gildeuretinol decreased vitamin A dimerization down to the normal rate and prevented retinal degeneration and loss of visual function in animals with Stargardt disease. A randomized, placebo-controlled, double-masked clinical trial of gildeuretinol in late-stage Stargardt patients (TEASE-1) showed clinically and statistically significant slowing of the growth of retinal lesions over two years of treatment. Additional clinical trials of gildeuretinol in Stargardt disease are ongoing. Gildeuretinol has received breakthrough therapy designation and orphan drug designation for Stargardt disease from the U.S. Food and Drug Administration. A study (SAGA) of gildeuretinol in 198 patients with geographic atrophy (GA) secondary to age-related macular degeneration (AMD) demonstrated a meaningful trend in the reduction of lesion growth rate and demonstrated a functional benefit in low luminance visual acuity (LLVA). In studies, gildeuretinol demonstrated a favorable safety and tolerability profile. About Alkeus Pharmaceuticals Alkeus Pharmaceuticals, Inc. is a private biopharmaceutical company with headquarters in Cambridge, Mass., backed by institutional investors led by Bain Capital Life Sciences. Founded in 2010, Alkeus is developing therapies for serious diseases of the eye with high unmet need, with the purpose to protect the sight of individuals impacted by retinal diseases. Alkeus’ breakthrough-designated lead candidate, gildeuretinol acetate (ALK-001), is a new chemical entity currently being evaluated in clinical trials for the treatment of Stargardt disease and for geographic atrophy (GA) secondary to age-related macular degeneration (AMD). For further information, please contact: Media Relations media@alkeuspharma.com Website:

Enhanced protection of vision with ANX007 treatment in healthier eyes Greater preservation of EZ in the central fovea by ANX007 in patients with less advanced GA Pivotal Phase 3 ARCHER II Data Expected Second Half 2026 BRISBANE, Calif., Oct. 21, 2024 (GLOBE NEWSWIRE) -- Annexon, Inc. (Nasdaq: ANNX), a biopharmaceutical company focused on upstream C1q to advance therapies for neuroinflammatory diseases of the body, brain and eye, today announced new findings from its Phase 2 ARCHER study for ANX007 in geographic atrophy (GA) due to dry age-related macular degeneration (AMD). ANX007 demonstrated enhanced protection of vision and greater preservation of central photoreceptor cells in a subpopulation of patients with less advanced disease as measured by the photoreceptor ellipsoid zone (EZ) in the central fovea. The data were presented at the American Academy of Ophthalmology (AAO) 2024 annual meeting. ANX007 is a first-in-kind, non-pegylated antigen-binding fragment (Fab) designed to block C1q locally in the eye with an intravitreal formulation. “Photoreceptors near the foveal center are necessary for high acuity vision like reading an eye chart or seeing faces. Protecting these cells is essential to preserving vision and we are encouraged by ANX007’s consistent and robust effect on this structural element of the eye,” said Douglas Love, president and chief executive officer of Annexon. “We are further encouraged by ANX007’s more pronounced treatment effect on both preservation of vision and photoreceptors in patients with less advanced disease. Importantly, these Phase 2 data highlight the potential of ANX007 to deliver a differentiated benefit, particularly with earlier intervention in a neurodegenerative disease, and we are encouraged by the promise ANX007 holds to help millions of patients worldwide with dry AMD and GA.” As previously described, in the randomized Phase 2 ARCHER trial, ANX007 demonstrated a visual function benefit consistently across multiple measures that was both dose and time dependent. This includes significant broad-based protection of vision in standard and low light conditions and significant protection of photoreceptors in the fovea region critical for visual acuity. These Phase 2 data are further reinforced in a subpopulation of patients with less advanced disease defined by low light visual acuity (LLVA) < 30 at baseline and in patients with more intact vision as defined by <80% EZ loss. Key highlights of the new data presented at AAO include: Protection from vision loss observed in patients with less advanced disease vs. overall patients through month 12 0% (0/56) ANX007 monthly-treated patients with less advanced disease lost 15 letters, or three lines on an eye chart, vs. 17% (10/59) sham patients (Nominal p-value 0.0013)6% (5/89) ANX007 monthly-treated overall patients lost 15 