Has the U.S. Biotech Industry valuation changed over the past few years?

Investors are relatively neutral on the American Biotechs industry at the moment, indicating that they anticipate long term growth rates to remain steady. The industry is trading close to its 3-year average PS ratio of 6.9x.

Which industries have driven the changes within the U.S. Healthcare industry?

There are no additional sub-industries under this industry.

U.S. Biotech Industry Analysis

Date	Market Cap	Revenue	Earnings	PE	Absolute PE	PS
Fri, 12 Jun 2026	US$1.2t	US$170.0b	-US$12,156,213,059.82	16.5x	-102.2x	7.3x
Sun, 10 May 2026	US$1.3t	US$170.4b	-US$11,735,587,251.14	17.7x	-110.3x	7.6x
Tue, 07 Apr 2026	US$1.3t	US$166.1b	-US$11,844,065,571.08	16.2x	-108.8x	7.8x
Thu, 05 Mar 2026	US$1.3t	US$169.6b	-US$13,987,007,729.05	21.6x	-94.4x	7.8x
Sat, 31 Jan 2026	US$1.3t	US$163.5b	-US$15,009,663,548.11	20.3x	-84.3x	7.7x
Mon, 29 Dec 2025	US$1.2t	US$163.6b	-US$15,776,614,106.35	22x	-78.8x	7.6x
Wed, 26 Nov 2025	US$1.2t	US$163.3b	-US$16,349,343,940.48	18.8x	-74.6x	7.5x
Fri, 24 Oct 2025	US$1.2t	US$163.4b	-US$18,379,211,811.07	17x	-63.3x	7.1x
Sun, 21 Sep 2025	US$1.1t	US$163.5b	-US$18,307,901,758.97	16.3x	-59.2x	6.6x
Tue, 19 Aug 2025	US$1.1t	US$163.6b	-US$18,805,727,983.06	15.6x	-57.2x	6.6x
Thu, 17 Jul 2025	US$964.8b	US$155.8b	-US$23,409,909,784.69	17.2x	-41.2x	6.2x
Sat, 14 Jun 2025	US$958.5b	US$155.9b	-US$23,959,805,126.31	16.3x	-40x	6.1x
Mon, 12 May 2025	US$861.1b	US$154.9b	-US$24,538,327,634.73	16.7x	-35.1x	5.6x
Wed, 09 Apr 2025	US$728.1b	US$118.6b	-US$36,894,652,377.23	19.3x	-19.7x	6.1x
Fri, 07 Mar 2025	US$848.3b	US$119.0b	-US$37,227,382,606.31	16.9x	-22.8x	7.1x
Sun, 02 Feb 2025	US$1.0t	US$149.5b	-US$26,306,804,829.57	17.2x	-38.1x	6.7x
Tue, 31 Dec 2024	US$977.8b	US$149.6b	-US$26,368,249,096.05	16.9x	-37.1x	6.5x
Thu, 28 Nov 2024	US$1.0t	US$150.0b	-US$26,605,248,182.60	16.6x	-38.7x	6.9x
Sat, 26 Oct 2024	US$886.8b	US$113.1b	-US$36,035,376,152.30	20.6x	-24.6x	7.8x
Mon, 23 Sep 2024	US$920.0b	US$113.2b	-US$35,983,947,157.41	21.9x	-25.6x	8.1x
Wed, 21 Aug 2024	US$905.2b	US$113.2b	-US$35,832,221,284.65	22.9x	-25.3x	8x
Fri, 19 Jul 2024	US$1.2t	US$164.5b	-US$28,050,002,699.28	29x	-43.2x	7.4x
Sun, 16 Jun 2024	US$1.2t	US$164.4b	-US$28,071,754,707.37	27.3x	-41.2x	7x
Tue, 14 May 2024	US$1.1t	US$164.7b	-US$26,999,224,352.94	23.2x	-41.7x	6.8x
Thu, 11 Apr 2024	US$1.1t	US$164.3b	-US$23,371,324,513.62	21.4x	-48.7x	6.9x
Sat, 09 Mar 2024	US$1.2t	US$167.3b	-US$22,121,973,439.03	19x	-54x	7.1x
Mon, 05 Feb 2024	US$1.4t	US$203.9b	-US$24,425,425,728.00	19.2x	-58.9x	7.1x
Wed, 03 Jan 2024	US$1.4t	US$204.8b	-US$22,201,360,571.00	21x	-63.9x	6.9x
Fri, 01 Dec 2023	US$1.2t	US$204.7b	-US$22,039,871,274.00	18.5x	-56x	6x
Sun, 29 Oct 2023	US$1.2t	US$206.6b	-US$15,166,070,486.00	16.3x	-77.7x	5.7x
Tue, 26 Sep 2023	US$1.3t	US$207.4b	-US$12,899,236,949.00	17x	-97.7x	6.1x
Thu, 24 Aug 2023	US$1.3t	US$207.6b	-US$12,449,828,498.00	17.5x	-103.1x	6.2x
Sat, 22 Jul 2023	US$1.2t	US$186.5b	-US$16,009,709,300.00	12.8x	-72x	6.2x
Mon, 19 Jun 2023	US$1.2t	US$186.3b	-US$16,034,836,469.00	12.1x	-72.3x	6.2x


