AHR AGONISTS Field The present disclosure relates to novel AHR agonist compounds, to pharmaceutical compositions comprising the compounds, and to methods of using the compounds to treat certain immune-mediated diseases. Background The present disclosure is in the field of treatment of certain immune-mediated diseases (IMD), in particular psoriasis and atopic dermatitis, via the activation of the aryl hydrocarbon receptor (AHR). IMDs encompass a broad range of chronic and debilitating inflammatory conditions that affect approximately 4% of the population worldwide. In view of the limited efficacy of currently available treatments, and few small molecule treatment options, there is significant unmet need for alternative, potent, selective, and safer drugs for the treatment of IMDs. AHR is a transcription factor which regulates many aspects of immunological function, most notably the suppression of adaptive immune responses (Ehrlich et al., Curr. Opin. Toxicol., 2, 72-78 (2017)). Prototypical AHR agonists include halogenated dibenzodioxins, such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD), tryptophan metabolites, such as L-kynurenine, bilirubin, and PGE2. Results from studies on AHR agonists, especially TCDD, suggest that immune suppression occurs as the result of AHR-induced expression of regulatory T cells (Tregs), TH17 cells, and dendritic cells (DCs) (Rothhammer et al., Nat. Rev, Immunol., 19, 184- 197 (2019)). TCDD has been shown to be effective in the prevention of several murine models of IMD, including type-1 diabetes (Kerkvliet et al., Immunotherapy, 1, 539-547 (2009)), autoimmune encephalomyelitis (Quintana et al., Nature, 453, 65-71, (2008)), autoimmune uveoretinitis (Zhang et al., Invest. Opthalmol. Vis. Sci., 51, 2109-2117 (2010)), inflammatory bowel disease (Takamura et al., Immunol. Cell. Biol., 88, 685-689 (2010), Benson et al., Toxicol. Sci., 120, 68-78 (2011), Singh et al., PLoS One, 6(8), e23522 (2011)), as well as several models of transplant tolerance (Pauly at al., Toxicol. Environ. Chem., 94, 1175-1187 (2012)) and allergic diseases (Schulz et al., Toxicol. Sci., 123, 491-500 (2011), Li et al, PloS One, 11, e0150551 (2016), Luebke et al., Toxicol. Sci., 62, 71-79 (2001)). AHR also regulates the expression of CYP1A1, CYP1A2, and CYP1B1, which catalyze the metabolism of polycyclic aromatic hydrocarbon (PAH) and other aromatic compounds (e.g., estrogen). While in some cases (for example in the case of benzo[a]pyrene) this metabolism results in the formation of reactive species, CYP induction is also believed to be critical for the detoxification and metabolic clearance of PAHs, which reduces the probability of bioactivation, and DNA adduct formation. Several marketed drugs were found to activate AHR (thus upregulating CYP1A1, CYP1A2, and CYP1B1) after their FDA approval, yet their long-term use is not associated with dioxin-like toxicities (Ehrlich et al., Curr. Opin. Toxicol., 2, 72-78 (2017)). As such, CYP induction is no longer viewed as a barrier to the adoption of AHR agonists in therapy (Ehrlich et al., Curr. Opin. Toxicol., 2, 72-78 (2017)). WO 2008/014307 discloses certain bicyclic heteroaryl amides as inhibitors of undecaprenyl pyrophosphate synthase. EP 0059698 discloses certain heterocyclic carboxamides, compositions containing these compounds and methods of treatment with these compositions. The bacterial stilbenoid DMVT-505 (VTAMA® (tapinarof)) 1% cream, an aryl hydrocarbon receptor agonist, indicated for the topical treatment of plaque psoriasis in adults, has been approved by the U.S. Food and Drug Administration (FDA). Despite this, there remains a need for alternative novel, oral, selective, and potent AHR agonists for the treatment of IMDs. The present disclosure provides certain compounds that are agonists of AHR and potential treatment options. Detailed Description Various embodiments for AHR agonists and their treatment options are presented below. When a later embodiment refers to a previous “embodiment X”, such reference also includes references to “embodiment XA”, “embodiment XB”, and so on, unless such later embodiment cannot be properly construed as a dependent embodiment (e.g. falling outside the scope of the referenced embodiment or having improper antecedent basis). For example, when “Embodiment 18” below refers to “any of embodiments 1-17”, such reference also includes reference to “embodiment 13A” among others. Likewise, when “Embodiment 21” below refers to “embodiment 19 or 20”, such reference generally also includes reference to “embodiment 19A”, “embodiment 19B”, “embodiment 19C”, “embodiment 20A”, and “embodiment 20B”. Embodiment 1. A compound of the formula: , wherein: Z is CH ₂ , O, or NH; ring A is pyridyl or phenyl, each optionally substituted with halo; and Y is 5-membered heteroaryl fused with thiophene or fused with 5-membered or 6-membered carbocycle, wherein the 5-membered heteroaryl contains 1 or 2 N, and the 5-membered or 6-membered carbocycle is optionally substituted with halo or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, provided that the compound is not one of the following: (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetrahydro-3 - cyclopentapyrazolyl)methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(4,5,6,7-tetrahydro-1 ,2-benzisoxazol-3-yl)- methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(5,6,7,8-tetrahydro-4 H- cyclohept[d]isoxazol-3-yl)-methanone, (7-fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tet rahydro-3- cyclopentapyrazolyl)-methanone, (7-bromo-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetr ahydro-3- cyclopentapyrazolyl)-methanone, (6-Chloro-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2-benzazepin- 2-yl)methanone, (5-Chloro-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2-benzazepin- 2-yl)methanone, (1,3,4,5-Tetrahydro-2H-2-benzazepin-2-yl)-1H-thieno[2,3-c]py razol-5-ylmethanone, 1H-Benzimidazol-6-yl(7-chloro-2,3-dihydro-1,4-benzoxazepin-4 (5H)-yl)methanone, and (6-Fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)-1H-indazol- 7-ylmethanone. Embodiment 2. A compound of the formula: , wherein: Z is O or NH; ring A is pyridyl or phenyl, each optionally substituted with halo; and Y is 5-membered heteroaryl fused with thiophene or fused with 5-membered or 6-membered carbocycle, wherein the 5-membered heteroaryl contains 1 or 2 N, and the 5-membered or 6-membered carbocycle is optionally substituted with halo or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, provided that the compound is not one of the following: (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetrahydro-3 - cyclopentapyrazolyl)methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(4,5,6,7-tetrahydro-1 ,2-benzisoxazol-3-yl)- methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(5,6,7,8-tetrahydro-4 H- cyclohept[d]isoxazol-3-yl)-methanone, (7-fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tet rahydro-3- cyclopentapyrazolyl)-methanone, (7-bromo-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetr ahydro-3- cyclopentapyrazolyl)-methanone, 1H-Benzimidazol-6-yl(7-chloro-2,3-dihydro-1,4-benzoxazepin-4 (5H)-yl)methanone, and (6-Fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)-1H-indazol- 7-ylmethanone. Embodiment 3. A compound of the formula: , wherein: ring A is pyridyl or phenyl, each optionally substituted with halo; and Y is 5-membered heteroaryl fused with thiophene or fused with 5-membered or 6-membered carbocycle, wherein the 5-membered heteroaryl contains 1 or 2 N, and the 5-membered or 6-membered carbocycle is optionally substituted with halo or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, provided that the compound is not one of the following: (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetrahydro-3 - cyclopentapyrazolyl)methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(4,5,6,7-tetrahydro-1 ,2-benzisoxazol-3-yl)- methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(5,6,7,8-tetrahydro-4 H- cyclohept[d]isoxazol-3-yl)-methanone, (7-fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tet rahydro-3- cyclopentapyrazolyl)-methanone, (7-bromo-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetr ahydro-3- cyclopentapyrazolyl)-methanone, 1H-Benzimidazol-6-yl(7-chloro-2,3-dihydro-1,4-benzoxazepin-4 (5H)-yl)methanone, and (6-Fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)-1H-indazol- 7-ylmethanone. Embodiment 4. A compound of the formula: , wherein: ring A is pyridyl or phenyl, each optionally substituted with halo; and Y is 5-membered heteroaryl fused with thiophene or fused with 5-membered or 6-membered carbocycle, wherein the 5-membered heteroaryl contains 1 or 2 N, and the 5-membered or 6-membered carbocycle is optionally substituted with halo or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof. Embodiment 5. The compound of any of embodiments 1-4, wherein ring A is phenyl optionally substituted with halo, or a pharmaceutically acceptable salt thereof. Embodiment 6. The compound of any of embodiments 1-4, wherein ring A is pyridyl, or a pharmaceutically acceptable salt thereof. Embodiment 7. The compound of any preceding embodiment, wherein Y is a bicyclic heteroaryl, or a pharmaceutically acceptable salt thereof. Embodiment 8. The compound of any of embodiments 1 to 6, wherein Y is selected from: each optionally substituted with halo or cyano, or a pharmaceutically acceptable salt thereof. Embodiment 9. The compound of any of embodiments 1 to 6, wherein wherein ring B is a carbocycle, or a pharmaceutically acceptable salt thereof. Embodiment 10. The compound of embodiment 9, wherein substituted with fluoro or cyano, or a pharmaceutically acceptable salt thereof. Embodiment 11. The compound of embodiment 9, wherein pharmaceutically acceptable salt thereof. Embodiment 12. The compound of embodiment 1, wherein: Z is O or NH; ring A is phenyl optionally substituted with fluoro, or is pyridyl; and Y is , wherein ring B is a 5-membered or 6-membered carbocycle, or a pharmaceutically acceptable salt thereof. Embodiment 13. A compound selected from: ,

or a pharmaceutically acceptable salt thereof. Embodiment 13A. A compound selected from Table 1 below, or a pharmaceutically acceptable salt thereof: Table 1

