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

Investors are optimistic on the American Biotechs industry, and appear confident in long term growth rates. The 3-year average PS ratio of 6.9x is lower than the industry's current PS ratio of 7.6x.

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
Thu, 18 Jun 2026	US$1.3t	US$170.0b	-US$12,153,726,792.88	16.4x	-106.1x	7.6x
Sat, 16 May 2026	US$1.3t	US$171.4b	-US$12,310,644,857.95	17.4x	-106.5x	7.7x
Mon, 13 Apr 2026	US$1.3t	US$166.2b	-US$11,968,946,358.80	17.5x	-107.7x	7.8x
Wed, 11 Mar 2026	US$1.3t	US$169.1b	-US$15,388,798,482.88	21.5x	-86.5x	7.9x
Fri, 06 Feb 2026	US$1.3t	US$164.4b	-US$14,752,166,736.35	19.7x	-86.5x	7.8x
Sun, 04 Jan 2026	US$1.2t	US$163.5b	-US$15,345,571,210.77	21.1x	-79x	7.4x
Tue, 02 Dec 2025	US$1.2t	US$163.6b	-US$16,204,397,732.22	18.7x	-77.1x	7.6x
Thu, 30 Oct 2025	US$1.2t	US$164.0b	-US$17,953,607,163.74	17.4x	-65.9x	7.2x
Sat, 27 Sep 2025	US$1.1t	US$163.5b	-US$18,316,421,423.95	16.3x	-58.1x	6.5x
Mon, 25 Aug 2025	US$1.1t	US$163.6b	-US$18,584,724,159.63	15.1x	-57.8x	6.6x
Wed, 23 Jul 2025	US$961.0b	US$155.2b	-US$23,253,955,254.01	16.5x	-41.3x	6.2x
Fri, 20 Jun 2025	US$929.9b	US$155.9b	-US$23,930,083,012.02	16.9x	-38.9x	6x
Sun, 18 May 2025	US$895.3b	US$155.9b	-US$24,392,718,921.60	16.3x	-36.7x	5.7x
Tue, 15 Apr 2025	US$740.5b	US$119.2b	-US$36,459,397,381.90	19.9x	-20.3x	6.2x
Thu, 13 Mar 2025	US$834.6b	US$118.7b	-US$37,659,545,163.68	18.4x	-22.2x	7x
Sat, 08 Feb 2025	US$857.1b	US$117.3b	-US$30,948,989,158.04	17.2x	-27.7x	7.3x
Mon, 06 Jan 2025	US$980.2b	US$149.6b	-US$26,354,792,434.12	17x	-37.2x	6.6x
Wed, 04 Dec 2024	US$1.0t	US$149.9b	-US$26,584,927,055.40	16.5x	-39.1x	6.9x
Fri, 01 Nov 2024	US$1.1t	US$147.3b	-US$30,454,139,694.27	17.1x	-34.7x	7.2x
Sun, 29 Sep 2024	US$893.6b	US$113.2b	-US$36,006,680,210.71	21.3x	-24.8x	7.9x
Tue, 27 Aug 2024	US$909.0b	US$113.1b	-US$35,851,266,005.46	23.3x	-25.4x	8x
Thu, 25 Jul 2024	US$1.2t	US$164.5b	-US$28,090,976,401.93	28.2x	-43x	7.3x
Sat, 22 Jun 2024	US$1.1t	US$164.4b	-US$27,943,646,272.00	28.1x	-41.1x	7x
Mon, 20 May 2024	US$1.1t	US$164.6b	-US$26,835,738,666.64	23.9x	-42.8x	7x
Wed, 17 Apr 2024	US$1.1t	US$164.2b	-US$23,402,696,044.05	20.5x	-46.3x	6.6x
Fri, 15 Mar 2024	US$1.2t	US$167.4b	-US$22,100,849,384.54	16.3x	-54.1x	7.1x
Sun, 11 Feb 2024	US$1.2t	US$169.3b	-US$26,263,046,791.87	19.8x	-44.2x	6.9x
Tue, 09 Jan 2024	US$1.4t	US$204.8b	-US$22,499,844,981.00	20.8x	-63.1x	6.9x
Thu, 07 Dec 2023	US$1.3t	US$204.6b	-US$22,056,080,007.00	19.4x	-58.1x	6.3x
Sat, 04 Nov 2023	US$1.2t	US$206.7b	-US$20,531,174,316.00	18.8x	-60.4x	6x
Mon, 02 Oct 2023	US$1.3t	US$207.4b	-US$13,122,605,528.00	17.1x	-95.8x	6.1x
Wed, 30 Aug 2023	US$1.3t	US$207.6b	-US$12,432,896,963.00	17.8x	-103.8x	6.2x
Fri, 28 Jul 2023	US$1.1t	US$186.8b	-US$16,232,166,533.00	14.3x	-69.6x	6x
Sun, 25 Jun 2023	US$1.1t	US$186.2b	-US$16,162,116,001.00	13.6x	-70.3x	6.1x