US Market	-2.36%
Healthcare	0.99%
Biotech	-0.93%
Biotech	-0.93%

Company	Last Price	7D	1Y	Valuation
AMGN Amgen	US$354.06	2.4% +US$4.6b	19.1%	PE24.5x
NUVL Nuvalent	US$123.45	31.3% +US$2.3b	58.5%	PB8.3x
INCY Incyte	US$107.83	6.5% +US$1.3b	55.8%	PE15x
TNGX Tango Therapeutics	US$29.82	34.6% +US$1.1b	490.5%	PS75.7x
TGTX TG Therapeutics	US$48.05	18.5% +US$1.1b	28.6%	PE14.7x

Announcement • Jun 09

Kymera Therapeutics Presents New Preclinical Data for Kt-579, Oral Irf5 Degrader, At Eular and Focis Congresses

Kymera Therapeutics, Inc. presented new preclinical data for KT-579, its potent, selective, oral IRF5 degrader, demonstrating disease-modifying activity in lupus models. KT-579 demonstrated consistent disease-modifying activity comparable or superior to approved and clinically active therapies in multiple preclinical lupus models. The findings show that by selectively targeting and degrading IRF5, KT-579 offers a novel oral approach for complex, heterogeneous autoimmune diseases driven by multiple validated inflammatory pathways, including Type I interferons, pro-inflammatory cytokines and autoantibody responses. These data were presented at the European Alliance of Associations for Rheumatology (EULAR) Annual Meeting held June 3-6, 2026, in London, UK, and will be presented at the Federation of Clinical Immunology Societies (FOCIS) Annual Meeting being held June 9-12, 2026, in San Francisco, CA. The Company previously reported data demonstrating KT-579’s compelling profile in preclinical studies using human primary cell systems, patient-derived cells and in vivo disease models of lupus, rheumatoid arthritis, and inflammatory bowel disease showing activity comparable or superior to existing standards of care. New data presented at EULAR and FOCIS further validate KT-579’s broad and consistent activity across preclinical models of lupus. In healthy donor and lupus patient-derived human cells, with or without a common SLE-associated polymorphism, KT-579 selectively degraded IRF5, blocked TLR-induced IRF5 nuclear translocation, and reduced key downstream inflammatory mediators, including Type I IFN and pro-inflammatory cytokines, as well as plasmablast differentiation and IgG production. In vivo, KT-579 demonstrated dose-dependent IRF5 degradation and inhibition of TLR7- and TLR9-induced cytokine release, including TNFa, IL-6, IL-12 and IFNß. Across multiple lupus models spanning low to high Type I IFN signaling, KT-579 treatment led to reductions in disease-relevant biomarkers, including proteinuria, serum autoantibodies and kidney pathology, with activity comparable or superior to approved and clinically active agents tested. Together, these findings demonstrate consistent modulation of pro-inflammatory, Type I IFN and B cell-driven pathways, supporting KT-579’s potential as a first-in-class, oral approach in lupus and other chronic autoimmune diseases. The KT-579 Phase 1 healthy volunteer trial is ongoing. The Phase 1 study is evaluating the safety, tolerability, pharmacokinetics and pharmacodynamics of single- and multiple-ascending doses of orally administered KT-579 compared to placebo. The key study aim is to show that KT-579 can robustly degrade IRF5 in blood at doses that are safe and well tolerated. The functional impact of IRF5 degradation on the induction of Type I interferons, pro-inflammatory cytokines, and inflammatory pathway gene transcripts will also be assessed with whole blood ex vivo stimulation assays. The Company expects to report data from the trial in the second half of 2026 and, following the healthy volunteer study, plans to initiate a patient proof-of-concept trial, likely in lupus. European Alliance of Associations for Rheumatology (EULAR) Title: First-in-class Oral IRF5 Degrader, KT-579, Demonstrates Selective and Potent In Vitro and In Vivo Activity in Human Cellular Assays and Mouse Models of Lupus Type/Session: Poster, Poster View VIII Date/Time: Saturday, June 6, 2026, at 10:15 AM BST Federation of Clinical Immunology Societies (FOCIS) Title: Potent and Selective First-in-Class Oral IRF5 Degrader, KT-579, Inhibits Endosomal TLR-Induced Responses in SLE Derived PBMCs and Significantly Reduces Disease Activity in the MRL.lpr Mouse Lupus Model Type/Session: Poster, Autoimmune Diseases Date/Time: Thursday, June 11, 2026, at 7:00 PM PT Copies of the EULAR and FOCIS posters will be available in the Resource Library section of Kymera's website. KT-579 is an investigational, first-in-class, oral degrader of IRF5, a genetically validated transcription factor and master regulator of immunity, and currently in Phase 1 testing. By selectively degrading IRF5, KT-579 is designed to modulate multiple disease-driving pathways simultaneously, including Type I interferons, pro-inflammatory cytokines and autoantibody responses, offering the potential for biologics-like activity in a convenient oral medicine. In preclinical studies, KT-579 degraded IRF5 across multiple preclinical species and in all disease-relevant tissues. In preclinical models of lupus, rheumatoid arthritis (RA), and inflammatory bowel disease (IBD), KT-579 activity was equal to or more efficacious than small molecule inhibitors and biologics currently marketed or in the clinic. In preclinical safety studies, KT-579 did not show any adverse effects of any type at all doses tested. KT-579 has the potential to be the first novel mechanism with broad utility in diseases where effective and well tolerated oral therapies are needed, such as lupus, IBD, RA, Sjögren's and others.