Embodiment 14. A compound of the formula or a pharmaceutically acceptable salt thereof. Embodiment 15. A compound of the formula acceptable salt thereof. Embodiment 16. A compound of the formula pharmaceutically acceptable salt thereof. Embodiment 17. A compound of the formula , or a pharmaceutically acceptable salt thereof. Embodiment 18. A pharmaceutical composition, comprising a compound of any of embodiments 1-17, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients. Embodiment 19. A pharmaceutical composition, comprising a compound of formula: , wherein: Z is CH2, NH, or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C _1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C _1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients, provided that the compound is not (7-methyl-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2- benzazepin-2-yl)methanone. Embodiment 19A. A pharmaceutical composition, comprising a compound of formula: , wherein: Z is CR ¹ R ² , NR ³ , or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C _1-3 alkyl, or C _1-3 alkoxyl; Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C1-3 alkoxyl, halo, C1-3 alkyl, C1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon; and R ¹ , R ² , and R ³ are each H, C _1-3 alkyl, or C _3-4 cycloalkyl, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients, provided that the compound is not (7-Methyl-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2- benzazepin-2-yl)methanone. Embodiment 19B. The pharmaceutical composition of embodiment 19A wherein R ¹ and R ² are each H. Embodiment 19C. The pharmaceutical composition of embodiment 19A wherein R ¹ , R ² , and R ³ are each H. Embodiment 20. A pharmaceutical composition, comprising a compound of formula: , wherein: Z is NH or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C _1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C _1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients. Embodiment 20A. A pharmaceutical composition, comprising a compound of formula: , wherein: Z is NR ³ or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C1-3 alkyl, or C1-3 alkoxyl; Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C _1-3 alkoxyl, halo, C _1-3 alkyl, C _1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon; and R ³ is H, C _1-3 alkyl, or C _3-4 cycloalkyl, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients. Embodiment 20B. The pharmaceutical composition of embodiment 20A wherein R ³ is H. Embodiment 21. The pharmaceutical composition of embodiment 19 or 20, wherein the compound is not 1,3-benzodioxol-5-yl(1,2,3,5-tetrahydro-4H-1,4-benzodiazepin -4- yl)methanone, is not 1-naphthalenyl(1,2,3,5-tetrahydro-4H-1,4-benzodiazepin-4- yl)methanone, and is not 1-naphthalenyl(1,2,3,5-tetrahydro-4H-pyrido[2,3-e]-1,4-diaze pin-4- yl)methanone. Embodiment 22. The pharmaceutical composition of any of embodiments 19-21, wherein Z is O. Embodiment 23. A pharmaceutical composition, comprising a compound of formula: , wherein: ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C _1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C _1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients. Embodiment 23A. A pharmaceutical composition, comprising a compound of formula: , wherein: ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C _1-3 alkyl, or C _1-3 alkoxyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C _1-3 alkoxyl, halo, C _1-3 alkyl, C _1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients. Embodiment 24. The pharmaceutical composition of any of embodiments 19-23, wherein the aromatic unit is an aryl or a heteroaryl containing 1 or 2 N. Embodiment 25. A method of treating a disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound according to any of embodiments 1 to 17, a pharmaceutically acceptable salt thereof, or the pharmaceutical composition according to any embodiments 18 to 24. Embodiment 26. A method of treating a disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound of formula: , wherein: Z is CH2, NH, or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C _1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C _1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, provided that the compound is not (7-methyl-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2- benzazepin-2-yl)methanone. Embodiment 26A. A method of treating a disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound of formula: , wherein: Z is CR ¹ R ² , NR ³ , or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C _1-3 alkyl, or C _1-3 alkoxyl; Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C _1-3 alkoxyl, halo, C _1-3 alkyl, C _1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon; and R ¹ , R ² , and R ³ are each H, C1-3 alkyl, or C3-4 cycloalkyl, or a pharmaceutically acceptable salt thereof, provided that the compound is not (7-methyl-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2- benzazepin-2-yl)methanone. Embodiment 26B. The method of embodiment 26A wherein R ¹ and R ² are each H. Embodiment 26C. The method of embodiment 26A wherein R ¹ , R ² , and R ³ are each H. Embodiment 27. The method of embodiment 25 or 26, wherein the disease or disorder is an immune-mediated disease or disorder. Embodiment 28. A method of treating an immune-mediated disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound of formula: , wherein: Z is CH ₂ , NH, or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof. Embodiment 28A. A method of treating an immune-mediated disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound of formula: , wherein: Z is CR ¹ R ² , NR ³ , or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C1-3 alkyl, or C1-3 alkoxyl; Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C1-3 alkoxyl, halo, C1-3 alkyl, C1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon; and R ¹ , R ² , and R ³ are each H, C _1-3 alkyl, or C _3-4 cycloalkyl, or a pharmaceutically acceptable salt thereof. Embodiment 28B. The method of embodiment 28A wherein R ¹ and R ² are each H. Embodiment 28C. The method of embodiment 28A wherein R ¹ , R ² , and R ³ are each H. Embodiment 29. The method of embodiment 27 or 28, wherein the compound is not 1,3- benzodioxol-5-yl(1,2,3,5-tetrahydro-4H-1,4-benzodiazepin-4-y l)methanone, is not 1-naphthalenyl(1,2,3,5-tetrahydro-4H-1,4-benzodiazepin-4-yl) methanone, and is not 1- naphthalenyl(1,2,3,5-tetrahydro-4H-pyrido[2,3-e]-1,4-diazepi n-4-yl)methanone. Embodiment 30. The method of any of embodiments 27 to 29, wherein Z is NR ³ or O. Embodiment 30A. A method of treating an immune-mediated disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound of formula: , wherein: ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C _1-3 alkyl, or C _1-3 alkoxyl; Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C _1-3 alkoxyl, halo, C _1-3 alkyl, C _1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon; and R ³ is H, C1-3 alkyl, or C3-4 cycloalkyl, or a pharmaceutically acceptable salt thereof. Embodiment 30B. The method of embodiment 30A wherein R ³ is H. Embodiment 31. A method of treating an immune-mediated disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound of formula: , wherein: ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof. Embodiment 31A. A method of treating an immune-mediated disease or disorder in a patient in need thereof, comprising administering to the patient an effective amount of a compound of formula: , wherein: ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C _1-3 alkyl, or C _1-3 alkoxyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C _1-3 alkoxyl, halo, C _1-3 alkyl, C _1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof. Embodiment 32. The method of any of embodiments 27 to 31, wherein the aromatic unit is an aryl or a heteroaryl containing 1 or 2 N. Embodiment 33. The method of any of embodiments 27 to 32, wherein the immune- mediated disease or disorder is selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis. Embodiment 34. The method of embodiment 33, wherein the disease or disorder is psoriasis. Embodiment 35. The method of embodiment 33, wherein the disease or disorder is atopic dermatitis. Embodiment 36. The method of embodiment 33, wherein the disease or disorder is ulcerative colitis. Embodiment 37. The method of embodiment 33, wherein the disease or disorder is Crohn’s disease. Embodiment 38. The method of embodiment 33, wherein the disease or disorder is graft- versus-host disease. Embodiment 39. The method of embodiment 33, wherein the disease or disorder is rheumatoid arthritis. Embodiment 40. The method of embodiment 33, wherein the disease or disorder is multiple sclerosis. Embodiment 41. A compound according to any one of embodiments 1 to 17, or a pharmaceutically acceptable salt thereof, for use in therapy. Embodiment 42. A compound of formula: , wherein: Z is CH2, NH, or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C _1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof, for use in therapy, provided that the compound is not (7-methyl-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2- benzazepin-2-yl)methanone. Embodiment 42A. A compound of formula: , wherein: Z is CR ¹ R ² , NR ³ , or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C1-3 alkyl, or C1-3 alkoxyl; Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C1-3 alkoxyl, halo, C1-3 alkyl, C1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon; and R ¹ , R ² , and R ³ are each H, C _1-3 alkyl, or C _3-4 cycloalkyl, or a pharmaceutically acceptable salt thereof, for use in therapy, provided that the compound is not (7-Methyl-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2- benzazepin-2-yl)methanone. Embodiment 43. The compound for use of embodiment 41 or 42, wherein the use in therapy is a use in treating an immune-mediated disease or disorder. Embodiment 44. A compound of formula: , wherein: Z is CH ₂ , NH, or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof for use in treating an immune-mediated disease or disorder. Embodiment 44A. A compound of formula: , wherein: Z is CR ¹ R ² , NR ³ , or O; ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C1-3 alkyl, or C1-3 alkoxyl; Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C1-3 alkoxyl, halo, C1-3 alkyl, C1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon; and R ¹ , R ² , and R ³ are each H, C _1-3 alkyl, or C _3-4 cycloalkyl, or a pharmaceutically acceptable salt thereof for use in treating an immune-mediated disease or disorder. Embodiment 45. The compound for use of embodiment 44, wherein the compound is not 1,3-benzodioxol-5-yl(1,2,3,5-tetrahydro-4H-1,4-benzodiazepin -4-yl)methanone, is not 1-naphthalenyl(1,2,3,5-tetrahydro-4H-1,4-benzodiazepin-4-yl) methanone, and is not 1- naphthalenyl(1,2,3,5-tetrahydro-4H-pyrido[2,3-e]-1,4-diazepi n-4-yl)methanone. Embodiment 46. The compound for use of embodiment 44 or 45, wherein Z is NH or O. Embodiment 46A. The compound for use of embodiment 44 or 45, wherein Z is NR ³ or O. Embodiment 46B. The compound for use of embodiment 44 or 45, wherein Z is CH ₂ . Embodiment 47. A compound of formula: , wherein: ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo or C _1-3 alkyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with halo, C _1-3 alkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof for use in treating an immune-mediated disease or disorder. Embodiment 47A. A compound of formula: , wherein: ring A is a 6-membered aromatic group containing C or N, each optionally substituted with halo, C _1-3 alkyl, or C _1-3 alkoxyl; and Y is a bicyclic group including a 5- or 6- membered aromatic unit fused with a 5-, 6-, or 7- membered monocycle, and the bicyclic group is optionally substituted with oxo, C _1-3 alkoxyl, halo, C _1-3 alkyl, C _1-3 haloalkyl, or cyano, wherein Y attaches to the carbonyl with a sp ² carbon, or a pharmaceutically acceptable salt thereof for use in treating an immune-mediated disease or disorder. Embodiment 48. The compound for use of any of embodiments 44 to 47, wherein the aromatic unit is an aryl or a heteroaryl containing 1 or 2 N. Embodiment 49. The compound for use of any of embodiments 43 to 48, wherein the immune-mediated disease or disorder is selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis. Embodiment 50. The compound for use of embodiment 49, wherein the immune-mediated disease or disorder is psoriasis. Embodiment 51. The compound for use of embodiment 49, wherein the immune-mediated disease or disorder is atopic dermatitis. Embodiment 52. The compound for use of embodiment 49, wherein the immune-mediated disease or disorder is ulcerative colitis. Embodiment 53. The compound for use of embodiment 49, wherein the immune-mediated disease or disorder is Crohn’s disease. Embodiment 54. The compound for use of embodiment 49, wherein the immune-mediated disease or disorder is graft-versus-host disease. Embodiment 55. The compound for use of embodiment 49, wherein the immune-mediated disease or disorder is rheumatoid arthritis. Embodiment 56. The compound for use of embodiment 49, wherein the immune-mediated disease or disorder is multiple sclerosis. Embodiment 57. A compound for use in treating an immune-mediated disease or disorder, the compound being selected from: (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetrahydro-3 - cyclopentapyrazolyl)methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(4,5,6,7-tetrahydro-1 ,2-benzisoxazol-3-yl)- methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(5,6,7,8-tetrahydro-4 