US Market	1.98%
Healthcare	-0.71%
Biotech	4.63%
Biotech	4.63%

Company	Last Price	7D	1Y	Valuation
MRNA Moderna	US$61.80	34.4% +US$6.3b	143.3%	PS11x
VRTX Vertex Pharmaceuticals	US$458.99	5.3% +US$5.9b	2.4%	PE26.9x
GILD Gilead Sciences	US$125.45	3.3% +US$4.9b	16.2%	PE16.9x
RVMD Revolution Medicines	US$157.77	9.4% +US$2.9b	295.1%	PB22.4x
AMGN Amgen	US$341.66	1.2% +US$2.1b	18.0%	PE23.6x

Announcement • 16h

Neurocrine Biosciences, Inc. Presents First Retrospective Case Series Of CRENESSITY (Crinecerfont) In Patients With Classic Congenital Adrenal Hyperplasia Due To 11B-Hydroxylase Deficiency At ENDO 2026

Neurocrine Biosciences, Inc. announced clinical findings from the first retrospective case series in pediatric and adult patients with classic congenital adrenal hyperplasia (CAH) due to 11ß-hydroxylase deficiency. This subtype was not previously studied in clinical trials of CRENESSITY (crinecerfont) and is the second most common form of classic CAH after 21-hydroxylase deficiency, accounting for approximately 5% of cases. Androstenedione and other adrenal hormone levels in 11ß-hydroxylase-deficient patients improved substantially after initiation of CRENESSITY, with greater than 90% median reductions in 11-deoxycortisol and 11-deoxycorticosterone. Nearly all patients (14/15) reduced their total glucocorticoid dose with CRENESSITY, and 2 of 5 patients on antihypertensive medications reduced or discontinued these drugs. Reductions in androstenedione (A4) were observed across all patients with elevated baseline levels following initiation of CRENESSITY. Steroid precursors also decreased, with values reaching within normal ranges, and blood pressure improved in adult patients. This retrospective case series outlines clinical responses to CRENESSITY treatment in 15 pediatric (n=11) and adult (n=4) patients with classic CAH due to 11ß-OHD. Across all patients with elevated A4 and/or adrenal steroid precursors at baseline, initiation of CRENESSITY was associated with reduction of levels. A4 and precursor normalization were observed as early as one month following treatment initiation, including in patients whose hormone excess had persisted despite prior supraphysiologic glucocorticoid (GC) therapy. Among patients with elevated hormones at baseline, median decreases of -92% (DOC, n=5), -95% (11-dF, n=7), and -65% (A4, n=3) were observed after CRENESSITY initiation. Among patients receiving antihypertensive treatment, two of five were able to reduce or discontinue these medications. Following the initiation of CRENESSITY, 14 of 15 patients were able to reduce their total GC dose. This case series provides early, foundational evidence supporting the efficacy and safety of CRENESSITY treatment in patients with classic CAH due to 11ß-OHD. Although CRENESSITY is approved as an adjunctive treatment to GCs for patients with classic CAH regardless of