Announcement • Jun 06

Vertex Pharmaceuticals Incorporated Presents New Data On ALYFTREK And TRIKAFTA At European Cystic Fibrosis Conference

Vertex Pharmaceuticals Incorporated announced data demonstrating the potentially transformative impact of treating cystic fibrosis (CF) with ALYFTREK (vanzacaftor/tezacaftor/deutivacaftor) in children ages 2 to 5, as well as data from 96-week interim analyses of two open-label extension studies of ALYFTREK in children 6 to 11 years and people 12 years and older demonstrating the long-term safety and efficacy profile of the medicine. The data, presented at the European Cystic Fibrosis Conference, show children ages 2 to 5 with vanzacaftor/tezacaftor/deutivacaftor-responsive genotypes including those who are homozygous for the F508del mutation (F/F) and those who have F508del/minimal function mutations (F/MF)on ALYFTREK had further improvement in CFTR function from a TRIKAFTA baseline as measured by sweat chloride (SwCl), with 65% having achieved SwCl <30 mmol/L after treatment with ALYFTREK. Vertex also presented Phase 3 data of children ages 1 to <2 with TRIKAFTA (elexacaftor/tezacaftor/ivacaftor). Vertex plans to submit for global regulatory approvals of ALYFTREK in children ages 2 to 5 in the first half of 2026, and the company has begun global regulatory submissions for TRIKAFTA in children ages 1 to <2. “A Phase 3 open-label clinical trial of vanzacaftor/tezacaftor/deutivacaftor in children aged 2-5 years with cystic fibrosis”was presented as a late-breaking abstract and oral presentation in the “Late-Breaking Science” session on June 5 from 5:00 p.m. to 6:30 p.m. GMT+1. Data from 67 children who all completed the 24-week, Phase 3, open-label study show that ALYFTREK was generally safe and well tolerated, consistent with the established safety profile. The primary endpoint of the study was safety and tolerability. Treatment with ALYFTREK resulted in a rapid, clinically meaningful improvement in CFTR function with a mean reduction in sweat chloride from a baseline on TRIKAFTA of -9.6 mmol/L (95% CI -12.1 to -7.0) through Week 24, with 92% of children achieving SwCl concentrations of <60 mmol/L (the diagnostic threshold for CF), and 65% of children reaching SwCl values of <30 mmol/L. These improvements in CFTR function surpass those seen in trials with any other CFTR modulator in this age group. Vertex also presented multiple abstracts on clinical and real-world evidence on ALYFTREK and TRIKAFTA as listed below. These abstracts will be published in the Journal of Cystic Fibrosis: “Long-term safety and efficacy of vanzacaftor/tezacaftor/deutivacaftor in people with cystic fibrosis aged 12 years and older: 96-week interim analysis from an open-label extension study.” (Poster 143) “Long-term safety and efficacy of vanzacaftor/tezacaftor/deutivacaftor in children with cystic fibrosis aged 6 years and older: 96-week interim analysis from an open-label extension study”; also presented as an oral presentation (WS01.3) during the symposium “Clinical and functional impact of highly effective modulators” on June 4 from 3:00–4:30 p.m. GMT+1. “Demographic and clinical characteristics of children with CF aged 2-5 years initiating ELX/TEZ/IVA in LONGITUDE — a UK CF Registry observational study.” (Poster P432). “A Phase 3, 24-Week, Open-Label Study of Elexacaftor/Tezacaftor/Ivacaftor in Children with Cystic Fibrosis 12 to <24 Months of Age” (WS01.2)was featured in an oral presentation as part of the symposium “Clinical and functional impact of highly effective modulators” on June 4 from 3:00–4:30 p.m. GMT+1 and the abstract will be published in the Journal of Cystic Fibrosis:. Results from a 24-week, Phase 3, open-label study of TRIKAFTA in 54 enrolled children aged 12 to <24 months was presented. The primary endpoint was safety and tolerability. TRIKAFTA was generally safe and well tolerated; the safety data are consistent with the established safety profile. Treatment with TRIKAFTA in this age group resulted in rapid, statistically significant and clinically meaningful decrease in SwCl, with a mean reduction of -71.8 mmol/L from a baseline without CFTR modulator treatment through Week 24, with 98.0% of children achieving concentrations <60 mmol/L and 68.6% reaching <30 mmol/L. The uses of ALYFTREK in children with CF 2 to 5 years old, and TRIKAFTA in children with CF 1 to <2 years old, are investigational.

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