H-cyclohept[d]isoxazol-3- yl)-methanone, (7-fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tet rahydro-3- cyclopentapyrazolyl)-methanone, (7-bromo-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6-tetr ahydro-3- cyclopentapyrazolyl)-methanone, (6-Chloro-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2-benzazepin- 2-yl)methanone, (5-Chloro-1H-indol-2-yl)(1,3,4,5-tetrahydro-2H-2-benzazepin- 2-yl)methanone, (1,3,4,5-Tetrahydro-2H-2-benzazepin-2-yl)-1H-thieno[2,3-c]py razol-5-ylmethanone, 1H-Benzimidazol-6-yl(7-chloro-2,3-dihydro-1,4-benzoxazepin-4 (5H)-yl)methanone, and (6-Fluoro-2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)-1H-indazol- 7-ylmethanone. Embodiment 1’. A compound of the formula: , wherein: Z is CH2, O, or NH; ring A is pyridyl or phenyl, each optionally substituted with halo; and Y is 5-membered heteroaryl fused with thiophene or fused with 5-membered or 6- membered carbocycle, wherein the 5-membered heteroaryl contains 1 or 2 N, and the 5-membered or 6-membered carbocycle is optionally substituted with halo or cyano, or a pharmaceutically acceptable salt thereof. Embodiment 2’. The compound of embodiment 1A, wherein ring A is phenyl optionally substituted with halo, or a pharmaceutically acceptable salt thereof. Embodiment 3’. The compound of embodiment 1A, wherein ring A is pyridyl, or a pharmaceutically acceptable salt thereof. Embodiment 4’. The compound of any preceding embodiments 1A-3A, wherein Z is O or NH, or a pharmaceutically acceptable salt thereof. Embodiment 5’. The compound of any preceding embodiments 1A-4A, wherein Z is O, or a pharmaceutically acceptable salt thereof. Embodiment 6’. The compound of any of embodiments 1A-4A, wherein Z is NH, or a pharmaceutically acceptable salt thereof. Embodiment 7’. The compound of any preceding embodiments 1A-6A, wherein Y is a bicyclic heteroaryl, or a pharmaceutically acceptable salt thereof. Embodiment 8’. The compound of any of embodiments 1A-6A, wherein Y is selected from the group consisting of: each optionally substituted with halo or cyano, or a pharmaceutically acceptable salt thereof. Embodiment 9’. The compound of any of embodiments 1A-6A, wherein Y wherein ring B is a carbocycle, or a pharmaceutically acceptable salt thereof. Embodiment 10’. The compound of embodiment 9A, wherein Y is optionally substituted with fluoro or cyano, or a pharmaceutically acceptable salt thereof. Embodiment 11’. The compound of embodiment 9A, wherein pharmaceutically acceptable salt thereof. Embodiment 12’. The compound of embodiment 1A, wherein: Z is O or NH; ring A is phenyl optionally substituted with fluoro, or pyridyl; and wherein ring B is a 5-membered or 6-membered carbocycle, or a pharmaceutically acceptable salt thereof. Embodiment 13’. A compound selected from the group consisting of: ,

or a pharmaceutically acceptable salt thereof. Embodiment 14’. A compound of the formula , or a pharmaceutically acceptable salt thereof. Embodiment 15’. A compound of the formula , or a pharmaceutically acceptable salt thereof. Embodiment 16’. A compound of the formula , or a pharmaceutically acceptable salt thereof. Embodiment 17’. A compound of the formula , or a pharmaceutically acceptable salt thereof. Embodiment 18’. A pharmaceutical composition, comprising a compound of any of embodiments 1’-17’, or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable carriers, diluents, or excipients. Embodiment 19’. A method of treating an immune-mediated disease in a patient in need thereof, comprising administering to the patient an effective amount of a compound according to any of embodiments 1’ to 17’, a pharmaceutically acceptable salt thereof, or the pharmaceutical composition according to embodiment 18’. Embodiment 20’. A method of treating a disease or disorder selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis in a patient in need thereof, comprising administering to the patient an effective amount of a compound according to any one of embodiments 1’ to 17’, a pharmaceutically acceptable salt thereof, or the pharmaceutical composition according to embodiment 18’. Embodiment 21’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in therapy. Embodiment 22’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating a disease or disorder selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis. Embodiment 23’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating psoriasis. Embodiment 24’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating atopic dermatitis. Embodiment 25’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating ulcerative colitis. Embodiment 26’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating Crohn’s disease. Embodiment 27’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating graft-versus-host disease. Embodiment 28’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating rheumatoid arthritis. Embodiment 29’. A compound according to any one of embodiments 1’ to 17’, or a pharmaceutically acceptable salt thereof, for use in treating multiple sclerosis. Furthermore, the present disclosure provides a compound of Formula I: , wherein: Z is CH2, O, or NH; ring A is pyridyl or phenyl, each optionally substituted with halo; Y is 5-membered heteroaryl fused with thiophene or fused with 5-membered or 6- membered carbocycle, wherein the 5-membered heteroaryl contains 1 or 2 N, and the 5-membered or 6-membered carbocycle is optionally substituted with halo or cyano; or a pharmaceutically acceptable salt thereof. In some embodiments, the compound of Formula I is as described above, provided that when Y of the compound of Formula I is , then ring A is substituted phenyl or optionally substituted pyridyl. In some embodiments, the compound of Formula I is as described above, provided that when Y of the compound of Formula I , then ring A is substituted phenyl or optionally substituted pyridyl, wherein n is 1 or 2. In some embodiments, ring A of the compound of Formula I in any preceding embodiment is a phenyl optionally substituted with halo. In some embodiments, ring A of the compound of Formula I in any preceding embodiment is a phenyl optionally substituted with fluoro. In some embodiments, ring A of the compound of Formula I in any preceding embodiment is a pyridyl. In some embodiments, the moiety of the compound of Formula I in any preceding embodiment is selected from: wherein R is H or halo. In some embodiments, the halo is fluoro. In some embodiments, the moiety of the compound of Formula I in any preceding embodiment i In some embodiments, Z of the compound of Formula I in any preceding embodiment is O or NH. In some embodiments, Z of the compound of Formula I in any preceding embodiment is O. In some embodiments, Z of the compound of Formula I in any preceding embodiment is NH. In some embodiments, Y of the compound of Formula I in any preceding embodiment is a bicyclic heteroaryl. In some embodiments, Y of the compound of Formula I in any preceding embodiment is selected from the group consisting of: each optionally substituted with halo or cyano. In some embodiments, Y of the compound of Formula I in any preceding embodiment is selected from the group consisting of: each optionally substituted with halo or cyano. In some embodiments, Y of the compound of Formula I in any preceding embodiment is wherein ring B is a carbocycle. In some embodiments, Y of the compound of Formula I in any preceding embodiment is wherein ring B is a carbocycle, and ring A of the compound of Formula I is pyridyl. In some embodiments, Y of the compound of Formula I in any preceding embodiment is optionally substituted with fluoro or cyano. In some embodiments, Y of the compound of Formula I in any preceding embodiment is substituted with fluoro. In some embodiments, Y of the compound of Formula I in any preceding embodiment is . In some embodiments, Y of the compound of Formula I in any preceding embodiment is and ring A of the compound of Formula is pyridyl. In some embodiments, Y of the compound of Formula I in any preceding embodiment is and Z is O. In some embodiments, Y of the compound of Formula I in any preceding embodiment is ring A of the compound of Formula is pyridyl, and Z is O. In some embodiments, the moiety of the compound of Formula I in any preceding embodiment i the compound of Formula I is . In some embodiments, provided here is the compound of Formula I as described in any preceding embodiments, wherein: Z is O or NH; ring A is phenyl optionally substituted with fluoro, or pyridyl; and Y is , wherein ring B is a 5-membered or 6-membered carbocycle, or a pharmaceutically acceptable salt thereof. In some embodiments, the compound of Formula I is as described in any preceding embodiments, provided that it is not (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6- tetrahydro-3-cyclopentapyrazolyl)methanone. In some embodiments, the compound of Formula I is as described in any preceding embodiments, provided that it is not (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(4,5,6,7- tetrahydro-1,2-benzisoxazol-3-yl)-methanone. In some embodiments, the compound of Formula I is as described in any preceding embodiments, provided that it is not (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(5,6,7,8- tetrahydro-4H-cyclohept[d]isoxazol-3-yl)-methanone. In some embodiments, provided here is a compound selected from the group consisting of: ,

or a pharmaceutically acceptable salt thereof. The present disclosure further provides pharmaceutical composition, comprising a compound or a pharmaceutically acceptable salt thereof according to any of the above embodiments with one or more pharmaceutically acceptable carriers, diluents, or excipients. The present disclosure provides a method of treating an immune-mediated disease in a patient, comprising administering to a patient in need of such treatment an effective amount of a compound, a pharmaceutically acceptable salt thereof, or pharmaceutical composition according to any of the above embodiments. The present disclosure also provides a method of treating a disease or disorder selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis in a patient, comprising administering to a patient in need of such treatment an effective amount of a compound, a pharmaceutically acceptable salt thereof, or pharmaceutical composition according to any of the above embodiments. The present disclosure provides a compound according to any of the above embodiments, or a pharmaceutically acceptable salt thereof, for use in therapy. The present disclosure also provides (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6- tetrahydro-3-cyclopentapyrazolyl)methanone, or a pharmaceutically acceptable salt thereof, for use in therapy. The present disclosure also provides (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(4,5,6,7- tetrahydro-1,2-benzisoxazol-3-yl)-methanone, or a pharmaceutically acceptable salt thereof, for use in therapy. The present disclosure also provides (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(5,6,7,8- tetrahydro-4H-cyclohept[d]isoxazol-3-yl)-methanone, or a pharmaceutically acceptable salt thereof, for use in therapy. The present disclosure also provides a compound according to any of the above embodiments, or a pharmaceutically acceptable salt thereof, for use in the treatment of a disease or disorder selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft- versus-host disease, rheumatoid arthritis, and multiple sclerosis. The present disclosure also provides (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(1,4,5,6- tetrahydro-3-cyclopentapyrazolyl)methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(4,5,6,7- tetrahydro-1,2-benzisoxazol-3-yl)-methanone, (2,3-dihydro-1,4-benzoxazepin-4(5H)-yl)(5,6,7,8- tetrahydro-4H-cyclohept[d]isoxazol-3-yl)-methanone, or a pharmaceutically acceptable salt of each thereof, for use in the treatment of a