enzyme deficiency, there is limited evidence on its use in this rare subtype. These findings support further exploration of CRENESSITY in this classic CAH subtype. Presentations at the ENDO 2026 annual meeting included: CAHtalyst Adult Study Two-Year Results, CAHtalyst Pediatric Study Two-Year Results, and additional presentations on long-term risk of cardiometabolic comorbidities, crinecerfont treatment of classic congenital adrenal hyperplasia due to 11ß-hydroxylase deficiency, and a modified Delphi panel of U.S. endocrinologists. CRENESSITY is a potent and selective oral corticotropin-releasing factor type 1 receptor (CRF1) antagonist that reduces and controls excess adrenocorticotropic hormone (ACTH) and adrenal androgens through a non-glucocorticoid (GC) mechanism for the treatment of classic congenital adrenal hyperplasia (CAH). Antagonism of CRF1 receptors in the pituitary has been shown to decrease ACTH levels, which in turn decreases the production of adrenal androgens and potentially the symptoms associated with CAH. The robust clinical study data demonstrate that lowering adrenal androgen levels with CRENESSITY enables lower, more physiologic dosing of GCs to replace missing cortisol. CRENESSITY comes in capsules and an oral solution. For adults 18 years of age and older, the recommended dosage is 100 mg twice daily taken orally with a meal. For pediatric patients four to 17 years of age weighing less than 55 kg (121 lbs), the recommended dosage is based on body weight and is administered twice daily, taken orally with a meal. For pediatric patients weighing more than 55 kg (121 lbs), the recommended dosage is 100 mg twice daily taken orally with a meal. Healthcare providers can work with patients to determine the appropriate formulation for use depending on patient needs. Patients receiving CRENESSITY should continue GC therapy for cortisol replacement. CRENESSITY is available in 50 mg and 100 mg capsules, and as an oral solution of 50 mg/mL. CRENESSITY is a prescription medicine used together with glucocorticoids (steroids) to control androgen (testosterone-like hormone) levels in adults and children 4 years of age and older with classic congenital adrenal hyperplasia (CAH). CRENESSITY may cause serious side effects, including allergic reactions and risk of sudden adrenal insufficiency or adrenal crisis with too little glucocorticoid (steroid) medicine. The most common side effects of CRENESSITY in adults include tiredness, headache, dizziness, joint pain, back pain, decreased appetite, and muscle pain. The most common side effects of CRENESSITY in children include headache, stomach pain, tiredness, nasal congestion, and nosebleeds.

Announcement • 22h

Elicio Therapeutics Reports Multiple Complete Responses After ELI-002 7P Treatment And Subsequent Therapy With Checkpoint Inhibition In Metastatic MKRAS Pancreatic Cancer