letters vs. 21% (19/89) sham overall patients (Nominal p-value 0.0021) ANX007 enhanced protection against EZ loss in central subdomains in patients with more EZ intact at baseline 61% decrease in EZ loss between ANX007 and sham in patients with < 80% EZ loss at baseline (Nominal p-value 0.0575)48% decrease in EZ loss between ANX007 and sham in patients with < 98% EZ loss at baseline (Nominal p-value 0.0218) About ANX007 and Phase 2 ARCHER TrialANX007 is an antigen-binding fragment (Fab) antibody designed as a first-in-kind therapeutic to selectively inhibit C1q, the initiating molecule of the classical complement pathway and a key driver of neurodegeneration. In dry age-related macular degeneration (AMD) or geographic atrophy (GA), C1q binds to photoreceptor synapses, causing aberrant activation of the classical pathway with synapse loss, inflammation and neuronal damage that results in vision loss. Intravitreal administration of ANX007 fully stopped C1q and classical pathway activation. In animal models, the murine analog of ANX007 protected against loss of photoreceptor synapses and cells to preserve function. ANX007 has been granted Fast Track designation from the Food and Drug Administration and is the first therapeutic candidate for the treatment of GA to receive Priority Medicine (PRIME) designation in the EU, which provides early and proactive support to developers of promising medicines that may offer a major therapeutic advantage over existing treatments or benefit to patients without treatment options. In the randomized, multi-center, double-masked, sham-controlled Phase 2 ARCHER clinical trial, ANX007 demonstrated consistent protection against vision loss across multiple measures in a broad population of patients with GA. ANX007 provided statistically significant, time and dose-dependent protection from vision loss as measured by ≥ 15 letter loss on reading an eye chart with best corrected visual acuity (BCVA≥15), the widely accepted and clinically-meaningful functional endpoint. Significant protection from vision loss was also shown in other prespecified measures of BCVA and visual function, including low luminance visual acuity (LLVA) and low luminance visual deficit (LLVD). ANX007’s treatment effect increased over the course of the on-treatment portion of the study, suggesting that ANX007 may provide a growing and durable treatment effect over time. While benefit gained against vision loss was maintained during the subsequent six-month off-treatment period, the rate of decline for BCVA ≥ 15-letter vision after treatment termination began to parallel that of sham, providing additional support for the observed on-treatment protection. ANX007 was also shown to protect key retinal structures important for vision, including significant protection of photoreceptors as measured by optical coherence tomography (OCT) and supported by slowing of loss of retinal pigment epithelial cells (RPE) near the fovea, as measured by fundus autofluorescence (FAF). ANX007 was generally well-tolerated through month 12, with no increase in choroidal neovascularization (CNV) rates between the treated and sham arms and no events of retinal vasculitis reported. About Dry AMD and Geographic AtrophyDry age-related macular degeneration (AMD) is the most common form of AMD and geographic atrophy (GA) is an advanced form of dry AMD, an eye disease that is the leading cause of blindness in the elderly. Dry AMD and GA are chronic progressive neurodegenerative disorders of the retina involving the loss of photoreceptor synapses and cells in the outer retina. GA affects an estimated one million people in the United States and eight million people globally, severely limiting their independence and causing frustration, anxiety and emotional hardship. Effective treatments that preserve vision are still needed, as no currently approved therapies have been shown in clinical trials to significantly prevent vision loss. About AnnexonAnnexon Biosciences (Nasdaq: ANNX) is harnessing neuroinflammation to advance potentially first-in-kind treatments for millions of people living with serious neuroinflammatory diseases of the body, brain and eye. Our novel scientific approach focuses on C1q, the initiating molecule of a potent inflammatory pathway that when misdirected can lead to tissue damage and loss. By targeting C1q, our immunotherapies are designed to stop neuroinflammatory diseases where they start. Our pipeline spans three diverse therapeutic areas – neurodegenerative, ophthalmic and autoimmune diseases – and includes investigational drug candidates designed