disease or disorder selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis. Furthermore, the present disclosure provides the use of a compound according to any of the above embodiments, or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for the treatment of an immune-mediated disease. In addition, the present disclosure provides the use of a compound according to any of the above embodiments, or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for the treatment of a disease or disorder selected from psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis. As used herein, the term “alkyl”, used alone or as part of a larger moiety, refers to a saturated, straight, or branched chain hydrocarbon group containing one or more carbon atoms. As used herein, the term “alkoxy”, used alone or as part of a larger moiety, refers to a moiety having an oxygen directly attached to an alkyl group with the attachment point of the moiety on the oxygen atom. The term may be preceded with an indication of number of carbon atoms of the alkoxy. Accordingly, the term “C1-3 alkoxy” refers to -O-C1-3 alkyl. Representative alkoxyl groups include methoxy, ethoxy, propyloxy, tert-butoxy, and the like. As used herein, the term “aryl”, used alone or as part of a larger moiety, refers to an aromatic hydrocarbon group, having 6, 10, or 14 π-electrons shared in a cyclic array. Aryl can be monocyclic (having one ring), bicyclic (having two rings), or polycyclic (having two or more rings). Exemplary aryl includes phenyl, naphthyl, anthracenyl, and phenanthrenyl. As used herein, the terms “aromatic group” and “aromatic unit”, refers to aryl and heteroaryl (as defined below) groups. As used herein, the term “monocycle”, refers to a ring system of one cycle, where each ring atom of the cycle can be a carbon or a heteroatom. In other words, the monocycle can be a carbocycle or a heterocycle (each defined below). As used herein, the term “cycloalkyl” refers to a saturated ring system containing at least three carbon atoms. Cycloalkyl can be monocyclic (having one ring), bicyclic (having two rings), or polycyclic (having two or more rings). Exemplary monocyclic cycloalkyl rings include cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, and cycloheptyl. As used herein, the term “carbocycle” refers to a saturated or unsaturated ring system containing only carbons. Carbocycles include cycloalkyls and aryls and partially saturated rings. As used herein, the term “halo” refers to halogen as a substituent, and specifically chloro, fluoro, bromo, or iodo. As used herein, the term “heterocyclic” and “heterocycle” refers to an optionally substituted saturated ring system containing at least two carbon atoms and at least one heteroatom. Exemplary heteroatoms are oxygen, nitrogen, and sulfur. Exemplary heterocyclic rings (or heterocycles) include oxirane, aziridine, oxetane, oxolane, pyrrolidine, piperidine, and morpholine. Heterocycles can be monocycles (having one ring), bicycles (having two rings), or polycycles (having two or more rings) that may be, for example, fused with each other. As used herein, the term “heteroaryl” refers to groups having 5 to 10 ring atoms, preferably 5, 6, 9, or 10 ring atoms, having 6, 10, or 14 π-electrons shared in a cyclic array, and having, in addition to carbon atoms, from one to five heteroatoms. The term “heteroatom” refers to nitrogen, oxygen, or sulfur, and includes any oxidized form of nitrogen or sulfur, and any quaternized form of a basic nitrogen. Heteroaryl groups include, for example, thienyl, furanyl, pyrrolyl, imidazolyl, pyrazolyl, triazolyl, tetrazolyl, oxazolyl, isoxazolyl, oxadiazolyl, thiazolyl, isothiazolyl, thiadiazolyl, pyridyl, pyridazinyl, pyrimidinyl, and pyrazinyl. The term “bicyclic heteroaryl” includes groups in which a heteroaryl ring is fused to one or more aryl, or heteroaryl rings. Nonlimiting examples include indolyl, isoindolyl, benzothienyl, benzofuranyl, dibenzofuranyl, indazolyl, benzimidazolyl, benzthiazolyl, quinolyl, isoquinolyl, cinnolinyl, phthalazinyl, quinazolinyl, and quinoxalinyl. When there are two or more rings, the rings may be arranged separate from each other or connected with each other. When two rings are connected with each other, they may be connected in a “fuse” arrangement (or connection motif), a “spiro” arrangement, or a “bridge” arrangement. As used herein, the term “fuse” refers to an arrangement where the two rings are connected with each other, side-by-side, sharing two “bridgehead” atoms that are directly and immediately connected to each other. The “fuse” connection motif differs from “spiro” connection motif in that there is one and only one “bridgehead” atom in the “spiro” motif; and differs from “bridge” connection motif in that the two “bridgehead” atoms are not immediately connected to each other in the “bridge” motif. When a first ring is “fused with” a second ring, the "bridgehead” atoms are construed as belonging to both rings. Accordingly, if an embodiment provided here describes one such ring being a six-membered “carbocycle,” then the six ring atoms include two “bridgehead” atoms and four additional atoms. And all these six ring atoms are carbons in order to be a “carbocycle.” For example, the group falls outside the scope of “a 5-membered heteroaryl fused with a 6-membered carbocycle” because one bridgehead atom is not carbon. As used herein, the term “oxo” refers to the oxygen atom as a substituent connected to another atom by a double bond. It may be denoted as “=O”. The term oxo is the carbonyl group less the carbon atom. As used herein, the term “immune-mediated disease” encompasses a group of autoimmune or inflammatory disorders in which immunological pathways play an important etiological and/or pathogenetic role. Such diseases are sometimes characterized by an alteration in cellular homeostasis. Immune-mediated diseases may be triggered by environmental factors, dietary habits, infectious agents, and genetic predisposition. Immune-mediated disease includes, for example, psoriasis, atopic dermatitis, ulcerative colitis, Crohn’s disease, graft-versus-host disease, rheumatoid arthritis, and multiple sclerosis. As used herein, the term “treating” includes restraining, slowing, stopping, or reversing the progression or severity of an existing symptom or disorder. As used herein, the term "patient" refers to a human. As used herein, the term “effective amount” refers to the amount or dose of compound of the disclosure, or a pharmaceutically acceptable salt thereof which, upon single or multiple dose administration to the patient, provides the desired effect in the patient under diagnosis or treatment. An effective amount can be readily determined by one skilled in the art by the use of known techniques. In determining the effective amount for a patient, a number of factors are considered, including, but not limited to: the species of patient; its size, age, and general health; the specific disease or disorder involved; the degree of or involvement or the severity of the disease or disorder; the response of the individual patient; the particular compound administered; the mode of administration; the bioavailability characteristics of the preparation administered; the dose regimen selected; the use of concomitant medication; the individual patient’s medical history; and other relevant circumstances. The compounds of the present disclosure are generally effective over a wide dosage range. For example, dosages per day normally fall within the range of about 0.1 to about 15 mg/kg of body weight. In some instances, dosage levels below the lower limit of the aforesaid range may be more than adequate, while in other cases still larger doses may be employed with acceptable side effects, and therefore the above dosage range is not intended to limit the scope of the disclosure in any way. The compounds of the present disclosure are preferably formulated as pharmaceutical compositions administered by any route which makes the compound bioavailable, including oral and transdermal routes. Most preferably, such compositions are for oral administration. Such pharmaceutical compositions and processes for preparing same are well known in the art (See, e.g., Remington: The Science and Practice of Pharmacy, A. Adejare, Editor, 23 ^rd Edition, Elsevier Academic Press, 2020). The compounds of the present disclosure, or pharmaceutically acceptable salts thereof, may be prepared according to the following Preparations and Examples by methods well known and appreciated in the art. Suitable reaction conditions for the steps of these Preparations and Examples are well known in the art and appropriate substitutions of solvents and co-reagents are within the skill of the art. Likewise, it will be appreciated by those skilled in the art that synthetic intermediates may be isolated and/or purified by various well-known techniques as needed or desired, and that frequently, it will be possible to use various intermediates directly in subsequent synthetic steps with little or no purification. As an illustration, compounds of the preparations and examples can be isolated, for example, by silica gel purification, isolated directly by filtration, or crystallization. Furthermore, the skilled artisan will appreciate that in some circumstances, the order in which moieties are introduced is not critical. The particular order of steps required to produce the compounds of the present disclosure is dependent upon the particular compound being synthesized, the starting compound, and the relative lability of the substituted moieties, and is well appreciated by the skilled chemist. All substituents, unless otherwise indicated, are as previously defined, and all reagents are well known and appreciated in the art. Certain abbreviations are as follows: “ACN” refers to acetonitrile; “BSA” refers to bovine serum albumin; “CMV” refers to cytomegalovirus; “DCM” refers to dichloromethane; “DIEA” refers to N, N-diisopropylethylamine; “DMEM” refers to Dulbecco's modified eagle medium; “DMF” refers to dimethylformamide; “DMSO” refers to dimethyl sulfoxide; “DPBS” refers to Dulbecco's phosphate-buffered saline; “EDCI” refers to 1-ethyl-3-(3- dimethylaminopropyl)carbodiimide; “EGFP” refers to enhanced green fluorescence protein; “EtOAc” refers to ethyl acetate; “FBS” refers to fetal bovine serum; “HATU” refers to (1- [bis(dimethylamino)methylene]-1H-1,2,3-triazolo[4,5-b]pyridi nium 3-oxide hexafluorophosphate “HOBt” refers to hydroxybenzotriazole; “hr/hrs” refers to hour/hours; “MeOH” refers to methanol and methyl alcohol; “min” refers to minute/minutes; “NMI” refers to N-methylimidazole; “TCFH” refers to tetramethylchloroformamidinium hexafluorophosphate; “T3P”refers to propanephosphonic acid anhydride; and “THF” refers to tetrahydrofuran. In an optional step, a pharmaceutically acceptable salt of a compound according to any of the above embodiments can be formed by reaction of an appropriate free base of the compound with an appropriate pharmaceutically acceptable acid in a suitable solvent under standard conditions. The formation of such salts is well known and appreciated in the art. See, for example, Gould, P.L., “Salt selection for basic drugs,” International Journal of Pharmaceutics, 33: 201-217 (1986); Bastin, R.J., et al. “Salt Selection and Optimization Procedures for Pharmaceutical New Chemical Entities,” Organic Process Research and Development, 4: 427- 435 (2000); and Berge, S.M., et al., “Pharmaceutical Salts,” Journal of Pharmaceutical Sciences, 66: 1-19, (1977). “Salt selection for basic drugs,” International Journal of Pharmaceutics, 33: 201-217 (1986). One of ordinary skill in the art will appreciate that a compound according to any of the above embodiments is readily converted to and may be isolated as a pharmaceutically acceptable salt. The compounds of Formula I or pharmaceutically acceptable salts