Elicio Therapeutics, Inc. reported preliminary clinical observations which the Company believes support the evaluation of ELI-002 7P in combination with checkpoint inhibition. Three patients who received ELI-002 7P during Elicio’s recently completed Phase 2 AMPLIFY-7P study experienced disease progression after treatment and subsequently achieved confirmed complete radiographic and complete metabolic responses after receiving nivolumab-based therapy with concurrent normalization of tumor biomarker CA19-9 levels. Two of the three patients maintained complete responses for at least eight months, with one ongoing complete response at >13 months. In addition, all three patients demonstrated persistent mKRAS-specific T cell responses. These observations provide preliminary clinical support for the hypothesis that ELI-002 7P-induced immune responses may enhance sensitivity to checkpoint inhibition and support prospective evaluation of ELI-002 7P and anti–PD-1 combination strategies. These observations represent the first three patients identified following recurrence after treatment with ELI-002 7P during the Phase 2 AMPLIFY-7P study and subsequent gemcitabine/nab-paclitaxel chemotherapy and nivolumab. Elicio intends to continue monitoring additional patients who participated in the AMPLIFY-7P study and are currently following a similar course of treatment. All three patients were microsatellite stable (MSS) /mismatch repair proficient (MMR-p), a population that has historically demonstrated limited responsiveness to immune checkpoint inhibitors. Published studies evaluating chemotherapy-, checkpoint inhibitor-, or RAS inhibitor-based regimens in metastatic pancreatic cancer have reported complete response rates of approximately 0% to 8%, with durable complete responses rarely observed. Elicio intends to initiate a Phase 1 study in metastatic pancreatic ductal adenocarcinoma designed to provide a rapid assessment of clinical activity through a focused, confirmatory study, subject to funding. Elicio plans to use the study findings to further evaluate checkpoint inhibitor combinations and help inform future development strategies in metastatic PDAC and the adjuvant PDAC Phase 3 trial. Elicio is hosting a virtual key opinion leader event on Wednesday, June 24, 2026, at 1:00 PM ET, to further discuss these observations. Elicio’s lead product candidate, ELI-002, is a structurally novel investigational AMP cancer immunotherapy that targets cancers that are driven by mutations in the KRAS-gene—a prevalent driver of many human cancers. ELI-002 is comprised of two powerful components that are built with Elicio’s proprietary AMP technology consisting of AMP-modified mutant KRAS peptide antigens and ELI-004, an AMP-modified CpG oligodeoxynucleotide adjuvant that is available as an off-the-shelf subcutaneous administration. ELI-002 7P (7-peptide formulation) was evaluated in the randomized Phase 2 AMPLIFY-7P trial in patients with mKRAS-driven pancreatic cancer (NCT05726864). The Phase 2 AMPLIFY-7P trial included patients with mKRAS-positive pancreatic cancer who completed standard therapy but remain at high risk of relapse. Based on topline results and post-hoc analyses, Elicio has refined its Phase 3 development strategy to focus on patients with lower residual disease burden and extended treatment duration. Elicio intends to initiate a Phase 1 study in metastatic PDAC designed to provide a rapid assessment of clinical activity through a focused, confirmatory study, subject to funding. Elicio plans to use the study findings to further evaluate checkpoint inhibitor combinations and help inform future development strategies in metastatic PDAC and the adjuvant PDAC Phase 3 trial. At the time of the Phase 2 AMPLIFY-7P analysis, data for overall survival remained immature. The ELI-002 7P formulation is designed to provide immune response coverage against seven of the most common KRAS mutations present in 25% of all solid tumors, thereby increasing the potential patient population for ELI-002. Elicio’s proprietary AMP platform delivers investigational immunotherapy directly to the “brain center” of the immune system – the lymph nodes. Elicio believes this site-specific delivery of disease-specific antigens, adjuvants and other immunomodulators may efficiently educate, activate and amplify critical immune cells, potentially resulting in induction and persistence of potent adaptive immunity required to treat many diseases. In pre-clinical models, Elicio observed lymph node-specific engagement driving therapeutic immune responses of increased magnitude, function and durability. Elicio’s AMP platform, originally developed at the Massachusetts Institute of Technology, has broad potential in the cancer space to advance a number of development initiatives through internal activities, in-licensing arrangements or development collaborations and partnerships. The AMP platform has been shown to deliver immunotherapy directly to the lymph nodes by latching on to the protein albumin, found in the local injection site, as it travels to lymphatic tissue. ELI-002 also has been studied in patients with mKRAS-positive colorectal cancer in Phase 1 studies. In the future, Elicio plans to expand ELI-002 7P to other indications, including mKRAS positive lung cancer and other mKRAS positive cancers. Elicio’s pipeline includes additional off-the-shelf therapeutic cancer immunotherapy candidates, including ELI-007 and ELI-008, that target BRAF-driven cancers and p53 hotspot mutations, respectively.

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