to address the unmet needs of over 8 million people worldwide. Annexon’s mission is to deliver potentially game-changing therapies to patients so that they can live their best lives. When they thrive, we thrive. To learn more visit annexonbio.com. Forward Looking StatementsThis press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. In some cases, you can identify forward-looking statements by terminology such as “aim,” “anticipate,” “assume,” “believe,” “contemplate,” “continue,” “could,” “design,” “due,” “estimate,” “expect,” “goal,” “intend,” “may,” “objective,” “plan,” “positioned,” “potential,” “predict,” “seek,” “should,” “suggest,” “target,” “on track,” “will,” “would” and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology. All statements other than statements of historical facts contained in this press release are forward-looking statements. These forward-looking statements include, but are not limited to, the ability of ANX007 to block upstream C1q, the clinical and regulatory status of ANX007; ANX007’s distinct potential neuroprotective mechanism of action and potential to provide protection from vision loss; the potential therapeutic benefit of ANX007; Annexon’s ability to stop neuroinflammatory diseases where they start; and Annexon’s ability to deliver game-changing therapies to millions of patients. Forward-looking statements are not guarantees of future performance and are subject to risks and uncertainties that could cause actual results and events to differ materially from those anticipated, including, but not limited to, risks and uncertainties related to: the ongoing off-treatment follow-up portion of the Phase 2 ARCHER trial; the company’s history of net operating losses; the company’s ability to obtain necessary capital to fund its clinical programs; the early stages of clinical development of the company’s product candidates; the effects of public health crises on the company’s clinical programs and business operations; the company’s ability to obtain regulatory approval of and successfully commercialize its product candidates; any undesirable side effects or other properties of the company’s product candidates; the company’s reliance on third-party suppliers and manufacturers; the outcomes of any future collaboration agreements; and the company’s ability to adequately maintain intellectual property rights for its product candidates. These and other risks are described in greater detail under the section titled “Risk Factors” contained in the company’s Annual Report on Form 10-K and Quarterly Reports on Form 10-Q and the company’s other filings with the SEC. Any forward-looking statements that the company makes in this press release are made pursuant to the Private Securities Litigation Reform Act of 1995, as amended, and speak only as of the date of this press release. Except as required by law, the company undertakes no obligation to publicly update any forward-looking statements, whether as a result of new information, future events or otherwise. Investor Contact:Joyce AllaireLifeSci Advisors, LLCjallaire@lifesciadvisors.com Media Contact:Sheryl SeapyReal Chemistry949-903-4750sseapy@realchemistry.com

97% reduction in treatment burden at nine months after treatment with ABBV-RGX-314 Data consistent with that from multiple previous studies demonstrating favorable safety and efficacy profile Well tolerated with zero cases of intraocular inflammation in a setting of no prophylactic steroids Data highlight the potential of ABBV-RGX-314 to treat both eyes in wet AMD ROCKVILLE, Md., Oct. 21, 2024 /PRNewswire/ -- REGENXBIO Inc. (Nasdaq: RGNX) today announced positive data from the Phase II fellow eye sub-study evaluating the subretinal delivery of ABBV-RGX-314 in patients with bilateral wet age-related macular degeneration (wet AMD). The new data were presented at the American Academy of Ophthalmology (AAO) meeting by Arshad Khanani, M.D., M.A., FASRS, Director of Clinical Research at Sierra Eye Associates, Reno, NV. "The results presented at AAO from the Phase II sub-study, the first to evaluate a gene therapy in fellow eyes for wet AMD, demonstrate that ABBV-RGX-314 could be a treatment for patients with bilateral disease and add to the already-robust data demonstrating ABBV-RGX-314's potential to impact the treatment paradigm for patients with wet AMD," said Curran Simpson, President and Chief Executive Officer of REGENXBIO. "With more treated patients and the longest-term data of any gene therapy program for wet AMD, REGENXBIO, with our partner AbbVie, are well-positioned to bring the first gene