thereof, may be prepared by a variety of procedures known in the art, some of which are illustrated in the Schemes, Preparations, and Examples below. The specific synthetic steps for each of the routes described may be combined in different ways, or in conjunction with steps from different schemes, to prepare compounds of Formula I, or pharmaceutically acceptable salts thereof. The products of each step in the scheme below can be recovered by conventional methods well known in art, including e.g., extraction, evaporation, precipitation, chromatography, filtration, trituration, and crystallization. In the scheme below, all variables and substituents unless otherwise indicated, are as previously defined. The reagents and starting materials are readily available to one of ordinary skill in the art. Scheme 1. General scheme for the preparation of intermediate compound 7 Scheme 1 depicts a general scheme for the synthesis of intermediate compound 7. PG is a suitable protecting group (such as t-butyloxycarbonyl or BOC); and X is Cl or Br. Moreover, R can be H (that is, ring A being unsubstituted) or another suitable substituent defined for Formula I. A halo-bearing compound 1 is contacted with alkylamine compound 2 under conditions sufficient to provide compound 3. For example, compound 1 is dissolved in a suitable solvent (e.g. acetonitrile), adding an appropriate base (e.g. DIEA) and a mono-protected ethane-1,2- diamine (such as tert-butyl N-(2-aminoethyl)carbamate) 2. The mixture is then agitated at a suitable temperature (e.g., >50 °C) for several hrs., until the reaction completes. The reaction progress can be monitored, for example, with thin layer chromatography (TLC) or other suitable methods. The reaction mixture is concentrated under reduced pressure and purified (e.g., via silica gel chromatography) to give compound 3. The compound 3 is reduced under conditions sufficient to provide compound 4. For example, compound 3 is dissolved in a suitable solvent (e.g., THF) and cooled (e.g., using ice bath). This mixture is treated with a suitable reducing agent (e.g., lithium aluminum hydride) and stirred at the reduced temperature (e.g., in ice bath) for several hrs., until the reaction completes. The reaction mixture is quenched with water and a base (e.g., 15% aqueous sodium hydroxide), filtered, and the filtrate concentrated under reduced pressure to give compound 4. Compound 4 is oxidized under conditions sufficient to provide aldehyde compound 5. For example, compound 4 is dissolved in a suitable solvent (e.g., 1,2-dichloroethane), treated with a suitable oxidizing agent (e.g., manganese dioxide), and heated at a suitable temperature (e.g., 70 °C) for several hrs., until the reaction completes. The reaction mixture is filtered, and the filtrate concentrated under reduced pressure to give compound 5. Compound 5 is contacted with an acid under conditions sufficient to provide cyclic imine compound 6, such as by deprotecting the amine group and allowing cyclization to occur with the aldehyde group. For example, compound 5 is dissolved in a suitable solvent (e.g., DCM), treated with an appropriate acid (e.g., trifluoroacetic acid), and stirred at ambient temperature for several hrs., until reaction completes. The reaction mixture is concentrated under reduced pressure and the residue purified (e.g., prep-HPLC) to give compound 6. Compound 6 is then reduced under conditions sufficient to provide compound 7. For example, compound 6 is dissolved in a suitable solvent (e.g., MeOH), treated with a suitable reducing agent (e.g., sodium borohydride), and stirred at ambient temperature for several hrs., until the reaction completes. The reaction mixture is concentrated under reduced pressure and the residue purified (e.g., prep-HPLC) to give compound 7. Scheme 2 General scheme for the preparation of intermediate compound 17 Scheme 2 depicts a general scheme for the synthesis of intermediate compound 17. Moreover, R can be H (that is, ring A being unsubstituted) or another suitable substituent defined for Formula I. Hydroxy-bearing compound 8 is contacted with halo-bearing compound 9 under conditions sufficient to provide compound 10. For example, a solution of compound 8 and compound 9 in a suitable solvent (e.g., DMF) is heated at a suitable temperature (e.g.40-80 °C) for several hrs until the reaction completes. The reaction is quenched with water, extracted with a suitable solvent (e.g., EtOAc), dried (e.g., over anhydrous Na2SO4), concentrated under reduced pressure, and purified (e.g. via silica gel chromatography) to give compound 10. Compound 10 is contacted with an acid under conditions sufficient to provide a cyclized compound 11, such as by deprotecting the amine group and allowing intramolecular ester-amide exchange reaction to occur. For example, a solution of compound 10 in a suitable solvent (e.g., DCM) is treated with an appropriate acid (e.g., trifluoroacetic acid) and stirred at ambient temperature for several hrs until the reaction completes. The reaction solution is concentrated under reduced pressure to give compound 11. Compound 11 is then reduced under conditions sufficient (e.g., with borane) to compound 17. For example, compound 11 is dissolved in a solution of borane-THF complex and stirred at a suitable temperature (e.g., 60-80 °C) for several hrs until the reaction completes. The reaction mixture is quenched with an appropriate alcohol (e.g., MeOH), stirred at a suitable temperature (e.g., 80-90 °C) for several hrs, and concentrated under reduced pressure to give compound 17. In an alternative route, aldehyde compound 12 is contacted with alkylamine compound 13 under conditions sufficient to provide compound 14. For example, a mixture of compound 12 and compound 13 in a suitable solvent (e.g., acetonitrile) is stirred with a drying agent (e.g., MgSO4) for several hrs until the reaction completes. The reaction mixture is filtered and concentrated under reduced pressure. The residue is dissolved in a suitable solvent (e.g., MeOH), treated with a reducing agent (e.g., sodium borohydride), and stirred at a suitable temperature (e.g., 0-20 °C) for several hrs. The mixture is concentrated under reduced pressure and purified (e.g., prep-TLC) to give compound 14. Compound 14 is converted under conditions sufficient into compound 17. For example, a solution of compound 14 in a suitable solvent (e.g., DMF) is treated with an appropriate base (e.g., potassium t-butoxide) and heated at a suitable temperature (e.g., 60-100 °C) for several hrs until the reaction completes. The reaction mixture is concentrated under reduced pressure and purified (e.g., via silica gel chromatography) to give compound 17. In another example, compound 14 is first converted under conditions sufficient to provide compound 16 having its amine group protected; and the compound 16 is then converted under conditions sufficient to provide compound 17. For example, a mixture of compound 14, an appropriate catalyst (e.g. palladium acetate), an appropriate ligand (e.g.2-(di-t- butylphosphino)biphenyl), and an appropriate base (e.g. cesium carbonate) in a suitable solvent (e.g.1,4-dioxane) is heated at a suitable temperature (e.g.80-110 °C) for several hrs. The reaction mixture is diluted with an appropriate solvent (e.g., EtOAc) and washed with water. The organics are dried (e.g., over sodium sulfate), filtered, concentrated under reduced pressure, and purified (e.g., via silica gel chromatography) to give compound 16. A solution of compound 16 in a suitable solvent (e.g., 1,4-dioxane) is treated with an appropriate acid (e.g., hydrogen chloride in 1,4-dioxane) and stirred at ambient temperature for several hrs. The reaction mixture is quenched with an appropriate base (e.g., aqueous sodium bicarbonate) to pH ~7 and concentrated under reduced pressure. The residue is purified (e.g., prep-TLC) to give compound 17. Scheme 3. General scheme for the preparation of compounds of Formula I Scheme 3 depicts a general scheme for the synthesis of compounds of Formula I. Z is CH2, NH, or O. Moreover, R can be H (that is, ring A being unsubstituted) or another suitable substituent defined for Formula I. Compound 18 is contacted with an appropriate carboxylic acid compound 19 under conditions sufficient (e.g., through an amide coupling reaction) to provide compound of Formula I. For example, compounds 18 and 19 are dissolved in a suitable solvent (e.g., DMF, or THF) and treated with an appropriate amide coupling agent (e.g., HATU) and an appropriate base (e.g., DIEA, or triethylamine) and stirred at ambient temperature for several hrs until reaction completes. The reaction mixture is concentrated under reduced pressure and the residue purified (e.g., prep-HPLC) to give compound of Formula I. In some embodiments, compounds of Formula I-1 may be prepared according to Schemes 1A-5A described below:

Scheme 1A. General scheme for the preparation of intermediate compound 7 Scheme 1A depicts a general scheme for the synthesis of intermediate compound 7. PG is a suitable protecting group (such as t-butyloxycarbonyl or BOC); and X is Cl or Br. Moreover, R can be H (that is, ring A being unsubstituted) or another suitable substituent defined with respect to embodiment 19 or embodiment 19A. A halo-bearing compound 1 is contacted with alkylamine compound 2 under conditions sufficient to provide compound 3. For example, compound 1 is dissolved in a suitable solvent (e.g. acetonitrile), adding an appropriate base (e.g. DIEA) and a mono-protected ethane-1,2- diamine (such as tert-butyl N-(2-aminoethyl)carbamate) 2. The mixture is then agitated at a suitable temperature (e.g., >50 °C) for several hrs., until the reaction completes. The reaction progress can be monitored, for example, with thin layer chromatography (TLC) or other suitable methods. The reaction mixture is concentrated under reduced pressure and purified (e.g. via silica gel chromatography) to give compound 3. The compound 3 is reduced under conditions sufficient to provide compound 4. For example, compound 3 is dissolved in a suitable solvent (e.g. THF) and cooled (e.g. using ice bath). This mixture is treated with a suitable reducing agent (e.g., lithium aluminum hydride) and stirred at the reduced temperature (e.g., in ice bath) for several hrs., until the reaction completes. The reaction mixture is quenched with water and a base (e.g.15% aqueous sodium hydroxide), filtered, and the filtrate concentrated under reduced pressure to give compound 4. The compound 4 is oxidized under conditions sufficient to provide aldehyde compound 5. For example, compound 4 is dissolved in a suitable solvent (e.g., 1,2-dichloroethane), treated with a suitable oxidizing agent (e.g., manganese dioxide), and heated at a suitable temperature (e.g., 70 °C) for several hrs., until the reaction completes. The reaction mixture is filtered and the filtrate concentrated under reduced pressure to give compound 5. Compound 5 is contacted with an acid under conditions sufficient to provide cyclic imine compound 6, such as by deprotecting the amine group and allowing cyclization to occur with the aldehyde group. For example, compound 5 is dissolved in a suitable solvent (e.g., DCM), treated with an appropriate acid (e.g., trifluoroacetic acid), and stirred at ambient temperature for several hrs., until reaction completes. The reaction mixture is concentrated under reduced pressure and the residue purified (e.g. prep-HPLC) to give compound 6. Compound 6 is then reduced under conditions sufficient to provide compound 7. For example, compound 6 is dissolved in a suitable solvent (e.g., MeOH), treated with a suitable reducing agent (e.g., sodium borohydride), and stirred at ambient temperature for several hrs., until the reaction completes. The reaction mixture is concentrated under reduced pressure and the residue purified (e.g. prep-HPLC) to give compound 7.

Scheme 2A. General scheme for the preparation of intermediate compound 17 Scheme 2A depicts a general scheme for the synthesis of intermediate compound 17. Moreover, R can be H (that is, ring A being unsubstituted) or another suitable substituent defined with respect to embodiment 19 or embodiment 19A. Hydroxy-bearing compound 8 is contacted with halo-bearing compound 9 under conditions sufficient to provide compound 10. For example, a solution of compound 8 and compound 9 in a suitable solvent (e.g., DMF) is heated at a suitable temperature (e.g., 40-80 °C) for several hrs., until the reaction completes. The reaction is quenched with water, extracted with a suitable solvent (e.g. EtOAc), dried (e.g. over anhydrous Na2SO4), concentrated under reduced pressure, and purified (e.g. via silica gel chromatography) to give compound 10. Compound 10 is contacted with an acid under conditions sufficient to provide a cyclized compound 11, such as by deprotecting the amine group and allowing intramolecular ester-amide exchange reaction to occur. For example, a solution of compound 10 in a suitable solvent (e.g., DCM) is treated with an appropriate acid (e.g., trifluoroacetic acid) and stirred at ambient temperature for several hrs., until the reaction completes. The reaction solution is concentrated under reduced pressure to give compound 11. Compound 11 is then reduced under conditions sufficient (e.g. with borane) to compound 17. For example, compound 11 is dissolved in a solution of borane-THF complex and stirred at a suitable temperature (e.g., 60-80 °C) for several hrs., until reaction completes. The reaction mixture is quenched with an appropriate alcohol (e.g., MeOH), stirred at a suitable temperature (e.g., 80-90 °C) for several hrs., and concentrated under reduced pressure to give compound 17. In an alternative route, aldehyde compound 12 is contacted with alkylamine compound 13 under conditions sufficient to provide compound 14. For example, a mixture of compound 12 and compound 13 in a suitable solvent (e.g., acetonitrile) is stirred with a drying agent (e.g., MgSO ₄ ) for several hrs., until the reaction completes. The reaction mixture is filtered and concentrated under reduced pressure. The residue is dissolved in a suitable solvent (e.g., MeOH), treated with a reducing agent (e.g., sodium borohydride), and stirred at a suitable temperature (e.g., 0-20 °C) for several hrs. The mixture is concentrated under reduced pressure and purified (e.g. prep-TLC) to give compound 14. Compound 14 is converted under conditions sufficient into compound 17. For example, a solution of compound 14 in a suitable solvent (e.g., DMF) is treated with an appropriate base (e.g., potassium t-butoxide) and heated at a suitable temperature (e.g., 60-100 °C) for several hrs., until the reaction completes. The reaction mixture is concentrated under reduced pressure and purified (e.g. via silica gel chromatography) to give compound 17. In another example, compound 14 is first converted under conditions sufficient to provide compound 16 having its amine group protected; and the compound 16 is then converted under conditions sufficient to provide compound 17. For example, a mixture of compound 14, an appropriate catalyst (e.g. palladium acetate), an appropriate ligand (e.g.2-(di-t- butylphosphino)biphenyl), and an appropriate base (e.g. cesium carbonate) in a suitable solvent (e.g.1,4-dioxane) is heated at a suitable temperature (e.g.80-110 °C) for several hrs. The reaction mixture is diluted with an appropriate solvent (e.g. EtOAc) and washed with water. The organics are dried (e.g. over sodium sulfate), filtered, concentrated under reduced pressure, and purified (e.g. via silica gel chromatography) to give compound 16. A solution of compound 16 in a suitable solvent (e.g., 1,4-dioxane) is treated with an appropriate acid (e.g., hydrogen chloride in 1,4-dioxane) and stirred at ambient temperature for several hrs. The reaction mixture is quenched with an appropriate base (e.g. aqueous sodium bicarbonate) to pH ~7 and concentrated under reduced pressure. The residue is purified (e.g. prep-TLC) to give compound 17. Scheme 3A. General scheme for the preparation of intermediate compound 23     Scheme 3A depicts a general scheme for the synthesis of compound 23. Moreover, R can be H (that is, ring A being unsubstituted) or another suitable substituent defined with respect to embodiment 19 or embodiment 19A. Amine compound 20 is protected with a suitable protecting group under conditions sufficient to provide compound 21. For example, a solution of compound 20 and di-tert- butyldicarbonate in a suitable solvent (e.g., THF) is stirred at a suitable temperature (e.g., 25- 50 °C) for several hrs., until the reaction completes. The reaction is quenched with water, extracted with a suitable solvent (e.g. EtOAc), dried (e.g. over anhydrous Na ₂ SO ₄ ), concentrated under reduced pressure, and purified (e.g. via silica gel chromatography) to give compound 21. Compound 21 is reacted with an appropriate alkylating agent such as an alkyl halide under basic conditions or an alcohol under Mitsunobu conditions. For example, a solution of compound 21 in a suitable solvent (e.g. THF) is treated with a suitable base (e.g. NaH) and stirred at a suitable temperature (e.g.0-30 °C) for several minutes (e.g.30 minutes). The alkylating agent is then added, and the solution heated at a suitable temperature (e.g.25-80 °C) until the reaction completes. The reaction is quenched with water, extracted with a suitable solvent (e.g. EtOAc), dried (e.g. over anhydrous Na2SO4), concentrated under reduced pressure, and purified (e.g. via silica gel chromatography) to give compound 22. Compound 22 is deprotected under such conditions to provide compound 23. For example, in the case of a tert-butoxy carbonyl protecting group, compound 22 in a suitable solvent (e.g., DCM) is treated with a suitable acid (e.g., TFA) and stirred for a suitable time (e.g., 1 to 12 hrs. The solvents are concentrated under reduced pressure and the residue is diluted with water and treated with a base (e.g. saturated aqueous sodium bicarbonate solution) and extracted with a suitable solvent (e.g. EtOAc), dried (e.g. over anhydrous Na2SO4), concentrated under reduced pressure, and purified (e.g. via silica gel chromatography) to give compound 23. Scheme 4A. General scheme for the preparation of intermediate compound 26     Scheme 4A depicts a general scheme for the synthesis of compound 26. Moreover, R can be H (that is, ring A being unsubstituted) or another suitable substituent defined with respect to embodiment 19 or embodiment 19A. Ketone compound 24 is reacted under conditions sufficient to provide compound 25. For example, sodium azide is added portionwise to a solution of compound 24 in concentrated hydrochloric acid at a suitable temperature (e.g., 0-25 °C) for 12-18 hrs. The reaction is poured into ice water and the solution neutralized with a suitable base (e.g. potassium carbonate). The mixture is extracted with a suitable solvent (e.g. DCM), dried (e.g. over anhydrous Na2SO4), concentrated under reduced pressure, and purified (e.g. via silica gel chromatography) to give compound 25. Compound 25 is then reduced under conditions sufficient (e.g. with borane) to give compound 26. For example, compound 25 is dissolved in a solution of borane-THF complex and stirred at a suitable temperature (e.g., 60-80 °C) for several hrs., until reaction completes. The reaction mixture is quenched with an appropriate alcohol (e.g., MeOH), stirred at a suitable temperature (e.g., 80-90 °C) for several hrs., and concentrated under reduced pressure to give compound 26.   Scheme 5A. General scheme for the preparation of compounds of Formula I-1: Scheme 5A depicts a general scheme for the synthesis of compounds of Formula I-1. Z is CH2, NR, or O. Compound 18 is contacted with an appropriate carboxylic acid compound 19 under conditions sufficient (e.g. through an amide coupling reaction) to provide compound of Formula I-1. For example, compound 18 and compound 19 are dissolved in a suitable solvent (e.g., DMF) and treated with an appropriate amide coupling agent (e.g. HATU) and an appropriate base (e.g. DIEA) and stirred at ambient temperature for several hrs., until reaction completes. The reaction mixture is concentrated under reduced pressure and the residue purified (e.g. prep- HPLC) to give compound of Formula I-1. In some embodiments, compounds of table 1 may be prepared according to Schemes 1A- 5A described above. Preparation 1 7-Fluoro-2,3,4,5-tetrahydro-1H-1,4-benzodiazepine Step 1 7-Fluoro-3,4-dihydro-1H-1,4-benzodiazepine-2,5-dione F 6-Fluoro-1H-3,1-benzoxazine-2,4-dione (2.75 g, 15.2 mmol), and glycine ethyl ester hydrochloride (2.14 g, 15.2 mmol) were stirred in pyridine (12.25M in water; 20 mL) for 16 hrs., at 120 °C. After this time, the reaction mixture was poured into water (50 mL) and washed with EtOAc (30 mL × 3). The aqueous layer was brought to about pH 3 with 6N HCl and the resulting solid filtered to give 7-fluoro-3,4-dihydro-1H-1,4-benzodiazepine-2,5-dione as a yellow solid (1.34 g, 45.3%). ¹ H NMR (DMSO-d ₆ ) δ 10.37 (s, 1H), 8.67 (br t, J=5.5 Hz, 1H), 7.53 - 7.38 (m, 2H), 7.15 (dd, J=4.9, 9.0 Hz, 1H), 3.67 - 3.55 (m, 2H). Step 2 7-Fluoro-2,3,4,5-tetrahydro-1H-1,4-benzodiazepine 7-Fluoro-3,4-dihydro-1H-1,4-benzodiazepine-2,5-dione (151 mg, 0.778 mmol) was dissolved in THF (10 mL) and the mixture cooled in an ice bath. To the cold mixture lithium aluminum hydride (0.176 g, 4.64 mmol) was added portion-wise. After complete