therapy to market with the hope of preserving long-term vision for millions of patients globally with wet AMD." "The majority of our patients with wet AMD eventually have bilateral disease and face a substantial treatment burden with frequent lifelong injections in both eyes. This leads to suboptimal real-world vision outcomes with current standard of care," said Dr. Khanani. "The fellow eye dosing data with ABBV-RGX-314 is a milestone for the field of gene therapy for common retinal diseases, as this is the first time we have performed bilateral treatment for wet AMD patients. These results, combined with the durable treatment effect up to four years shown in long-term follow up, highlight the potential of ABBV-RGX-314 as a one-time effective treatment option for patients with wet AMD." Data and Safety Summary The fellow eye sub-study was designed to evaluate the safety and efficacy of a single dose (1.3x1011 GC/eye) of ABBV-RGX-314 using subretinal delivery in the fellow eye of previously treated patients. The second eye was treated with ABBV-RGX-314 approximately one year or more after administration of ABBV-RGX-314 in the first eye. This dose is being evaluated in the ongoing pivotal trials of ABBV-RGX-314 and is similar to one of the doses evaluated in the Phase I/IIa trial, which demonstrated durable treatment effect up to four years in a long-term follow up study. The fellow eye sub-study data at nine months includes nine patients who received ABBV-RGX-314 using subretinal delivery in the Phase I/IIa or bridging studies and elected to receive treatment in their second eye. Prior to ABBV-RGX-314 administration, these patients had a high treatment burden in the fellow eye and had received an average of nine anti-VEGF injections in the year prior to entering the study, including anti-VEGF injections intended to be longer-lasting treatments. At nine months post-administration of ABBV-RGX-314, key findings from the Phase II fellow eye sub-study include: 97% reduction in annualized anti-VEGF treatment burden 100% of patients required either zero or one supplemental injection 78% of patients were completely injection-free Additionally, patients demonstrated sustained best-corrected visual acuity (BCVA) and central retinal thickness (CRT) at nine months. ABBV-RGX-314 produced similar levels of aqueous protein in both treated eyes. As of September 11, 2024, ABBV-RGX-314 was well tolerated in the treated fellow eye with no drug related serious adverse events. No cases of intraocular inflammation, chorioretinitis, vasculitis, occlusion or hypotony were observed. No prophylactic steroids were used in this trial, other than those typically used in vitrectomy surgery. Common adverse events included mild retinal pigmentary changes occurring in periphery and post-operative conjunctival hemorrhage, which all resolved within days to weeks. Data presented is available on the "Publications" section of the REGENXBIO website at . About ABBV-RGX-314 ABBV-RGX-314, being developed in collaboration with AbbVie, is being investigated as a potential one-time treatment for wet AMD, diabetic retinopathy, and other chronic retinal conditions. ABBV-RGX-314 consists of the NAV® AAV8 vector, which encodes an antibody fragment designed to inhibit vascular endothelial growth factor (VEGF). ABBV-RGX-314 is believed to inhibit the VEGF pathway by which new, leaky blood vessels grow and contribute to the accumulation of fluid in the retina. REGENXBIO is advancing research in two separate routes of administration of ABBV-RGX-314 to the eye, through a standardized subretinal delivery procedure as well as delivery to the suprachoroidal space. REGENXBIO has licensed certain exclusive rights to the SCS Microinjector® from Clearside Biomedical, Inc. to deliver gene therapy treatments to the suprachoroidal space of the eye. About Wet AMD Wet AMD is characterized by loss of vision due to new, leaky blood vessel formation in the retina. Wet AMD is a significant cause of vision loss in the United States, Europe and Japan, with up to 2 million people living with wet AMD in these geographies alone. Current anti-VEGF therapies have significantly changed the landscape for treatment of wet AMD, becoming the standard of care due to their ability to prevent progression of vision loss in the majority of patients. These therapies, however, require life-long frequent, repeated intraocular injections to maintain efficacy. Due to the burden of treatment, it is difficult for patients to adhere to frequent injections, which can lead to a decline in vision over time. ABOUT REGENXBIO