addition, the mixture was heated to 75 °C for 6 hrs. The reaction was then cooled in an ice bath and quenched with water (10 mL) and an aqueous NaOH solution (15%, 10 mL). After quenching, the mixture was diluted with EtOAc (30 mL) and washed with water (10 mL × 2). The organic layer was collected, dried over magnesium sulfate, filtered, and concentrated under reduced pressure. The residue was purified via silica gel chromatography eluting with 41% MeOH in DCM to give 7- fluoro-2,3,4,5-tetrahydro-1H-1,4-benzodiazepine as a yellow solid (105 mg, 81.2%). ¹ H NMR (DMSO-d ₆ ) δ 6.90 (dd, J=2.4, 9.4 Hz, 1H), 6.86 - 6.78 (m, 2H), 5.38 (br s, 1H), 5.43 - 5.33 (m, 1H), 3.67 (s, 2H), 3.17 (s, 2H), 2.92 - 2.79 (m, 4H). Preparation 2 9-Fluoro-2,3,4,5-tetrahydro-1H-1,4-benzodiazepine 9-Fluoro-2,3,4,5-tetrahydro-1H-1,4-benzodiazepine was prepared using a method analogous to that of preparation 1 using the corresponding suitable reagents, with the reaction time adjusted to reach completion, to give a green oil (1.5 g). ES/MS (m/z): 167.1 (M+H). Preparation 3 6-Fluoro-2,3,4,5-tetrahydro-1H-1,4-benzodiazepine 6-Fluoro-2,3,4,5-tetrahydro-1H-1,4-benzodiazepine was prepared using a method analogous to preparation 1 using the corresponding appropriate reagents, with the reaction time adjusted to reach completion, to give a white solid (237 mg, 57.4%). ¹ H NMR (CDCl ₃ ) δ 7.05 - 6.96 (m, 1H), 6.64 - 6.50 (m, 2H), 4.02 (s, 2H), 3.20 - 3.14 (m, 2H), 3.11 - 3.04 (m, 2H), 2.06 - 1.93 (m, 1H). Preparation 4 2,3,4,5-Tetrahydropyrido[3,4-f][1,4]oxazepine Step 1 2-[(4-Chloro-3-pyridyl)methylamino]ethanol 4-Chloropyridine-3-carbaldehyde (10 g, 68.5 mmol) was dissolved in DCM (150 mL) and 2-aminoethanol (6.3 g, 100 mmol) and acetic acid (4.12 g, 68.5 mmol) were added. The mixture was stirred at ambient temperature for 1 hr. After this time, the reaction mixture was concentrated under reduced pressure and purified via silica gel chromatography (0-10% MeOH in DCM) to give 2-[(4-chloro-3-pyridyl)methylamino]ethanol as a light-yellow oil (10 g, 75.1%). ES/MS (m/z): 187.0 (M+H). Step 2 2,3,4,5-Tetrahydropyrido[3,4-f][1,4]oxazepine 2-[(4-Chloro-3-pyridyl)methylamino]ethanol (15 g, 77.2 mmol) was dissolved in DMF (600 mL). Potassium t-butoxide (27 g, 228.6 mmol) was added and the reaction mixture stirred at 80 °C for 18 hrs. The reaction mixture was concentrated under reduced pressure, and purified via silica gel chromatography (0-15% MeOH in DCM) to give 2,3,4,5-tetrahydropyrido[3,4- f][1,4]oxazepine as a light-yellow oil (6.6 g, 54%). ES/MS (m/z): 151.1 (M+H). Preparation 5 2,3,4,5-Tetrahydropyrido[3,2-f][1,4]oxazepine 2,3,4,5-Tetrahydropyrido[3,2-f][1,4]oxazepine was prepared using a method analogous to Preparation 4 using the corresponding appropriate reagents with the reaction time adjusted to reach completion, to give a colorless oil (776 mg, 65.6%). ES/MS (m/z): 151.9 (M+H). Preparation 6 2,3,4,5-Tetrahydro-1H-pyrido[4,3-e][1,4]diazepine Step 1 4-[2-(tert-Butoxycarbonylamino)ethylamino]pyridine-3-carboxy lic acid 4-Chloropyridine-3-carboxylic acid (40 g, 253.9 mmol) was dissolved in acetonitrile (400 mL), and DIEA (88.7 mL, 508 mmol) and tert-butyl N-(2-aminoethyl)carbamate (49.3 g, 305 mmol) were added. The mixture was stirred at 100 °C for 16 hrs under nitrogen atmosphere. After this time, the reaction mixture was concentrated under reduced pressure and the resulting residue purified via silica gel chromatography (0-50% EtOAc in petroleum ether) to give 4-[2- (tert-butoxycarbonylamino)ethylamino]pyridine-3-carboxylic acid as a yellow oil (23 g, 25.8%). ES/MS (m/z): 282.1 (M+H). Step 2 tert-Butyl N-[2-[[3-(hydroxymethyl)-4-pyridyl]amino]ethyl]carbamate 4-[2-(tert-Butoxycarbonylamino)ethylamino]pyridine-3-carboxy lic acid (23 g, 65.4 mmol) was stirred in THF (400 mL) and the mixture cooled in an ice bath. To this cold mixture, lithium aluminum hydride (12.5 g, 329 mmol) was added slowly. After complete addition, stirring in the ice bath was maintained for 2 hrs. After this time, the reaction mixture was quenched with water (18 mL) and a 15% aqueous sodium hydroxide solution (27 mL), filtered, and concentrated under reduced pressure to give tert-butyl N-[2-[[3-(hydroxymethyl)-4- pyridyl]amino]ethyl]carbamate as a yellow oil (18 g, 72.1%). ES/MS (m/z): 268.2 (M+H). Step 3 tert-Butyl N-[2-[(3-formyl-4-pyridyl)amino]ethyl]carbamate tert-Butyl N-[2-[[3-(hydroxymethyl)-4-pyridyl]amino]ethyl]carbamate (15 g, 44.9 mmol) was stirred in 1,2-dichloroethane (200 mL). To this mixture, manganese dioxide (78 g, 897.2 mmol) was added and heated to 70 °C for 16 hrs under nitrogen atmosphere. After this time, the reaction mixture was filtered and the filtrate concentrated under reduced pressure to give tert- butyl N-[2-[(3-formyl-4-pyridyl)amino]ethyl]carbamate as a yellow oil (12 g, 50.4%). ES/MS (m/z): 266.0 (M+H). Step 4 2,3-Dihydro-1H-pyrido[4,3-e][1,4]diazepine tert-Butyl N-[2-[(3-formyl-4-pyridyl)amino]ethyl]carbamate (12 g, 45.5 mmol) was dissolved in DCM (70 mL), and to this mixture trifluoroacetic acid (70 mL) was added. The mixture was stirred at ambient temperature for 3 hrs. After this time, the reaction mixture was concentrated under reduced pressure and the residue purified via prep-HPLC (Phenomenex luna C18250*50mm*10µm; 0-20% water (ammonium carbonate)/ACN over 20 min; 110 mL/min) to give 2,3-dihydro-1H-pyrido[4,3-e][1,4]diazepine as a yellow oil (3 g, 41.7%). ES/MS (m/z): 148.2 (M+H). Step 5 2,3,4,5-Tetrahydro-1H-pyrido[4,3-e][1,4]diazepine 2,3-Dihydro-1H-pyrido[4,3-e][1,4]diazepine (40 mg, 0.163 mmol) was dissolved in MeOH (1 mL) and sodium borohydride (20 mg, 0.51 mmol) added. The mixture was stirred at ambient temperature for 1 hr. After this time, the reaction mixture was concentrated under reduced pressure and the residue purified via prep-HPLC (Phenomenex Luna® C18 75*30mm*3µm; 0-35% water (ammonium carbonate)/ACN over 11 min; 25 mL/min) to give 2,3,4,5-tetrahydro-1H-pyrido[4,3-e][1,4]diazepine as a white solid (12 mg, 31.1%). ES/MS (m/z): 150.2 (M+H). Preparation 7 2,3,4,5-Tetrahydropyrido[2,3-f][1,4]oxazepine Step 1 2-[(3-Bromo-2-pyridyl)methylamino]ethanol 3-Bromopyridine-2-carbaldehyde (2 g, 10.9 mmol), 2-aminoethanol (1.56 g, 25.6 mmol) and magnesium sulfate (10.37 g, 86.16 mmol) were mixed in DCM (30 mL) and stirred at ambient temperature for 3 hrs. The reaction mixture was filtered and concentrated under reduced pressure. The residue was dissolved in MeOH (30 mL) and treated with sodium borohydride (1.67 g, 43.34 mmol) at 0 °C for 2 hrs. The mixture was concentrated under reduced pressure. The residue was purified by prep-TLC (50% EtOAc in petroleum ether) to give 2-[(3-bromo-2- pyridyl)methylamino]ethanol as a yellow solid (2.21 g, 88.0%). ¹ H NMR (DMSO-d ₆ ) δ 8.57 (d, J=4.0 Hz, 1H), 8.10 (d, J=8.0 Hz, 1H), 7.32 (dd, J=4.7, 8.1 Hz, 1H), 4.12 (s, 2H), 3.58 (t, J=5.5 Hz, 2H), 2.85 (t, J=5.5 Hz, 2H). Step 2 tert-Butyl N-[(3-bromo-2-pyridyl)methyl]-N-(2-hydroxyethyl)carbamate 2-[(3-Bromo-2-pyridyl)methylamino]ethanol (2.21 g, 9.56 mmol) and di-tert-butyl dicarbonate (10.8 g, 48.2 mmol) were stirred in 1,4-dioxane (15 mL). Sodium hydroxide (782 mg, 19.6 mmol) in water (15 mL) was added to this mixture and stirred at 30 °C for 0.5 hrs. The reaction mixture was extracted with EtOAc (100 mL × 3) and the organics dried over sodium sulfate, filtered, and concentrated under reduced pressure. The resulting residue was purified via silica gel chromatography (0-50% EtOAc in petroleum ether) to give tert-butyl N-[(3-bromo-2- pyridyl)methyl]-N-(2-hydroxyethyl)carbamate as a colorless liquid (2.44 g, 77.0%). ES/MS (m/z): 331.0 (M+H). Step 3 tert-Butyl 3,5-dihydro-2H-pyrido[2,3-f][1,4]oxazepine-4-carboxylate tert-Butyl N-[(3-bromo-2-pyridyl)methyl]-N-(2-hydroxyethyl)carbamate (1.90 g, 8.26 mmol), palladium acetate (0.103 g , 0.45 mmol), 2-(di-t-butylphosphino)biphenyl (0.211 g, 0.69 mmol), and cesium carbonate (4.22 g, 13.0 mmol) were mixed in 1,4-dioxane (200 mL) and stirred at 95 °C for 16 hrs. The reaction mixture was diluted with EtOAc (50 mL) and washed with water (20 mL × 3). The organics were dried over sodium sulfate, filtered, and concentrated under reduced pressure. The residue was purified via silica gel chromatography (0-100% EtOAc in petroleum ether) to give tert-butyl 3,5-dihydro-2H-pyrido[2,3-f][1,4]oxazepine-4-carboxylate as a light-yellow oil (878 mg, 42.5%). ¹ H NMR (DMSO-d6) δ 8.16 (br d, J=3.5 Hz, 1H), 7.33 (br d, J=7.9 Hz, 1H), 7.22 (dd, J=4.6, 8.1 Hz, 1H), 4.66 (br s, 2H), 4.20 (br s, 2H), 3.73 (br s, 2H), 1.40 - 1.21 (m, 9H). Step 4 2,3,4,5-Tetrahydropyrido[2,3-f][1,4]oxazepine tert-Butyl 3,5-dihydro-2H-pyrido[2,3-f][1,4]oxazepine-4-carboxylate (800 mg, 3.20 mmol) was stirred in 1,4-dioxane (5 mL) and hydrogen chloride solution (4M in 1,4-dioxane, 521 mg) added. The mixture was stirred for 2 hrs at 20 °C. After this time, the reaction mixture was quenched with aqueous sodium bicarbonate solution to pH ~7, and concentrated under reduced pressure. This residue was purified via prep-TLC (6% MeOH in DCM) to give 2,3,4,5- tetrahydropyrido[2,3-f][1,4]oxazepine as a yellow oil (464 mg, 96.7%). ¹ H NMR (DMSO-d ₆ ) δ 8.22 (dd, J=1.4, 4.6 Hz, 1H), 7.44 (dd, J=1.3, 8.1 Hz, 1H), 7.29 (dd, J=4.7, 8.1 Hz, 1H), 4.21 (s, 2H), 4.16 - 4.10 (m, 2H), 3.28 (br s, 2H). Preparation 8 2,3,4,5-Tetrahydropyrido[4,3-f][1,4]oxazepine 2,3,4,5-Tetrahydropyrido[4,3-f][1,4]oxazepine was prepared using a method analogous to Preparation 7 using the corresponding appropriate reagents with the reaction time adjusted to reach completion, to give a colorless oil (70 mg, 50.6%). ES/MS (m/z): 151 (M+H).

Example 1 (7-Fluoro-1H-indazol-3-yl)-(1,2,3,5-tetrahydropyrido[4,3-e][ 1,4]diazepin-4-yl)methanone In DMF (1 mL), 2,3,4,5-tetrahydro-1H-pyrido[4,3-e][1,4]diazepine (40 mg, 0.22 mmol), 7-fluoro-1H-indazole-3-carboxylic acid (46 mg, 0.253 mmol), HATU (123 mg, 0.316 mmol), and DIEA (137 mg, 1.056 mmol) were added and stirred at 25 °C for 1 hr. After this time the mixture was concentrated under reduced pressure and purified via prep-HPLC to give (7-fluoro- 1H-indazol-3-yl)-(1,2,3,5-tetrahydropyrido[4,3-e][1,4]diazep in-4-yl)methanone as a white solid (13 mg, 24.9%). ES/MS (m/z): 312.0 (M+H). The compounds in Table 2 were prepared in a manner analogous to Example 1 using the corresponding appropriate reagents with the reaction time adjusted to reach completion.

Example 29 3,5-Dihydro-2H-pyrido[4,3-f][1,4]oxazepin-4-yl(1H-indazol-3- yl)methanone 2,3,4,5-Tetrahydropyrido[4,3-f][1,4]oxazepine (563 mg, 3.6 mmol) and 1H-indazole-3- carboxylic acid (584 mg, 3.6 mmol) were dissolved in 1,2-dichloroethane (10 mL). To this was added DIEA (1.86 g, 14.4 mmol) followed by T3P (4.56 g, 7.18 mmol), and the mixture was stirred at 80 °C for 12 hrs. The reaction mixture was concentrated under reduced pressure and purified via prep-HPLC (Phenomenex Luna® C1875*30mm*3µm; 0-35% water (ammonium carbonate)/ACN over 11 min; 25 mL/min) to give 3,5-dihydro-2H-pyrido[4,3-f][1,4]oxazepin-4- yl(1H-indazol-3-yl)methanone as a white solid (144.5 mg, 13.4%). ES/MS (m/z): 295 (M+H). ^{1H NMR (DMSO-d} ₆ ^{) δ 8.31 - 8.21 (m, 1H), 8.31 - 8.21 (m, 1H), 8.31 - 8.21 (m, 1H), 8.16 (br d,} J=4.5 Hz, 1H), 8.02 - 7.90 (m, 1H), 7.60 (d, J=8.5 Hz, 1H), 7.47 - 7.36 (m, 2H), 7.20 (t, J=7.6 Hz, 1H), 5.27 (s, 1H), 4.88 (s, 1H), 4.47 (br s, 1H), 4.40 - 4.30 (m, 2H), 4.12 (br s, 1H). Example 30 (2,3-Dihydropyrido[3,4-f][1,4]oxazepin-4(5H)-yl)(1,4,5,6-tet rahydrocyclopenta[c]pyrazol-3- yl)methanone 2,3,4,5-Tetrahydropyrido[3,4-f][1,4]oxazepine (248 mg, 1.65 mmol) and 1,4,5,6- tetrahydrocyclopenta[c]pyrazole-3-carboxylic acid (298 mg, 1.86 mmol) were dissolved in acetonitrile (8 mL). TCFH (562 mg, 1.96 mmol) was added followed by NMI (505 mg, 5.84 mmol), and the reaction mixture was stirred at ambient temperature for 24 hrs. The reaction mixture was concentrated under reduced pressure and the residue purified via prep-HPLC to give (2,3-dihydropyrido[3,4-f][1,4]oxazepin-4(5H)-yl)(1,4,5,6-tet rahydrocyclopenta[c]pyrazol-3- yl)methanone as a yellow solid (131 mg, 23.9%). ES/MS (m/z): 285.1 (M+H). Compounds 31-33 in Table 3 were prepared in a manner analogous to the method of Example 30 using the corresponding appropriate reagents with the reaction time adjusted to reach completion. Table 3. Examples 31 to 33 Example 34 3,5-Dihydro-2H-pyrido[3,2-f][1,4]oxazepin-4-yl(1H-indazol-3- yl)methanone 2,3,4,5-Tetrahydropyrido[3,2-f][1,4]oxazepine (470 mg, 2.97 mmol) and 1H-indazole-3- carboxylic acid (483 mg, 2.92 mmol) were dissolved in DCM (12 mL). DIEA (1.2 g, 8.9 mmol), HOBt (404 mg, 2.93 mmol), and EDCI (696 mg, 3.56 mmol) were added. The mixture was stirred at ambient temperature for 16 hrs. After this time, the reaction mixture was concentrated under reduced pressure, and the residue purified via prep-HPLC (A: water with 0.05% NH3 ^HI B: ACN; Column: Phenomenex Luna® 30*30mm*10µm+YMC AQ 100*30*10 µm; B% increases from 18% to 48% over 20 min; Flow Rate: 25 mL/min) to give 3,5-dihydro-2H- pyrido[3,2-f][1,4]oxazepin-4-yl(1H-indazol-3-yl)methanone as an off-white solid (170.95 mg, ^{18.95%). ES/MS (m/z): 295.0 (M+H). 1 NMR (DMSO-d} ₆ ^{) δ 13.51 (br s, –H), 8.14 - 8.05 (m,} –H), 8.00 - 7.91 (m, 1H), 7.85 (br d, J=7.0 Hz, 1H), 7.60 (d, J=8.5 Hz, –H), 7.43 - 7.37 (m, 1H), 7.19 (t, J=7.5 Hz, –H), 7.16 - 7.08 (m, 1H), 7.04 (br d, J=5.6 Hz, 1H), 5.24 (s, 1H), 4.86 (s, –H), 4.48 - 4.34 (m, 3H), 4.10 (br s, 1H). Example 35 hAHR Nuclear Translocation Assay [00067][0071] The purpose of this assay is to measure the ability of compounds to bind to, activate, and induce the translocation of AhR into the nucleus of a cell for transcription. Stable cell lines were established using Jump-In™ T-REx™ HEK293 Retargeting Kit (Life Technologies). Human AhR cDNA was cloned into the pJTI R4 CMV-TO EGFP vector. The EGFP was cloned to the C-terminal of AHR to form AhR-EGFP chimera. The pJTI R4 CMV- TO AhR-EGFP vector was transfected using FuGENE® HD into Jump-In™ T-REx™ HEK293 cells. Transfected cells were selected using 2.5 mg/ml G418 for 10 to 14 days, then expanded, harvested, and suspended in freeze media (FBS with 8% DMSO) at 2x10 ⁷ cells/ml, and aliquots were stored in liquid nitrogen. One day before the assay date, cells were thawed and resuspended in DMEM with 5% FBS in the presence of 1µg/ml Doxycycline and plated into ploy-L-Lysine coated CELLCARRIER-384 ULTRA Microplates (Perkin Elmer) at 12,000 to 15,000 cells per well and incubated at 37 °C and 5% CO ₂ overnight. On the assay date, compound was serially diluted (1:2) into 384-well nunc plates with DMSO using acoustic dispensing (ECHO®). The dose response was a 20-point curve. Compound was resuspended in 40 µl of DMEM plus 0.1% BSA. The culture media was damped and 25 µl of DMEM plus 0.1% BSA was added, then 25 µL of compound in DMEM plus 0.1% BSA was added into cell plates. Cells were incubated compounds at 37 °C and 5% CO2 for 45 minutes. The final DMSO concentration was 0.2%. The media was damped after 45 minutes incubation. The cells were fixed with 40 µl of cold MeOH (-20 °C) for 20 minutes. The MeOH was damped and 50 µL of DPBS containing 1 µg/mL Hochst was added into the cell plates. The intensity of EGFP was quantitated by using Opera PHENIX® or OPERETTA® high content image system (Perkin Elmer) with 20x Water Objective and five field per well. The ratio of EGFP fluorescent intensity in nuclear over cytosol was analyzed using a 4-parameter nonlinear logistic equation to determine the potency of AhR agonists. Table 3 shows the hAHR nuclear translocation assay EC ₅₀ values for the exemplified compounds. Table 4. hAHR Nuclear Translocation Assay EC50 Values Compounds 1-34 of the present disclosure are novel agonists of the aryl hydrocarbon receptor (AHR), as demonstrate by hAHR Nuclear Translocation Assay illustrated above. These compounds, particularly the compounds of Formula I, and the examples provided herein, are believed to be useful in the treatment of immune-mediated diseases (IMD), in particular psoriasis and atopic dermatitis, among others. Additional compounds, such as compounds of Table 1, may be tested with the same or similar protocol to determine their EC ₅₀ values.