Inc. REGENXBIO is a leading clinical-stage biotechnology company seeking to improve lives through the curative potential of gene therapy. Since its founding in 2009, REGENXBIO has pioneered the development of AAV Therapeutics, an innovative class of gene therapy medicines. REGENXBIO is advancing a pipeline of AAV Therapeutics for retinal and rare diseases, including ABBV-RGX-314 for the treatment of wet AMD and diabetic retinopathy, being developed in collaboration with AbbVie, RGX-202 for the treatment of Duchenne and RGX-121 for the treatment of MPS II. Thousands of patients have been treated with REGENXBIO's AAV Therapeutic platform, including Novartis' ZOLGENSMA for children with spinal muscular atrophy. Designed to be one-time treatments, AAV Therapeutics have the potential to change the way healthcare is delivered for millions of people. For more information, please visit . FORWARD-LOOKING STATEMENTS This press release includes "forward-looking statements," within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. These statements express a belief, expectation or intention and are generally accompanied by words that convey projected future events or outcomes such as "believe," "may," "will," "estimate," "continue," "anticipate," "assume," "design," "intend," "expect," "could," "plan," "potential," "predict," "seek," "should," "would" or by variations of such words or by similar expressions. The forward-looking statements include statements relating to, among other things, REGENXBIO's future operations and clinical trials. REGENXBIO has based these forward-looking statements on its current expectations and assumptions and analyses made by REGENXBIO in light of its experience and its perception of historical trends, current conditions and expected future developments, as well as other factors REGENXBIO believes are appropriate under the circumstances. However, whether actual results and developments will conform with REGENXBIO's expectations and predictions is subject to a number of risks and uncertainties, including the timing of enrollment, commencement and completion and the success of clinical trials conducted by REGENXBIO, its licensees and its partners, the timing of commencement and completion and the success of preclinical studies conducted by REGENXBIO and its development partners, the timely development and launch of new products, the ability to obtain and maintain regulatory approval of product candidates, the ability to obtain and maintain intellectual property protection for product candidates and technology, trends and challenges in the business and markets in which REGENXBIO operates, the size and growth of potential markets for product candidates and the ability to serve those markets, the rate and degree of acceptance of product candidates, and other factors, many of which are beyond the control of REGENXBIO. Refer to the "Risk Factors" and "Management's Discussion and Analysis of Financial Condition and Results of Operations" sections of REGENXBIO's Annual Report on Form 10-K for the year ended December 31, 2023, and comparable "risk factors" sections of REGENXBIO's Quarterly Reports on Form 10-Q and other filings, which have been filed with the U.S. Securities and Exchange Commission (SEC) and are available on the SEC's website at . All of the forward-looking statements made in this press release are expressly qualified by the cautionary statements contained or referred to herein. The actual results or developments anticipated may not be realized or, even if substantially realized, they may not have the expected consequences to or effects on REGENXBIO or its businesses or operations. Such statements are not guarantees of future performance and actual results or developments may differ materially from those projected in the forward-looking statements. Readers are cautioned not to rely too heavily on the forward-looking statements contained in this press release. These forward-looking statements speak only as of the date of this press release. Except as required by law, REGENXBIO does not undertake any obligation, and specifically declines any obligation, to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise. Zolgensma® is a registered trademark of Novartis Gene Therapies. SCS Microinjector® is a trademark of Clearside Biomedical, Inc. All other trademarks referenced herein are registered trademarks of REGENXBIO. CONTACT: Dana Cormack Corporate Communications [email protected] George E. MacDougall Investor Relations [email protected] SOURCE REGENXBIO Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED