PEPTIDE CONJUGATES OF THERAPEUTICS FIELD OF THE INVENTION The present invention relates to conjugates of therapeutic molecules (e.g., cytotoxic  agents) and targeting moieties (e.g., peptides), which are useful in the treatment of diseases such as cancer. BACKGROUND OF THE INVENTION Cancer is a group of diseases characterized by aberrant control of cell growth. The  annual incidence of cancer is estimated to be in excess of 1.6 million in the United States alone. While surgery, radiation, chemotherapy, and hormones are used to treat cancer, it remains the second leading cause of death in the U.S., and additional strategies of treatment are needed. Drug conjugates have emerged as a viable and continuously explored approach to target malignant tumors.   Despite advances in the selectivity of chemotherapy drugs over the past several decades, traditional cytotoxic chemotherapy drugs often lack sufficient specificity and targeting effects, causing injury to normal, non-cancerous cells which can lead to serious adverse reactions. Drug conjugates, comprised of a drug (e.g., a cytotoxic agent) linked to a targeting moiety (e.g., a peptide, protein, or antibody) have been developed for use in tumor  targeted therapy. Drug conjugates can provide for the preferential delivery of drug to diseased tissue, reducing undesired side effects such as damage to non-cancerous tissue. See, for example, Vrettos, V., “On the design principles of peptide—drug conjugates for targeted drug delivery to the malignant tumor site,” Beilstein J. Org. Chem.2018, 14:930-954. The development of linkers, groups which join the drug to the targeting moiety, has  emerged as an important aspect in the design of new drug conjugates. Some linkers may rely on the local physiological environment to release the drug component of the conjugate (e.g., a high glutathione concentration can lead to cleavage of a disulfide linker). In contrast, some linkers are more stable to these physiological conditions, providing higher stability of the conjugate in plasma. In addition, it has been shown that certain linkers with higher plasma  stability provide conjugates that exhibit reduced off-target toxicity compared to analogous, more cleavable linker conjugates. See Lu, J., “Linkers Having a Crucial Role in Antibody- Drug Conjugates,” Int. J. Mol. Sci.2016, 17, 1-22. Thus, there is a need for the development of new drug conjugates containing linkers that improve targeted drug delivery and reduce systemic drug toxicity. SUMMARY The present disclosure provides, inter alia, a compound of Formula (I): (I),   or a pharmaceutically acceptable salt thereof, wherein constituent variables are defined herein. The present disclosure further provides a pharmaceutical composition comprising a compound of the disclosure, or a pharmaceutically acceptable salt thereof, and at least one pharmaceutically acceptable carrier or excipient.   The present disclosure also provides methods of treating a disease or condition (e.g., cancer) by administering to a human or other mammal in need of such treatment a therapeutically effective amount of a compound of the disclosure. The present disclosure also provides use of a compound described herein in the manufacture of a medicament for use in therapy. The present disclosure also provides the  compounds described herein for use in therapy. The present disclosure also provides methods for synthesizing the compounds of the disclosure and intermediates useful in these methods. BRIEF DESCRIPTION OF THE DRAWINGS   FIG.1A shows a plot of efficacy (in terms of mean tumor volume) of nude mice bearing HCT116 colorectal carcinoma flank tumors after the indicated intraperitoneal doses of Compound 2 dosed for four total doses. FIG.1B shows a plot of the percent change in body weight of nude mice bearing HCT116 colorectal carcinoma flank tumors after the indicated intraperitoneal doses of  Compound 2 dosed for four total doses. FIG.2A shows a plot of efficacy (in terms of mean tumor volume) of nude mice bearing HCT116 colorectal carcinoma flank tumors after the indicated intraperitoneal doses of Compound 11 dosed for four total doses. FIG.2B shows a plot of the percent change in body weight of nude mice bearing  HCT116 colorectal carcinoma flank tumors after the indicated intraperitoneal doses of Compound 11 dosed for four total doses. FIG.3A shows a plot of efficacy (in terms of mean tumor volume) of nude mice bearing MKN45 gastric cancer tumors after the indicated intraperitoneal doses of Compound 1 dosed for four total doses. FIG.3B shows a plot of the percent change in body weight of nude mice bearing  MKN45 gastric cancer tumors after the indicated intraperitoneal doses of Compound 1 dosed for four total doses. DETAILED DESCRIPTION Provided herein is a compound of Formula (I):   (I), or a pharmaceutically acceptable salt thereof, wherein R ¹ is a peptide; R ² is a therapeutic moiety; L is selected from -(CH ₂ ) _p1 -Cy ¹ -(CH ₂ ) _p2 - and -X-Y-Z-;   Cy ¹ is selected from C6-10 aryl and 5-10 membered heteroaryl, wherein the C6-10 aryl and 5-10 membered heteroaryl are each optionally substituted with 1, 2, or 3 substituents independently selected from halo, CN, NO2, OR ^a1 , SR ^a1 , C(O)R ^b1 , C(O)NR ^c1 R ^d1 , C(O)OR ^a1 , OC(O)R ^b1 , OC(O)NR ^c1 R ^d1 , NR ^c1 R ^d1 , NR ^c1 C(O)R ^b1 , NR ^c1 C(O)OR ^a1 , and NR ^c1 C(O)NR ^c1 R ^d1 ; X is selected from , wherein  the N atom of X is t Y is -(CH ₂ CH ₂ O) _n1 (CH ₂ ) _n2 -; Z is selected from –N(R ^z )C(O)(CH2)o-, –N(R ^z )C(O)( CH=CH)-, and ,  wherein the N atom of Z is the point of attachment to Y;  R ^a1 , R ^b1 , R ^c1 , and R ^d1 are each independently selected from H, C1-6 alkyl, C2-6  alkenyl, C2-6 alkynyl, C1-6 haloalkyl, OH, CN, NO2, and CO2CH3; wherein said C1-6 alkyl and C2-6 alkenyl are each optionally substituted with OH, CN, NO2, or CO2CH3; R ^x is selected from H and C1-4 alkyl; R ^z is selected from H and C _1-4 alkyl; m is an integer from 0 to 4; n1 is an integer from 0 to 5; n2 is an integer from 2 to 10; o is an integer from 0 to 4;   p1 is an integer from 0 to 4; and p2 is an integer from 0 to 4. In some embodiments, L is -(CH2)p1-Cy ¹ -(CH2)p2-. In some embodiments, Cy ¹ is C _6-10 aryl optionally substituted with 1, 2, or 3 substituents independently selected from halo, CN, NO2, OR ^a1 , SR ^a1 , C(O)R ^b1 , C(O)NR ^c1 R ^d1 ,  C(O)OR ^a1 , OC(O)R ^b1 , OC(O)NR ^c1 R ^d1 , NR ^c1 R ^d1 , NR ^c1 C(O)R ^b1 , NR ^c1 C(O)OR ^a1 , and NR ^c1 C(O)NR ^c1 R ^d1 . In some embodiments, Cy ¹ is phenyl optionally substituted with 1, 2, or 3 substituents independently selected from halo, CN, NO2, OR ^a1 , SR ^a1 , C(O)R ^b1 , C(O)NR ^c1 R ^d1 , C(O)OR ^a1 , OC(O)R ^b1 , OC(O)NR ^c1 R ^d1 , NR ^c1 R ^d1 , NR ^c1 C(O)R ^b1 , NR ^c1 C(O)OR ^a1 , and NR ^c1 C(O)NR ^c1 R ^d1 .  In some embodiments, Cy ¹ is phenyl. In some embodiments, p1 is 1 or 2. In some embodiments, p1 is 1. In some embodiments, p2 is 1 or 2. In some embodiments, p2 is 1. In some embodiments, p1 and p2 are each 1. In some embodiments, L is:   . In some embodiments, L is -X In some embodiments, X is -(CH2)mC(O)NR ^x -. In some embodiments, X is -(CH=CH)-C(O)NRx-. In some embodiment .     In some embodiment In some embodiments, m is an integer from 1 to 4. In some embodiments, m is 1 or 2. In some embodiments, m is 1. In some embodiments, m is 0. In some embodiments, n1 is an integer from 1 to 5. In some embodiments, n1 is 0. In some embodiments, n1 is 1. In some embodiments, n1 is 1, 2, or 3. In some embodiments, n2 is an integer from 2 to 8. In some embodiments, n2 is an integer from 4 to 8. In some embodiments, n2 is 2. In some embodiments, n2 is 4, 6, or 8. In  some embodiments, n2 is 4. In some embodiments, n2 is 6. In some embodiments, n2 is 8. In some embodiments, Z is –N(R ^z )C(O)(CH ₂ ) _o -. In some embodiments, Z is –N(R ^z )C(O)( CH=CH)-. In some embodiment .    In some embodiments, R ^z is H. In some embodiments, o is 0. In some embodiments, o is an integer from 1 to 4. In some embodiments, o is 1. In some embodiments, L is selected from the following:   , O ,   d . ents, L has the following structure: , n.   As used herein, “peptide” refers to a targeting moiety comprising a 10-50 amino acid sequence, made up of naturally-occurring amino acid residues and optionally one or more non-naturally-occurring amino acids. In some embodiments, the peptide of R ¹ is a peptide of 20 to 40 amino acid residues, 20 to 30 amino acid residues, or 30 to 40 amino acid residues. In some embodiments, the peptide is capped. For example the peptide may include an N-  terminal cap at the amino terminus such as an N-terminal acetyl group. In some embodiments, the peptide is capped at the carboxy terminus, for example, the carboxylic acid group can be converted to a carboxy ester or amide group. Additionally, the peptide may contain amino acids in which one or more amino acid side chains includes a protecting group. In some embodiments, the targeting moiety is a conformationally restricted peptide. A  conformationally restricted peptide can include, for example, macrocyclic peptides and stapled peptides. A stapled peptide is a peptide constrained by a covalent linkage between two amino acid side-chains, forming a peptide macrocycle. Conformationally restricted peptides are described, for example, in Guerlavais et al., Annual Reports in Medicinal Chemistry 2014, 49, 331-345; Chang et al., Proceedings of the National Academy of  Sciences of the United States of America (2013), 110(36), E3445-E3454; Tesauro et al., Molecules 2019, 24, 351-377; Dougherty et al., Journal of Medicinal Chemistry (2019), 62(22), 10098-10107; and Dougherty et al., Chemical Reviews (2019), 119(17), 10241- 10287, each of which is incorporated herein by reference in its entirety. In some embodiments, the targeting moiety is an environmentally sensitive peptide  described, for example, in U.S. Pat. Nos.8,076,451 and 9,289,508 and U.S. Pat. Pub. No. 2019/209580 (each of which are incorporated herein by reference in their entirety), although other peptides capable of such selective insertion could be used. Other suitable peptides are described, for example, in Weerakkody, et al., PNAS 110 (15), 5834-5839 (April 9, 2013), which is also incorporated herein by reference in its entirety. Without being bound by theory,  it is believed that the environmentally sensitive peptide undergoes a conformational change and inserts across cell membranes in response to physiological changes (e.g., pH). The peptide can target acidic tissue and selectively translocate polar, cell-impermeable molecules across cell membranes in response to low extracellular pH. In some embodiments, R ¹ is a peptide capable of selectively delivering R ² L- across a  cell membrane having an acidic or hypoxic mantle. In some embodiments, the peptide is capable of selectively delivering molecules across a cell membrane having an acidic or hypoxic mantle having a pH less than about 6.0. In some embodiments, the peptide is capable of selectively delivering a molecule across a cell membrane having an acidic or hypoxic mantle having a pH less than about 6.5. In some embodiments, the peptide is capable of  selectively delivering a molecule across a cell membrane having an acidic or hypoxic mantle having a pH less than about 5.5. In some embodiments, the peptide is capable of selectively delivering a molecule across a cell membrane having an acidic or hypoxic mantle having a pH between about 5.0 and about 6.0. The term acidic and/or hypoxic mantle refers to the environment of the cell in the diseased tissue in question having a pH lower than 7.0 and preferably lower than 6.5. An acidic or hypoxic mantle more preferably has a pH of about 5.5 and most preferably has a pH of about 5.0. The compounds of formula (I) insert across a cell membrane   having an acidic and/or hypoxic mantle in a pH dependent fashion to insert R ² - into the cell. Since the compounds of formula (I) are pH-dependent, they preferentially insert across a cell membrane only in the presence of an acidic or hypoxic mantle surrounding the cell and not across the cell membrane of “normal” cells, which do not have an acidic or hypoxic mantle. An example of a cell having an acidic or hypoxic mantle is a cancer cell.  The terms “pH-sensitive” or “pH-dependent” as used herein to refer to the peptide R ¹ or to the mode of insertion of the peptide R ¹ or of the compounds of the invention across a cell membrane, means that the peptide has a higher affinity to a cell membrane lipid bilayer having an acidic or hypoxic mantle than a membrane lipid bilayer at neutral pH. Thus, the compounds of the invention preferentially insert through the cell membrane  to insert R ² - to the interior of the cell (and thus deliver R ² H as described above) when the cell membrane lipid bilayer has an acidic or hypoxic mantle (a “diseased” cell) but does not insert through a cell membrane when the mantle (the environment of the cell membrane lipid bilayer) is not acidic or hypoxic (a “normal” cell). It is believed that this preferential insertion is achieved as a result of the peptide R ¹ forming a helical   configuration, which facilitates membrane insertion. In some embodiments, the environmentally sensitive peptide comprises at least one of the following sequences: ADDQNPWRAYLDLLFPTDTLLLDLLWCG (SEQ ID NO.1; Pv1), AEQNPIYWARYADWLFTTPLLLLDLALLVDADECG (SEQ ID NO.2; Pv2);  ADDQNPWRAYLDLLFPTDTLLLDLLWDADECG (SEQ ID NO.3; Pv3); Ac-AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTKCG (SEQ ID NO. 4; Pv4); and AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTC (SEQ ID No.5; Pv5). In some embodiments, the environmentally sensitive peptide comprises at least one of  the following sequences: ADDQNPWRAYLDLLFPTDTLLLDLLWCG (SEQ ID NO.1; Pv1), AEQNPIYWARYADWLFTTPLLLLDLALLVDADECG (SEQ ID NO. 2; Pv2), and ADDQNPWRAYLDLLFPTDTLLLDLLWDADECG (SEQ ID NO.3; Pv3). In some embodiments, the environmentally sensitive peptide comprises the sequence ADDQNPWRAYLDLLFPTDTLLLDLLWCG (SEQ ID NO.1; Pv1).   In some embodiments, the environmentally sensitive peptide comprises the sequence AEQNPIYWARYADWLFTTPLLLLDLALLVDADECG (SEQ ID NO.2; Pv2). In some embodiments, the environmentally sensitive peptide comprises the sequence ADDQNPWRAYLDLLFPTDTLLLDLLWDADECG (SEQ ID NO.3; Pv3). In some embodiments, the environmentally sensitive peptide comprises the sequence  Ac-AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTKCG (SEQ ID NO.4; Pv4). In some embodiments, the environmentally sensitive peptide comprises the sequence AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTC (SEQ ID NO.5; Pv5). In some embodiments, the environmentally sensitive peptide consists essentially of the sequence ADDQNPWRAYLDLLFPTDTLLLDLLWCG (SEQ ID NO.1; Pv1).   In some embodiments, the environmentally sensitive peptide consists essentially of the sequence AEQNPIYWARYADWLFTTPLLLLDLALLVDADECG (SEQ ID NO.2; Pv2). In some embodiments, the environmentally sensitive peptide consists essentially of the sequence ADDQNPWRAYLDLLFPTDTLLLDLLWDADECG (SEQ ID NO.3; Pv3).  In some embodiments, the environmentally sensitive peptide consists essentially of the sequence AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTKCG (SEQ ID NO. 4; Pv4). In some embodiments, the environmentally sensitive peptide consists essentially of the sequence AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTC (SEQ ID NO.5;  Pv5). Additional environmentally sensitive peptides are disclosed in in U.S. Patent Publication No. US 2019/209580, U.S. Patent Application No.16/925,094, U.S. Patent Application No.16/924,445, and WO 2020/160009 each of which is incorporated herein in its entirety.   The term “therapeutic moiety” refers to a moiety (e.g., R ² -) derived from a therapeutic molecule or agent. Suitable therapeutic molecules (e.g., R ² H) for use in the invention include cytotoxic agents (e.g., PARP inhibitors, topoisomerase I inhibitors, and maytansinoids) which have undesirable side effects when delivered systemically because of their possible deleterious effect on normal tissue. Three PARP inhibitors (olaparib, rucaparib, and niraparib) are currently commercially available and others are in development, such as AG-014699 (Agouron/Pfizer), KU-0059436 (KuDOS/AstraZeneca), INO-1001 (Inotek/Genentech), NT-125 (now E-7449; Eisai; 3H-Pyridazino[3,4,5-de]quinazolin-3-one, 8-[(1,3-dihydro-  2H-isoindol-2-yl)methyl]-1,2-dihydro-), 2X-121 (2X Oncology; 3H-pyridazino[3,4,5- de]quinazolin-3-one, 8-[(1,3-dihydro-2H-isoindol-2-yl)methyl]-1,2-dihydro-), and ABT- 888 (Abbvie). PARP inhibitors are disclosed in (for example) United States patents 6,100,283; 6,310,082; 6,495,541; 6,548,494; 6,696,437; 7,151,102; 7,196,085; 7,449,464; 7,692,006; 7,781,596; 8,067,613; 8,071,623; and 8,697,736, which patents are   incorporated herein by reference in their entirety. Compounds of Formula (I) containing a PARP inhibitor moiety are described in U.S. Patent Publication No. US 2019/209580. The term “small molecule topoisomerase I targeting moiety” or “topoisomerase I inhibitor” refers to a chemical group that binds to topoisomerase I. The small molecule  topoisomerase I targeting moiety can be a group derived from a compound that inhibits the activity of topoisomerase I. Topoisomerase inhibitors include camptothecin and derivatives and analogues thereof such as opotecan, irinotecan (CPT-11), silatecan (DB- 67, AR-67), cositecan (BNP-1350), lurtotecan, gimatecan (ST1481), belotecan (CKD- 602), rubitecan, topotecan, deruxtecan, and exatecan. Topoisomerase inhibitors are   described in, for example, Ogitani, Bioorg. Med. Chem. Lett.26 (2016), 5069-5072; Kumazawa, E., Cancer Chemother Pharmacol 1998, 42: 210-220; Tahara, M, Mol Cancer Ther 2014, 13(5): 1170-1180; Nakada, T., Bioorganic & Medicinal Chemistry Letters 2016, 26: 1542-1545. Compounds of Formula (I) having a topoisomerase I targeting moiety are described in  U.S. Patent Application No.16/925,094. In some embodiments of compounds of Formula (I), R ² is camptothecin, opotecan, irinotecan (CPT-11), silatecan (DB-67, AR-67), cositecan (BNP-1350), lurtotecan, gimatecan (ST1481), belotecan (CKD-602), rubitecan, topotecan, deruxtecan, or exatecan. In some embodiments of compounds of Formula (I), R ² is exatecan. Suitable small molecule microtubule targeting moieties (e.g., R ² ) can be cytotoxic  compounds like maytansinoids that may have undesirable side effects when delivered systemically because of their possible deleterious effect on normal tissue. Small molecule microtubule targeting agents include, but are not limited to, maytansinoids, aclitaxel, docetaxel, epothilones, discodermolide, the vinca alkaloids, colchicine, combretastatins, and derivatives and analogues of the aforementioned. Microtubule targeting agents are described in Tangutur, A. D., Current Topics in Medicinal Chemistry, 201717(22): 2523- 2537. Microtubule-targeting agents also include maytansinoids, such as maytansine (DM1) and derivatives and analogues thereof, which are described in Lopus, M, Cancer Lett., 2011, 307(2): 113-118; and Widdison, W., J. Med. Chem.2006, 49:4392-4408.   Compounds of Formula (I) having a microtubule targeting moiety are described in U.S. Patent Application No.16/924,445. In some embodiments, R ² is a maytansinoid. In some embodiments, R ² is DM1 or DM4. In some embodiments, R ² is DM1. In some embodiments, R ² is DM4. In some embodiments, R ² is:   .     In some embodiments, the compound of the invention has the formula:

nd  orementioned. In some embodiments, the compound of the invention has the formula:  , ,   , ,   y acceptable salt of any of the aforementioned. In some embodiments, the compound of the invention has the formula: , 

, ,

, ,

, ,

d , rementioned.  In some embodiments, the compound of formula (I) is selected from: , 

, , O O NH  

d or a pharmaceutically acceptable salt of any of the aforementioned. In some embodiments, the peptide of R ¹ includes a N-terminal cap, a C-terminal cap, an amino acid side chain  protecting group, or a combination thereof. Intermediates In some embodiments, provided herein is a compound of Formula (II): (I),   or a pharmaceutically acceptable salt thereof, wherein R ² is a therapeutic moiety; L’ is selected from -(CH2)p1-Cy ¹ -(CH2)p2R ^LG and -X-Y-Z’-; Cy ¹ is selected from C _6-10 aryl and 5-10 membered heteroaryl, wherein the C _6-10 aryl and 5-10 membered heteroaryl are each optionally substituted with 1, 2, or 3 substituents  independently selected from halo, CN, NO ₂ , OR ^a1 , SR ^a1 , C(O)R ^b1 , C(O)NR ^c1 R ^d1 , C(O)OR ^a1 , OC(O)R ^b1 , OC(O)NR ^c1 R ^d1 , NR ^c1 R ^d1 , NR ^c1 C(O)R ^b1 , NR ^c1 C(O)OR ^a1 , and NR ^c1 C(O)NR ^c1 R ^d1 ; X is selected from , wherein the N atom of X is t Y is -(CH ₂ CH ₂ O) _n1 (CH ₂ ) _n2 -; Z’ is selected fro ,   wherein the N atom R ^LG is halo;   R ^a1 , R ^b1 , R ^c1 , and R ^d1 are each independently selected from H, C _1-6 alkyl, C _2-6 alkenyl, C2-6 alkynyl, C1-6 haloalkyl, OH, CN, NO2, and CO2CH3; wherein said C1-6 alkyl and C2-6 alkenyl are each optionally substituted with OH, CN, NO2, or CO2CH3;   R ^x is selected from H and C1-4 alkyl; R ^z is selected from H and C1-4 alkyl; m is an integer from 0 to 4; n1 is an integer from 0 to 5; n2 is an integer from 2 to 10;   o is an integer from 0 to 4; p1 is an integer from 0 to 4; and p2 is an integer from 0 to 4. In some embodiments, the compound of Formula (II) has the formula:   , ,   , y acceptable salt of any of the aforementioned.   In some embodiments, the compound of Formula (II) has the formula: O H ^N ,

, O HN , , , , mentioned.   The molecules of the invention can be tagged, for example, with a probe such as a fluorophore, radioisotope, and the like. In some embodiments, the probe is a fluorescent probe, such as LICOR. A fluorescent probe can include any moiety that can re-emit light upon light excitation (e.g., a fluorophore).   The Amino acids are represented by the IUPAC abbreviations, as follows: Alanine (Ala; A), Arginine (Arg; R), Asparagine (Asn; N), Aspartic acid (Asp; D), Cysteine (Cys; C), Glutamine (Gln; Q), Glutamic acid (Glu; E), Glycine (Gly; G), Histidine (His; H), Isoleucine (Ile; I), Leucine (Leu; L), Lysine (Lys; K), Methionine (Met; M), Phenylalanine (Phe; F), Proline (Pro; P), Serine (Ser; S), Threonine (Thr; T), Tryptophan (Trp; W), Tyrosine (Tyr; Y), Valine (Val; V). The term “Pv1” means ADDQNPWRAYLDLLFPTDTLLLDLLWCG, which is  the peptide of SEQ ID No.1. The term “Pv2” means AEQNPIYWARYADWLFTTPLLLLDLALLVDADECG, which is the peptide of SEQ ID No.2. The term “Pv3” means ADDQNPWRAYLDLLFPTDTLLLDLLWDADECG, which is the peptide of SEQ ID No.3.   The term “Pv4” means Ac- AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTKCG, which is the peptide of SEQ ID NO.4. The term “Pv5” means AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGTC, which is the peptide of  SEQ ID NO.5. The term “Pv6” means AAEQNPIYWWARYADWLFTTPLLLLDLALLVDADEGTCG, which is the peptide of SEQ ID NO.6. In the compounds of the invention, the peptides R ¹ are attached to L through a cysteine moiety of R ¹ .   It is further appreciated that certain features of the invention, which are, for clarity, described in the context of separate embodiments, can also be provided in combination in a single embodiment (while the embodiments are intended to be combined as if written in multiply dependent form). Conversely, various features of the invention which are, for brevity, described in the context of a single embodiment, can also be provided separately or  in any suitable subcombination. Thus, it is contemplated as features described as embodiments of the compounds of Formula (I) can be combined in any suitable combination. At various places in the present specification, certain features of the compounds are disclosed in groups or in ranges. It is specifically intended that such a disclosure include each and every individual subcombination of the members of such groups and ranges. For  example, the term "C1-6 alkyl" is specifically intended to individually disclose (without limitation) methyl, ethyl, C ₃ alkyl, C ₄ alkyl, C ₅ alkyl and C ₆ alkyl. The term "n-membered," where n is an integer, typically describes the number of ring-forming atoms in a moiety where the number of ring-forming atoms is n. For example, piperidinyl is an example of a 6-membered heterocycloalkyl ring, pyrazolyl is an example of a 5-membered heteroaryl ring, pyridyl is an example of a 6-membered heteroaryl ring and 1,2,3,4-tetrahydro-naphthalene is an example of a 10-membered cycloalkyl group. At various places in the present specification, variables defining divalent linking groups may be described. It is specifically intended that each linking substituent include both  the forward and backward forms of the linking substituent. For example, -NR(CR'R'')n- includes both -NR(CR'R'') _n - and -(CR'R'') _n NR- and is intended to disclose each of the forms individually. Where the structure requires a linking group, the Markush variables listed for that group are understood to be linking groups. For example, if the structure requires a linking group and the Markush group definition for that variable lists "alkyl" or "aryl" then it  is understood that the "alkyl" or "aryl" represents a linking alkylene group or arylene group, respectively. The term "substituted" means that an atom or group of atoms formally replaces hydrogen as a "substituent" attached to another group. The term "substituted", unless otherwise indicated, refers to any level of substitution, e.g., mono-, di-, tri-, tetra- or   penta-substitution, where such substitution is permitted. The substituents are independently selected, and substitution may be at any chemically accessible position. It is to be understood that substitution at a given atom is limited by valency. It is to be understood that substitution at a given atom results in a chemically stable molecule. The phrase "optionally substituted" means unsubstituted or substituted. The term "substituted" means that a hydrogen atom is  removed and replaced by a substituent. A single divalent substituent, e.g., oxo, can replace two hydrogen atoms. The term "Cn-m" indicates a range which includes the endpoints, wherein n and m are integers and indicate the number of carbons. Examples include C _1-4 , C _1-6 and the like. The term "alkyl" employed alone or in combination with other terms, refers to a  saturated hydrocarbon group that may be straight-chained or branched. The term "C _n-m alkyl", refers to an alkyl group having n to m carbon atoms. An alkyl group formally corresponds to an alkane with one C-H bond replaced by the point of attachment of the alkyl group to the remainder of the compound. In some embodiments, the alkyl group contains from 1 to 6 carbon atoms, from 1 to 4 carbon atoms, from 1 to 3 carbon atoms, or 1 to 2 carbon atoms.  Examples of alkyl moieties include, but are not limited to, chemical groups such as methyl, ethyl, n-propyl, isopropyl, n-butyl, tert-butyl, isobutyl, sec-butyl; higher homologs such as 2- methyl-1-butyl, n-pentyl, 3-pentyl, n-hexyl, 1,2,2-trimethylpropyl and the like. The term "alkenyl" employed alone or in combination with other terms, refers to a straight-chain or branched hydrocarbon group corresponding to an alkyl group having one or more double carbon-carbon bonds. An alkenyl group formally corresponds to an alkene with one C-H bond replaced by the point of attachment of the alkenyl group to the remainder of the compound. The term "Cn-m alkenyl" refers to an alkenyl group having n to m carbons. In some embodiments, the alkenyl moiety contains 2 to 6, 2 to 4, or 2 to 3 carbon atoms.   Example alkenyl groups include, but are not limited to, ethenyl, n-propenyl, isopropenyl, n- butenyl, sec-butenyl and the like. The term "alkylene", employed alone or in combination with other terms, refers to a divalent alkyl linking group. An alkylene group formally corresponds to an alkane with two C-H bond replaced by points of attachment of the alkylene group to the remainder of the  compound. The term "C _n-m alkylene" refers to an alkylene group having n to m carbon atoms. Examples of alkylene groups include, but are not limited to, ethan-1,2-diyl, ethan-1,1-diyl, propan-1,3-diyl, propan-1,2-diyl, propan-1,1-diyl, butan-1,4-diyl, butan-1,3-diyl, butan-1,2- diyl, 2-methyl-propan-1,3-diyl and the like. The term "amino" refers to a group of formula –NH2.   The term "carbonyl", employed alone or in combination with other terms, refers to a -C(=O)- group, which also may be written as C(O). The term "cyano" or "nitrile" refers to a group of formula –C≡N, which also may be written as -CN. The terms "halo" or "halogen", used alone or in combination with other terms, refers  to fluoro, chloro, bromo and iodo. In some embodiments, "halo" refers to a halogen atom selected from F, Cl, or Br. In some embodiments, halo groups are F. The term "haloalkyl" as used herein refers to an alkyl group in which one or more of the hydrogen atoms has been replaced by a halogen atom. The term "C _n-m haloalkyl" refers to a Cn-m alkyl group having n to m carbon atoms and from at least one up to {2(n to m)+1}  halogen atoms, which may either be the same or different. In some embodiments, the halogen atoms are fluoro atoms. In some embodiments, the haloalkyl group has 1 to 6 or 1 to 4 carbon atoms. Example haloalkyl groups include CF ₃ , C ₂ F ₅ , CHF ₂ , CH ₂ F, CCl ₃ , CHCl ₂ , C ₂ Cl ₅ and the like. In some embodiments, the haloalkyl group is a fluoroalkyl group. The term "haloalkoxy", employed alone or in combination with other terms, refers to  a group of formula -O-haloalkyl, wherein the haloalkyl group is as defined above. The term "C _n-m haloalkoxy" refers to a haloalkoxy group, the haloalkyl group of which has n to m carbons. Example haloalkoxy groups include trifluoromethoxy and the like. In some embodiments, the haloalkoxy group has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. The term "oxo" refers to an oxygen atom as a divalent substituent, forming a carbonyl group when attached to carbon, or attached to a heteroatom forming a sulfoxide or sulfone group, or an N-oxide group. In some embodiments, heterocyclic groups may be optionally substituted by 1 or 2 oxo (=O) substituents.   The term “oxidized” in reference to a ring-forming N atom refers to a ring-forming N-oxide. The term “oxidized” in reference to a ring-forming S atom refers to a ring-forming sulfonyl or ring-forming sulfinyl. The term "aromatic" refers to a carbocycle or heterocycle having one or more  polyunsaturated rings having aromatic character (i.e., having (4n + 2) delocalized ^ (pi) electrons where n is an integer). The term "aryl," employed alone or in combination with other terms, refers to an aromatic hydrocarbon group, which may be monocyclic or polycyclic (e.g., having 2 fused rings). The term "Cn-m aryl" refers to an aryl group having from n to m ring carbon atoms.  Aryl groups include, e.g., phenyl, naphthyl, and the like. In some embodiments, aryl groups have from 6 to about 10 carbon atoms. In some embodiments aryl groups have 6 carbon atoms. In some embodiments aryl groups have 10 carbon atoms. In some embodiments, the aryl group is phenyl. The term "heteroaryl" or "heteroaromatic," employed alone or in combination with  other terms, refers to a monocyclic or polycyclic aromatic heterocycle having at least one heteroatom ring member selected from sulfur, oxygen and nitrogen. In some embodiments, the heteroaryl ring has 1, 2, 3 or 4 heteroatom ring members independently selected from nitrogen, sulfur and oxygen. In some embodiments, any ring-forming N in a heteroaryl moiety can be an N-oxide. In some embodiments, the heteroaryl has 5-14 ring atoms  including carbon atoms and 1, 2, 3 or 4 heteroatom ring members independently selected from nitrogen, sulfur and oxygen. In some embodiments, the heteroaryl has 5-10 ring atoms including carbon atoms and 1, 2, 3 or 4 heteroatom ring members independently selected from nitrogen, sulfur and oxygen. In some embodiments, the heteroaryl has 5-6 ring atoms and 1 or 2 heteroatom ring members independently selected from nitrogen, sulfur and  oxygen. In some embodiments, the heteroaryl is a five-membered or six-membered heteroaryl ring. In other embodiments, the heteroaryl is an eight-membered, nine-membered or ten-membered fused bicyclic heteroaryl ring. A five-membered heteroaryl ring is a heteroaryl group having five ring atoms wherein one or more (e.g., 1, 2 or 3) ring atoms are independently selected from N, O and S. A six-membered heteroaryl ring is a heteroaryl group having six ring atoms wherein one or more (e.g., 1, 2 or 3) ring atoms are independently selected from N, O and S. The term "cycloalkyl," employed alone or in combination with other terms, refers to a non-aromatic hydrocarbon ring system (monocyclic, bicyclic or polycyclic), including  cyclized alkyl and alkenyl groups. The term "Cn-m cycloalkyl" refers to a cycloalkyl that has n to m ring member carbon atoms. Cycloalkyl groups can include mono- or polycyclic (e.g., having 2, 3 or 4 fused rings) groups and spirocycles. Cycloalkyl groups can have 3, 4, 5, 6 or 7 ring-forming carbons (C _3-7 ). In some embodiments, the cycloalkyl group has 3 to 6 ring members, 3 to 5 ring members, or 3 to 4 ring members. In some embodiments, the cycloalkyl  group is monocyclic. In some embodiments, the cycloalkyl group is monocyclic or bicyclic. In some embodiments, the cycloalkyl group is a C3-6 monocyclic cycloalkyl group. Ring- forming carbon atoms of a cycloalkyl group can be optionally oxidized to form an oxo or sulfido group. Cycloalkyl groups also include cycloalkylidenes. In some embodiments, cycloalkyl is cyclopropyl, cyclobutyl, cyclopentyl or cyclohexyl. Also included in the  definition of cycloalkyl are moieties that have one or more aromatic rings fused (i.e., having a bond in common with) to the cycloalkyl ring, e.g., benzo or thienyl derivatives of cyclopentane, cyclohexane and the like. A cycloalkyl group containing a fused aromatic ring can be attached through any ring-forming atom including a ring-forming atom of the fused aromatic ring. Examples of cycloalkyl groups include cyclopropyl, cyclobutyl, cyclopentyl,  cyclohexyl, cycloheptyl, cyclopentenyl, cyclohexenyl, cyclohexadienyl, and the like. In some embodiments, the cycloalkyl group is cyclopropyl, cyclobutyl, cyclopentyl, or cyclohexyl. At certain places, the definitions or embodiments refer to specific rings (e.g., an azetidine ring, a pyridine ring, etc.). Unless otherwise indicated, these rings can be attached to any ring member provided that the valency of the atom is not exceeded. For example, an  azetidine ring may be attached at any position of the ring, whereas an azetidin-3-yl ring is attached at the 3-position. The compounds described herein can be asymmetric (e.g., having one or more stereocenters). All stereoisomers, such as enantiomers and diastereomers, are intended unless otherwise indicated. Compounds of the present invention that contain asymmetrically  substituted carbon atoms can be isolated in optically active or racemic forms. Methods on how to prepare optically active forms from optically inactive starting materials are known in the art, such as by resolution of racemic mixtures or by stereoselective synthesis. Many geometric isomers of olefins, C=N double bonds and the like can also be present in the compounds described herein, and all such stable isomers are contemplated in the present invention. Cis and trans geometric isomers of the compounds of the present invention are described and may be isolated as a mixture of isomers or as separated isomeric forms. Resolution of racemic mixtures of compounds can be carried out by any of numerous methods known in the art. One method includes fractional recrystallization using a chiral  resolving acid which is an optically active, salt-forming organic acid. Suitable resolving agents for fractional recrystallization methods are, e.g., optically active acids, such as the D and L forms of tartaric acid, diacetyltartaric acid, dibenzoyltartaric acid, mandelic acid, malic acid, lactic acid or the various optically active camphorsulfonic acids such as α- camphorsulfonic acid. Other resolving agents suitable for fractional crystallization methods  include stereoisomerically pure forms of α-methylbenzylamine (e.g., S and R forms, or diastereomerically pure forms), 2-phenylglycinol, norephedrine, ephedrine, N- methylephedrine, cyclohexylethylamine, 1,2-diaminocyclohexane and the like. Resolution of racemic mixtures can also be carried out by elution on a column packed with an optically active resolving agent (e.g., dinitrobenzoylphenylglycine). Suitable elution  solvent composition can be determined by one skilled in the art. In some embodiments, the compounds of the invention have the (R)-configuration. In other embodiments, the compounds have the (S)-configuration. In compounds with more than one chiral centers, each of the chiral centers in the compound may be independently (R) or (S), unless otherwise indicated.   Compounds of the invention also include tautomeric forms. Tautomeric forms result from the swapping of a single bond with an adjacent double bond together with the concomitant migration of a proton. Tautomeric forms include prototropic tautomers which are isomeric protonation states having the same empirical formula and total charge. Example prototropic tautomers include ketone – enol pairs, amide - imidic acid pairs, lactam – lactim  pairs, enamine – imine pairs, and annular forms where a proton can occupy two or more positions of a heterocyclic system, e.g., 1H- and 3H-imidazole, 1H-, 2H- and 4H- 1,2,4- triazole, 1H- and 2H- isoindole and 1H- and 2H-pyrazole. Tautomeric forms can be in equilibrium or sterically locked into one form by appropriate substitution. Compounds of the invention can also include all isotopes of atoms occurring in the  intermediates or final compounds. Isotopes include those atoms having the same atomic number but different mass numbers. For example, isotopes of hydrogen include tritium and deuterium. One or more constituent atoms of the compounds of the invention can be replaced or substituted with isotopes of the atoms in natural or non-natural abundance. In some embodiments, the compound includes at least one deuterium atom. For example, one or more hydrogen atoms in a compound of the present disclosure can be replaced or substituted by deuterium. In some embodiments, the compound includes two or more deuterium atoms. In some embodiments, the compound includes 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11 or 12 deuterium atoms. Synthetic methods for including isotopes into organic compounds are known in the art  (Deuterium Labeling in Organic Chemistry by Alan F. Thomas (New York, N.Y., Appleton- Century-Crofts, 1971; The Renaissance of H/D Exchange by Jens Atzrodt, Volker Derdau, Thorsten Fey and Jochen Zimmermann, Angew. Chem. Int. Ed.2007, 7744-7765; The Organic Chemistry of Isotopic Labelling by James R. Hanson, Royal Society of Chemistry, 2011). Isotopically labeled compounds can used in various studies such as NMR   spectroscopy, metabolism experiments, and/or assays. Substitution with heavier isotopes such as deuterium, may afford certain therapeutic advantages resulting from greater metabolic stability, for example, increased in vivo half-life or reduced dosage requirements, and hence may be preferred in some circumstances. (A. Kerekes et.al. J. Med. Chem.2011, 54, 201-210; R. Xu et.al. J. Label Compd. Radiopharm.  2015, 58, 308-312). The term, "compound," as used herein is meant to include all stereoisomers, geometric isomers, tautomers and isotopes of the structures depicted. The term is also meant to refer to compounds of the inventions, regardless of how they are prepared, e.g., synthetically, through biological process (e.g., metabolism or enzyme conversion), or a  combination thereof. All compounds, and pharmaceutically acceptable salts thereof, can be found together with other substances such as water and solvents (e.g., hydrates and solvates) or can be isolated. When in the solid state, the compounds described herein and salts thereof may occur in various forms and may, e.g., take the form of solvates, including hydrates. The compounds  may be in any solid state form, such as a polymorph or solvate, so unless clearly indicated otherwise, reference in the specification to compounds and salts thereof should be understood as encompassing any solid state form of the compound. In some embodiments, the compounds of the invention, or salts thereof, are substantially isolated. By "substantially isolated" is meant that the compound is at least  partially or substantially separated from the environment in which it was formed or detected. Partial separation can include, e.g., a composition enriched in the compounds of the invention. Substantial separation can include compositions containing at least about 50%, at least about 60%, at least about 70%, at least about 80%, at least about 90%, at least about 95%, at least about 97%, or at least about 99% by weight of the compounds of the invention, or salt thereof. The phrase "pharmaceutically acceptable" is employed herein to refer to those compounds, materials, compositions and/or dosage forms which are, within the scope of  sound medical judgment, suitable for use in contact with the tissues of human beings and animals without excessive toxicity, irritation, allergic response, or other problem or complication, commensurate with a reasonable benefit/risk ratio. The expressions, "ambient temperature" and "room temperature," as used herein, are understood in the art, and refer generally to a temperature, e.g., a reaction temperature, that is  about the temperature of the room in which the reaction is carried out, e.g., a temperature from about 20 ºC to about 30 ºC. The present invention also includes pharmaceutically acceptable salts of the compounds described herein. The term "pharmaceutically acceptable salts" refers to derivatives of the disclosed compounds wherein the parent compound is modified by  converting an existing acid or base moiety to its salt form. Examples of pharmaceutically acceptable salts include, but are not limited to, mineral or organic acid salts of basic residues such as amines; alkali or organic salts of acidic residues such as carboxylic acids; and the like. The pharmaceutically acceptable salts of the present invention include the non-toxic salts of the parent compound formed, e.g., from non-toxic inorganic or organic acids. The  pharmaceutically acceptable salts of the present invention can be synthesized from the parent compound which contains a basic or acidic moiety by conventional chemical methods. Generally, such salts can be prepared by reacting the free acid or base forms of these compounds with a stoichiometric amount of the appropriate base or acid in water or in an organic solvent, or in a mixture of the two; generally, non-aqueous media like ether, ethyl  acetate, alcohols (e.g., methanol, ethanol, iso-propanol or butanol) or acetonitrile (MeCN) are preferred. Lists of suitable salts are found in Remington's Pharmaceutical Sciences, 17 ^th Ed., (Mack Publishing Company, Easton, 1985), p.1418, Berge et al., J. Pharm. Sci., 1977, 66(1), 1-19 and in Stahl et al., Handbook of Pharmaceutical Salts: Properties, Selection, and Use, (Wiley, 2002). In some embodiments, the compounds described herein include the N-  oxide forms. Synthesis Compounds of the invention, including salts thereof, can be prepared using known organic synthesis techniques and can be synthesized according to any of numerous possible synthetic routes, such as those in the Schemes below.   The reactions for preparing compounds of the invention can be carried out in suitable solvents which can be readily selected by one of skill in the art of organic synthesis. Suitable solvents can be substantially non-reactive with the starting materials (reactants), the intermediates or products at the temperatures at which the reactions are carried out, e.g., temperatures which can range from the solvent's freezing temperature to the solvent's boiling  temperature. A given reaction can be carried out in one solvent or a mixture of more than one solvent. Depending on the particular reaction step, suitable solvents for a particular reaction step can be selected by the skilled artisan. Preparation of compounds of the invention can involve the protection and deprotection of various chemical groups. The need for protection and deprotection, and the  selection of appropriate protecting groups, can be readily determined by one skilled in the art. The chemistry of protecting groups is described, e.g., in Kocienski, Protecting Groups, (Thieme, 2007); Robertson, Protecting Group Chemistry, (Oxford University Press, 2000); Smith et al., March's Advanced Organic Chemistry: Reactions, Mechanisms, and Structure, 6 ^th Ed. (Wiley, 2007); Peturssion et al., "Protecting Groups in Carbohydrate Chemistry," J.  Chem. Educ., 1997, 74(11), 1297; and Wuts et al., Protective Groups in Organic Synthesis, 4th Ed., (Wiley, 2006). Reactions can be monitored according to any suitable method known in the art. For example, product formation can be monitored by spectroscopic means, such as nuclear magnetic resonance spectroscopy (e.g., ¹ H or ¹³ C), infrared spectroscopy, spectrophotometry  (e.g., UV-visible), mass spectrometry or by chromatographic methods such as high performance liquid chromatography (HPLC) or thin layer chromatography (TLC). The Schemes below provide general guidance in connection with preparing the compounds of the invention. One skilled in the art would understand that the preparations shown in the Schemes can be modified or optimized using general knowledge of organic  chemistry to prepare various compounds of the invention. Compounds of Formula (I) can be prepared, e.g., using a process as illustrated in the schemes below. Scheme 1:

. ., ) in the presence of a base (e.g., DIEA) to provide Compound 1-2. Compound 1-2 can be treated with R ¹ H (e.g., a peptide described herein such as, for example, Pv1) to provide   Compound 1-3. Scheme 2: O H ^N CH CH O CH R1 in the presence of a base (e.g., DBU) to provide Compound 2-2. Compound 2-2 can be   coupled with Compound 2-3 in the presence of a base (e.g., triethylamine) to provide Compound 2-4. Compound 2-4 can be treated with R ¹ H (e.g., a peptide described herein such as, for example, Pv1) in the presence of a base (e.g., triethylamine) to provide Compound 2-5. The peptides R ¹ may be prepared using the solid-phase synthetic method first   described by Merrifield in J.A.C.S., Vol.85, pgs.2149-2154 (1963), although other art- known methods may also be employed. The Merrifield technique is well understood and is a common method for preparation of peptides. Useful techniques for solid-phase peptide synthesis are described in several books such as the text "Principles of Peptide Synthesis" by Bodanszky, Springer Verlag 1984. This method of synthesis involves the stepwise addition of protected amino acids to a growing peptide chain which was bound by covalent bonds to a solid resin particle. By this procedure, reagents and by-products are removed by filtration,  thus eliminating the necessity of purifying intermediates. The general concept of this method depends on attachment of the first amino acid of the chain to a solid polymer by a covalent bond, followed by the addition of the succeeding protected amino acids, one at a time, in a stepwise manner until the desired sequence is assembled. Finally, the protected peptide is removed from the solid resin support and the protecting groups are cleaved off.   The amino acids may be attached to any suitable polymer. The polymer must be insoluble in the solvents used, must have a stable physical form permitting ready filtration, and must contain a functional group to which the first protected amino acid can be firmly linked by a covalent bond. Various polymers are suitable for this purpose, such as cellulose, polyvinyl alcohol, polymethylmethacrylate, and polystyrene.   Methods of Use Provided herein is the use of the compounds of formula (I) in the treatment of diseases, such as cancer or neurodegenerative disease. Another aspect of the present invention is the use of the compounds of formula (I) in the treatment of diseases involving  acidic or hypoxic diseased tissue, such as cancer. Hypoxia and acidosis are physiological markers of many disease processes, including cancer. In cancer, hypoxia is one mechanism responsible for development of an acid environment within solid tumors. As a result, hydrogen ions must be removed from the cell (e.g., by a proton pump) to maintain a normal pH within the cell. As a consequence of this export of hydrogen ions, cancer cells have an  increased pH gradient across the cell membrane lipid bilayer and a lower pH in the extracellular milieu when compared to normal cells. One approach to improving the efficacy and therapeutic index of cytotoxic agents is to leverage this physiological characteristic to afford selective delivery of compound to hypoxic cells over healthy tissue. In these methods of treatment, a therapeutically-effective amount of a compound of  formula (I) or a pharmaceutically-acceptable salt thereof may be administered as a single agent or in combination with other forms of therapy, such as ionizing radiation or cytotoxic agents in the case of cancer. In combination therapy, the compound of formula (I) may be administered before, at the same time as, or after the other therapeutic modality, as will be appreciated by those of skill in the art. Either method of treatment (single agent or combination with other forms of therapy) may be administered as a course of treatment involving multiple doses or treatments over a period of time. Examples of cancers that are treatable using the compounds of the present disclosure  include, but are not limited to, colorectal cancer, gastric cancer, bone cancer, pancreatic cancer, skin cancer, cancer of the head or neck, cutaneous or intraocular malignant melanoma, uterine cancer, ovarian cancer, rectal cancer, cancer of the anal region, stomach cancer, testicular cancer, uterine cancer, carcinoma of the fallopian tubes, carcinoma of the endometrium, endometrial cancer, carcinoma of the cervix, carcinoma of the vagina,  carcinoma of the vulva, Hodgkin's Disease, non-Hodgkin's lymphoma, cancer of the esophagus, cancer of the small intestine, cancer of the endocrine system, cancer of the thyroid gland, cancer of the parathyroid gland, cancer of the adrenal gland, sarcoma of soft tissue, cancer of the urethra, cancer of the penis, chronic or acute leukemias including acute myeloid leukemia, chronic myeloid leukemia, acute lymphoblastic leukemia, chronic  lymphocytic leukemia, solid tumors of childhood, lymphocytic lymphoma, cancer of the bladder, cancer of the kidney or urethra, carcinoma of the renal pelvis, neoplasm of the central nervous system (CNS), primary CNS lymphoma, tumor angiogenesis, spinal axis tumor, brain stem glioma, pituitary adenoma, Kaposi's sarcoma, epidermoid cancer, squamous cell cancer, T -cell lymphoma, environmentally induced cancers including those  induced by asbestos, and combinations of said cancers. In some embodiments, cancers treatable with compounds of the present disclosure include bladder cancer, bone cancer, glioma, breast cancer (e.g., triple-negative breast cancer), cervical cancer, colon cancer, colorectal cancer, endometrial cancer, epithelial cancer, esophageal cancer, Ewing's sarcoma, pancreatic cancer, gallbladder cancer, gastric  cancer, gastrointestinal tumors, head and neck cancer (upper aerodigestive cancer), intestinal cancers, Kaposi's sarcoma, kidney cancer, laryngeal cancer, liver cancer (e.g., hepatocellular carcinoma), lung cancer (e.g., non-small cell lung cancer, adenocarcinoma), melanoma, prostate cancer, rectal cancer, renal clear cell carcinoma, skin cancer, stomach cancer, testicular cancer, thyroid cancer, and uterine cancer.   In some embodiments, cancers treatable with compounds of the present disclosure include melanoma (e.g., metastatic malignant melanoma), renal cancer (e.g. clear cell carcinoma), prostate cancer (e.g. hormone refractory prostate adenocarcinoma), breast cancer, triple-negative breast cancer, colon cancer and lung cancer (e.g. non-small cell lung cancer and small cell lung cancer). Additionally, the disclosure includes refractory or recurrent malignancies whose growth may be inhibited using the compounds of the disclosure. In some embodiments, cancers that are treatable using the compounds of the present disclosure include, but are not limited to, solid tumors (e.g., prostate cancer, colon cancer,  esophageal cancer, endometrial cancer, ovarian cancer, uterine cancer, renal cancer, hepatic cancer, pancreatic cancer, gastric cancer, breast cancer, lung cancer, cancers of the head and neck, thyroid cancer, glioblastoma, sarcoma, bladder cancer, etc.), hematological cancers (e.g., lymphoma, leukemia such as acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia  (CML), DLBCL, mantle cell lymphoma, Non-Hodgkin lymphoma (including relapsed or refractory NHL and recurrent follicular), Hodgkin lymphoma or multiple myeloma) and combinations of said cancers. In certain embodiments, a compound of formula (I) or a pharmaceutically-acceptable salt thereof may be used in combination with a chemotherapeutic agent, a targeted cancer  therapy, an immunotherapy or radiation therapy. The agents can be combined with the present compounds in a single dosage form, or the agents can be administered simultaneously or sequentially as separate dosage forms. In some embodiments, the chemotherapeutic agent, targeted cancer therapy, immunotherapy or radiation therapy is less toxic to the patient, such as by showing reduced bone marrow toxicity, when administered  together with a compound of formula (I), or a pharmaceutically acceptable salt thereof, as compared with when administered in combination with the corresponding microtubule targeting agent (e.g., R ² -H). Suitable chemotherapeutic or other anti-cancer agents include, for example, alkylating agents (including, without limitation, nitrogen mustards, ethylenimine derivatives,  alkyl sulfonates, nitrosoureas and triazenes) such as uracil mustard, chlormethine, cyclophosphamide (Cytoxan ^TM ), ifosfamide, melphalan, chlorambucil, pipobroman, triethylene-melamine, triethylenethiophosphoramine, busulfan, carmustine, lomustine, streptozocin, dacarbazine, and temozolomide. Other suitable agents for use in combination with the compounds of the present  invention include: dacarbazine (DTIC), optionally, along with other chemotherapy drugs such as carmustine (BCNU) and cisplatin; the “Dartmouth regimen,” which consists of DTIC, BCNU, cisplatin and tamoxifen; a combination of cisplatin, vinblastine, and DTIC; or temozolomide. Compounds according to the invention may also be combined with immunotherapy drugs, including cytokines such as interferon alpha, interleukin 2, and tumor necrosis factor (TNF). Suitable chemotherapeutic or other anti-cancer agents include, for example, antimetabolites (including, without limitation, folic acid antagonists, pyrimidine analogs,  purine analogs and adenosine deaminase inhibitors) such as methotrexate, 5-fluorouracil, floxuridine, cytarabine, 6-mercaptopurine, 6-thioguanine, fludarabine phosphate, pentostatine, and gemcitabine. Suitable chemotherapeutic or other anti-cancer agents further include, for example, certain natural products and their derivatives (for example, vinca alkaloids, antitumor  antibiotics, enzymes, lymphokines and epipodophyllotoxins) such as vinblastine, vincristine, vindesine, bleomycin, dactinomycin, daunorubicin, doxorubicin, epirubicin, idarubicin, ara- C, paclitaxel (TAXOL ^TM ), mithramycin, deoxycoformycin, mitomycin-C, L-asparaginase, interferons (especially IFN-a), etoposide, and teniposide. Other cytotoxic agents that can be administered in combination with the compounds  of the invention include, for example, navelbene, CPT-11, anastrazole, letrazole, capecitabine, reloxafine, cyclophosphamide, ifosamide, and droloxafine. Also suitable are cytotoxic agents such as, for example, epidophyllotoxin; an antineoplastic enzyme; a topoisomerase inhibitor; procarbazine; mitoxantrone; platinum coordination complexes such as cis-platin and carboplatin; biological response modifiers;  growth inhibitors; antihormonal therapeutic agents; leucovorin; tegafur; and haematopoietic growth factors. Other anti-cancer agent(s) include antibody therapeutics such as trastuzumab (Herceptin), antibodies to costimulatory molecules such as CTLA-4, 4-1BB and PD-1, or antibodies to cytokines (IL-10, TGF-α, etc.).   Other anti-cancer agents also include those that block immune cell migration such as antagonists to chemokine receptors, including CCR2 and CCR4. Other anti-cancer agents also include those that augment the immune system such as adjuvants or adoptive T cell transfer. Anti-cancer vaccines that can be administered in combination with the compounds of  the invention include, for example, dendritic cells, synthetic peptides, DNA vaccines and recombinant viruses. Other suitable agents for use in combination with the compounds of the present invention include chemotherapy combinations such as platinum-based doublets used in lung cancer and other solid tumors (cisplatin or carboplatin plus gemcitabine; cisplatin or carboplatin plus docetaxel; cisplatin or carboplatin plus paclitaxel; cisplatin or carboplatin plus pemetrexed) or gemcitabine plus paclitaxel bound particles (Abraxane®). Compounds of this invention may be effective in combination with anti-hormonal agents for treatment of breast cancer and other tumors. Suitable examples are anti-estrogen  agents including but not limited to tamoxifen and toremifene, aromatase inhibitors including but not limited to letrozole, anastrozole, and exemestane, adrenocorticosteroids (e.g. prednisone), progestins (e.g. megastrol acetate), and estrogen receptor antagonists (e.g. fulvestrant). Suitable anti-hormone agents used for treatment of prostate and other cancers may also be combined with compounds of the present invention. These include anti-  androgens including but not limited to flutamide, bicalutamide, and nilutamide, luteinizing hormone-releasing hormone (LHRH) analogs including leuprolide, goserelin, triptorelin, and histrelin, LHRH antagonists (e.g. degarelix), androgen receptor blockers (e.g. enzalutamide) and agents that inhibit androgen production (e.g. abiraterone). Compounds of the present invention may be combined with or administered in  sequence with other agents against membrane receptor kinases especially for patients who have developed primary or acquired resistance to the targeted therapy. These therapeutic agents include inhibitors or antibodies against EGFR, Her2, VEGFR, c-Met, Ret, IGFR1, or Flt-3 and against cancer-associated fusion protein kinases such as Bcr-Abl and EML4-Alk. Inhibitors against EGFR include gefitinib and erlotinib, and inhibitors against EGFR/Her2  include but are not limited to dacomitinib, afatinib, lapitinib and neratinib. Antibodies against the EGFR include but are not limited to cetuximab, panitumumab and necitumumab. Inhibitors of c-Met may be used in combination with the compounds of the invention. These include onartumzumab, tivantnib, and INC-280. Agents against Abl (or Bcr-Abl) include imatinib, dasatinib, nilotinib, and ponatinib and those against Alk (or EML4-ALK) include  crizotinib. Angiogenesis inhibitors may be efficacious in some tumors in combination with compounds of the invention. These include antibodies against VEGF or VEGFR or kinase inhibitors of VEGFR. Antibodies or other therapeutic proteins against VEGF include bevacizumab and aflibercept. Inhibitors of VEGFR kinases and other anti-angiogenesis  inhibitors include but are not limited to sunitinib, sorafenib, axitinib, cediranib, pazopanib, regorafenib, brivanib, and vandetanib Activation of intracellular signaling pathways is frequent in cancer, and agents targeting components of these pathways have been combined with receptor targeting agents to enhance efficacy and reduce resistance. Examples of agents that may be combined with compounds of the present invention include inhibitors of the PI3K-AKT-mTOR pathway, inhibitors of the Raf-MAPK pathway, inhibitors of JAK-STAT pathway, and inhibitors of protein chaperones and cell cycle progression. Agents against the PI3 kinase include but are not limited topilaralisib, idelalisib,  buparlisib. Inhibitors of mTOR such as rapamycin, sirolimus, temsirolimus, and everolimus may be combined with compounds of the invention. Other suitable examples include but are not limited to vemurafenib and dabrafenib (Raf inhibitors) and trametinib, selumetinib and GDC-0973 (MEK inhibitors). Inhibitors of one or more JAKs (e.g., ruxolitinib, baricitinib, tofacitinib), Hsp90 (e.g., tanespimycin), cyclin dependent kinases (e.g., palbociclib),  HDACs (e.g., panobinostat), PARP (e.g., olaparib), and proteasomes (e.g., bortezomib, carfilzomib) can also be combined with compounds of the present invention. A further example of a PARP inhibitor that can be combined with a compound of the invention is talazoparib. Methods for the safe and effective administration of most of these chemotherapeutic  agents are known to those skilled in the art. In addition, their administration is described in the standard literature. For example, the administration of many of the chemotherapeutic agents is described in the "Physicians' Desk Reference" (PDR, e.g., 1996 edition, Medical Economics Company, Montvale, NJ), the disclosure of which is incorporated herein by reference as if set forth in its entirety.   The phrase "therapeutically effective amount" of a compound (therapeutic agent, active ingredient, drug, etc.) refers to an amount of the compound to be administered to a subject in need of therapy or treatment which alleviates a symptom, ameliorates a condition, or slows the onset of disease conditions, according to clinically acceptable standards for the disorder or condition to be treated. For instance, a therapeutically effective amount can be an  amount which has been demonstrated to have a desired therapeutic effect in an in vitro assay, an in vivo animal assay, or a clinical trial. The therapeutically effective amount can vary based on the particular dosage form, method of administration, treatment protocol, specific disease or condition to be treated, the benefit/risk ratio, etc., among numerous other factors. Said therapeutically effective amount can be obtained from a clinical trial, an  animal model, or an in vitro cell culture assay. It is known in the art that the effective amount suitable for human use can be calculated from the effective amount determined from an animal model or an in vitro cell culture assay. For instance, as reported by Reagan-Shaw et al., FASEB J.2008: 22(3) 659-61, “μg/ml” (effective amount based on in vitro cell culture assays) = “mg/kg body weight/day” (effective amount for a mouse). Furthermore, the effective amount for a human can be calculated from the effective amount for a mouse based on the fact that the metabolism rate of mice is 6 times faster than that of humans. As an example of treatment using a compound of formula (I) in combination with a  cytotoxic agent, a therapeutically-effective amount of a compound of formula (I) may be administered to a patient suffering from cancer as part of a treatment regimen also involving a therapeutically-effective amount of ionizing radiation or a cytotoxic agent. In the context of this treatment regimen, the term “therapeutically-effective” amount should be understood to mean effective in the combination therapy. It will be understood by  those of skill in the cancer-treatment field how to adjust the dosages to achieve the optimum therapeutic outcome. Similarly, the appropriate dosages of the compounds of the invention for treatment of non-cancerous diseases or conditions (such as cardiovascular diseases) may readily be determined by those of skill in the medical arts.   The term "treating" as used herein includes the administration of a compound or composition which reduces the frequency of, delays the onset of, or reduces the progression of symptoms of a disease involving acidic or hypoxic diseased tissue, such as cancer, stroke, myocardial infarction, or long-term neurodegenerative disease, in a subject relative to a subject not receiving the compound or composition. This can include reversing, reducing, or  arresting the symptoms, clinical signs, or underlying pathology of a condition in a manner to improve or stabilize a subject's condition (e.g., regression of tumor growth, for cancer or decreasing or ameliorating myocardial ischemia reperfusion injury in myocardial infarction, stroke, or the like cardiovascular disease). The terms "inhibiting" or "reducing" are used for cancer in reference to methods to inhibit or to reduce tumor growth (e.g., decrease the size of  a tumor) in a population as compared to an untreated control population. All publications (including patents) mentioned herein are incorporated herein by reference for the purpose of describing and disclosing, for example, the constructs and methodologies that are described in the publications, which might be used in connection with the disclosure herein described. The publications discussed throughout the text are provided  solely for their disclosure prior to the filing date of the present application. Disclosed herein are several types of ranges. When a range of any type is disclosed or claimed, the intent is to disclose or claim individually each possible number that such a range could reasonably encompass, including end points of the range as well as any sub-ranges and combinations of sub-ranges encompassed therein. When a range of therapeutically effective amounts of an active ingredient is disclosed or claimed, for instance, the intent is to disclose or claim individually every possible number that such a range could encompass, consistent with the disclosure herein. For example, by a disclosure that the therapeutically effective amount of a compound can be in a range from about 1 mg/kg to about 50 mg/kg (of body  weight of the subject). Formulation, Dosage Forms and Administration To prepare the pharmaceutical compositions of the present invention, a compound of Formula (I) or a pharmaceutically-acceptable salt thereof is combined as the active  ingredient in intimate admixture with a pharmaceutical carrier according to conventional pharmaceutical compounding techniques, which carrier may take a wide variety of forms depending on the form of preparation desired for administration, e.g., oral or parenteral. In preparing the compositions in oral dosage form, any of the usual pharmaceutical media may be employed, such as for example, water, glycols, oils, alcohols, flavoring agents,  preservatives, coloring agents, and the like in the case of oral liquid preparations such as for example, suspensions, elixirs, and solutions; or carriers such as starches, sugars, diluents, granulating agents, lubricants, binders, disintegrating agents, and the like in a case of oral solid preparations, such as for example, powders, capsules, and tablets. Because of their ease in administration, tablets and capsules represent the most   advantageous oral dosage unit form, in which case solid pharmaceutical carriers are obviously employed. If desired, tablets may be sugar coated or enteric coated by standard techniques. For parenterals, the carrier will usually comprise sterile water, although other ingredients, for example, to aid solubility or for preservative purposes, may be included. Injectable suspensions may also be prepared, in which case appropriate liquid carriers,  suspending agents, and the like may be employed. One of skill in the pharmaceutical and medical arts will be able to readily determine a suitable dosage of the pharmaceutical compositions of the invention for the particular disease or condition to be treated. EXAMPLES   As used herein, all abbreviations, symbols and conventions are consistent with those used in the contemporary scientific literature. See, e.g., Janet S. Dodd, ed., The ACS Style Guide: A Manual for Authors and Editors, 2nd Ed., Washington, D.C.: American Chemical Society, 1997. General experimental details Routine monitoring of reactions was performed using EM Science DC-Alufolien silica gel coated glass TLC plates or HPLC methods described below. Flash chromatography was performed on automated purification systems from Teledyne Isco (Rf, Rf+ or EZ Prep  instruments). HPLC Instruments and Methods HPLC analysis of reaction mixtures (IPC) and purified materials was performed on Agilent 1100/1200/1260 or 1290 systems (coupled or uncoupled with MS). Details for all  used methods are below: Method A: HPLC Parameters et od : HPLC Parameters Column Temperature 40 °C xampe : repara on o ompoun   Step 1: (1 ⁴ S, S,3S,3S, ,4S,0 , ,4 )-8-c oro- -yroxy-8,4-dimethoxy-  3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(2-(2,5-dioxo-2,5-dihydro-1H-pyrrol- 1-yl)ethyl)-2,5-dioxopyrrolidin-3-yl)thio)-4-methylpentanoyl )-N-methyl-L-alaninate

A solut g, 0.522 mmol) in DCM )1.5 mL) was added to solid (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ - hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-  oxirana-8(1,3)-benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-mercapto-4- methylpentanoyl)-N-methyl-L-alaninate (DM4, 37.7 mg, 0.0483 mmol). The resultant solution was treated with DIEA (0.040 mL, 0.229 mmol) and stirred at ambient temperature overnight. The solution was treated with acetic acid (0.020 mL) and applied to a RediSep silica gel cartridge (12 g). MeOH (gradient 0% to 14%) in DCM was used as the eluent (the  product eluted at 5% MeOH). The fractions were combined and evaporated in vacuo to afford the desired product (41 mg) in 85% yield as a white solid). LC (method A): 3.014 min. (~95%). MS: 982.2 (M+H-H2O) ⁺ , 1000 (M+H ⁺ ), 1022 (M+Na) ⁺ . Step 2. Compound 1.   (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -Chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(2-(2,5-dioxo-2,5-dihydro-1H-pyrrol- 1-yl)ethyl)-2,5-dioxopyrrolidin-3-yl)thio)-4-methylpentanoyl )-N-methyl-L-alaninate (from Step 1, 29 mg, 0.0290 mmol) and peptide Pv1 (89 mg, 0.0262 mmol) were dissolved in DMF  (1 mL), and treated with DIEA (0.040 mL, 0.229 mmol). The solution was stirred at ambient temperature for 16 hours, then made acidic with acetic acid (0.020 mL) and applied to a medium pressure reverse phase cartridge RediSep Aq C18 column (15.5 g). Acetonitrile (a gradient 10% to 95%) in water (solvents buffered with NH ₄ OAc, 10 mM) was used as the eluent (the product eluted at 56% acetonitrile). The purified fractions were combined, frozen  and lyophilized to afford the product as a white solid (87.5 mg) as the bis-AcOH salt in 78% yield. LC (method B): 5.273 min. (99%); MS: 2138.4 (M+2H)/2 ⁺ . Example 2. Preparation of Compound 2 Ste p . ( S, S,3 S,3 S, ,4S, 0 , , 4 )-8 -c oro- - y roxy-8 , 4- imethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)-   benzenacyclotetradecaphane-10,12-dien-4-yl N (4-((1-(2-(2-(2-(2,5-dioxo-2,5-dihydro-1H- pyrrol-1-yl)ethoxy)ethoxy)ethyl)-2,5-dioxopyrrolidin-3-yl)th io)-4-methylpentanoyl)-N- methyl-L-alaninate. So -2,5-dione)  (390 mg, 1.41 mmol) was added to a solution of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ - chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)- oxazinana-3(2,3)-oxirana-8(1,3)-benzenacyclotetradecaphane-1 0,12-dien-4-yl N-(4- mercapto-4-methylpentanoyl)-N-methyl-L-alaninate (DM4, 110 mg, 0.141 mmol) in DCM (4 mL) cooled in an ice-bath. The resultant solution was treated with DIEA (0.040 mL, 0.229  mmol), the ice-bath was removed, and the solution was stirred at ambient temperature overnight. The solution was applied to a RediSep silica gel cartridge (24 g), using MeOH (gradient 1% to 20%) in DCM as the eluent (the product eluted at 6% MeOH). The fractions were combined and evaporated in vacuo. The product was further purified by pHPLC on a Kinetex C8, 100Å, 5 micron, 150x30 mm column eluted with acetonitrile (10% step to 45%) in water (solvents buffered with 0.05% TFA). Fractions were combined, frozen and lyophilized to afford the product (98 mg) in 64% yield as a white solid. LC (method B): 6.491 & 6.565 min. (diastereomer doublet 99%). MS: 1070.4 (M+H-H2O) ⁺ , 1088.4 (M+H) ⁺ .   Step 2. Compound 2 A solution of peptide Pv1 (301 mg, 0.0858 mmol) in DMF (2.5 mL) was added to a solution of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N (4-((1-(2-(2-(2-(2,5-dioxo-2,5-dihydro-1H-  pyrrol-1-yl)ethoxy)ethoxy)ethyl)-2,5-dioxopyrrolidin-3-yl)th io)-4-methylpentanoyl)-N- methyl-L-alaninate (from Step 1, 92 mg, 0.0845 mmol) in DMF (1 mL) cooled in an ice-bath, and treated with DIEA (0.110 mL, 0.630 mmol). The ice-bath was removed and the solution was stirred at ambient temperature overnight. The solution was applied to a medium pressure reverse phase cartridge Biotage Aq C18300Å (25 g) and eluted with acetonitrile (a gradient  5% step to 25% gradient to 95%) in water (solvents buffered with NH4OAc 10 mM). The purified fractions were combined, frozen and lyophilized to afford the product as a white solid, 340 mg (bis-AcOH salt, 88%). LC (method B): 6.132 min. (94.3%); MS: 2184.1 (M+2H)/2 ⁺ and 1457.1 (M+3H)/3 ⁺ .   Example 3. Preparation of Compound 3 Step . ( , , , , , , , , )- -c oro- - y roxy- , - met oxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(2-(2-(2-(2-(2,5-dioxo-2,5-dihydro- 1H-pyrrol-1-yl)ethoxy)ethoxy)ethoxy)ethyl)-2,5-dioxopyrrolid in-3-yl)thio)-4- methylpentanoyl)-N-methyl-L-alaninate O O HN O N O A )bis(1H-  pyrrole-2,5-dione) (50 mg, 0.142 mmol) in DCM (1 mL) was added to solid (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10- tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-mercapto-4-methylpentanoyl)-N-methyl- L-alaninate (DM4, 13.8 mg, 0.0177 mmol). The resultant solution was treated with DIEA  (0.025 mL, 0.143 mmol) and stirred at ambient temperature for 20 hours. The solution was treated with acetic acid (0.010 mL) and applied to a RediSep silica gel cartridge (4 g). MeOH (gradient 0.6% to 20%) in DCM was used as the eluent (the product eluted at 6% to 7% MeOH). The fractions were combined and evaporated in vacuo to afford the product (12.1 mg) in 60% yield as a colorless glass. LC (method B): 6.406 and 6.477 min.   (diastereomer doublet 99%). MS: 1114.4 (M+H-H ₂ O) ⁺ , 1133 (M+H ⁺ ), 1154.4 (M+Na) ⁺ . Step 2. Compound 3 Solid peptide Pv1 (41.2 mg, 0.0118 mmol) was added to a solution of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-  tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(2-(2-(2-(2-(2,5-dioxo-2,5-dihydro- 1H-pyrrol-1-yl)ethoxy)ethoxy)ethoxy)ethyl)-2,5-dioxopyrrolid in-3-yl)thio)-4- methylpentanoyl)-N-methyl-L-alaninate (from Step 1, 12.1 mg, 0.107 mmol in DMF (1 mL), and treated with saturated aqueous sodium bicarbonate (0.1 mL). The mixture was stirred at  ambient temperature for 1 hour, then applied to a medium pressure reverse phase cartridge RediSep Aq C18 (15.5 g). Acetonitrile (a gradient 20% to 95%) in water (solvents buffered with NH4OAc 10 mM) was used as the eluent (the product eluted at 57% acetonitrile). The purified fractions were combined, frozen and lyophilized to afford the product as a white solid, 35.1 mg (bis-AcOH salt, 78%). LC (method B): 6.624 min. (99%); MS: 2206.2 (M+2H)/2 ⁺ and 1471.1 (M+3H)/3 ⁺ .   Example 4. Preparation of Compound 4 Ste p . ( , )-4,4-(octane- ,8- iy is(azane iy )) is(4-oxo ut- -enoic aci ) Solid octane-1 a mixture/solution of  maleic anhydride (2.17 g, 22.1 mmol) in chloroform (20 mL) cooled in an ice-bath. The resultant gummy solid mixture was sonicated for 10 minutes and agitated with a heavy magnetic stir bar overnight. The resultant solid was collected by filtration, washed with DCM, and dried in vacuo to afford the product (3.29 g) in 98% yield as a white solid. ¹ H NMR (dmso-d ₆ ): 1.27 (s, 8H), 1.46 (t, 4H), 3.16 (q, 4H), 6.23 (d, 2H), 6.39 (d, 2H) and 9.13  (br s, 2H); LC (method A): 2.016 min. (99%); MS: 341.2 (M+H ⁺ ) and 339.1 (M-H)-. Step 2.1,1'-(octane-1,8-diyl)bis(1H-pyrrole-2,5-dione) A suspension of (2E,2' anediyl))bis(4-oxobut-2-enoic acid) (from Step 1, 723 mg, 2.12 mmol) and sodium acetate (139 mg, 1.69 mmol) in acetonitrile (8 mL) was treated with triethylamine (0.192 mL, 1.38 mmol) and acetic  anhydride (1.2 mL, 12.7 mmol). The resultant mixture was stirred at ambient temperature for 1 day. The solvents were evaporated in vacuo, and the residue was triturated in water. The solid was collected by filtration, washed with water, and recrystallized from DMSO to afford the product (193 mg) in 30% yield. ¹ H NMR(CDCl3): 1.27 (br s, 8H), 1.56 (quin, 4H), 3.49 (t, 4H), and 6.67 (s, 4H); LC (method A): 2.776 min. (99%); MS: 305.1 (M+H) ⁺ .   Step 3. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(8-(2,5-dioxo-2,5-dihydro-1H-pyrrol- 1-yl)octyl)-2,5-dioxopyrrolidin-3-yl)thio)-4-methylpentanoyl )-N-methyl-L-alaninate   A p 2, 97.5 mg, 0.320 mmol) in DCM (1.5 mL) was added to solid (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ - chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)- oxazinana-3(2,3)-oxirana-8(1,3)-benzenacyclotetradecaphane-1 0,12-dien-4-yl N-(4-  mercapto-4-methylpentanoyl)-N-methyl-L-alaninate (DM4, 31.6 mg, 0.0405 mmol). The resultant solution was treated with DIEA (0.056 mL, 0.32 mmol), and the solution was stirred at ambient temperature for one day. Acetic acid (0.020 mL) was added to the solution. The solution was applied to a RediSep silica gel cartridge (12 g). MeOH (gradient 1% to 20%) in DCM was used as the eluent. The fractions were combined and evaporated in vacuo to afford the product, (16.6 mg) in 38% yield. LC (method B): 7.800 & 7.854 min. (diastereomer doublet 99%). MS: 1066.4 (M+H-H2O) ⁺ , 1106.4 (M+Na) ⁺ .   Step 4. Compound 4 Solid peptide Pv1 (59.4 mg, 0.0169 mmol) was added to a solution of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10- tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(8-(2,5-dioxo-2,5-dihydro-1H-pyrrol-  1-yl)octyl)-2,5-dioxopyrrolidin-3-yl)thio)-4-methylpentanoyl )-N-methyl-L-alaninate (from Step 3, 16.6 mg, 0.0153 mmol) in DMF (0.85 mL), then treated with saturated aqueous sodium bicarbonate (0.1 mL), and the mixture was stirred at ambient temperature for one hour and stored in a freezer overnight. The mixture was treated with water and applied to a medium pressure reverse phase cartridge Silicycle C8300Å (15 g) and eluted with   acetonitrile (a gradient 20% to 95%) in water (solvents buffered with NH4OAc 10 mM). The purified fractions were combined, frozen and lyophilized, then dissolved in acetonitrile/water/TFA (1/1/0.004), transferred to a vial, and lyophilized to afford the product as a white solid (29.5 mg) as the bis-TFA salt in 42% yield. LC (method B): 6.878 min. (99%); MS: 2182.1 (M+2H)/2 ⁺ and 1449.1 (M-H ₂ O+3H)/3 ⁺ .   Example 5. Preparation of Compound 5 O O NH A solutio ,4-diyl)bis(1H- pyrrole-2,5-dione) (42 mg, 0.168 mmol) in DMF (0.5 mL) was treated with NEt ₃ (0.0095 mL, 0.0645 mmol). When Pv1 was consumed the solution was applied to a reverse phase  RediSep C18 AQ cartridge and eluted with acetonitrile (10% step to 35% gradient to 65%) in water (solvents buffered with AcOH 0.05%). The purified fractions were combined, frozen and lyophilized to afford the product. LC (method B): 6.187 min. (>95%). MS: 1764.4 (M+2H)/2 ⁺ and 1176.3 (M+3H)/3 ⁺ .   Step 2. Compound 5 A solution of the compound of Step 1 (30 mg, 0.0085 mmol) and (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10- tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-mercapto-4-methylpentanoyl)-N-methyl-  L-alaninate (DM4, 13.2 mg, 0.017 mmol) in DMF (0.17 mL) was treated with aqueous sodium bicarbonate (1.14 M, 0.030 mL, 0.0342 mmol). The mixture was applied to a reverse phase RediSep C18 AQ cartridge, and the column was eluted with acetonitrile (10% step to 35% gradient to 65%) in water (solvents buffered with NH4OAc 10mM). The purified fractions were combined, frozen and lyophilized, to afford the product. LC (method B):  6.412 min. (97%); MS: 2154.9 (M+2H)/2 ⁺ and 1436.6 (M+3H)/3 ⁺ . Example 6. Preparation of Compound 6

  pyrrole-2,5-dione) (48 mg, 0.173 mmol) in DMF (0.5 mL) was treated with NEt ₃ (0.0095 mL, 0.0645 mmol). When Pv1 was consumed the solution was applied to a reverse phase RediSep C18 AQ cartridge and eluted with acetonitrile (10% step to 35% gradient to 65%) in water (solvents buffered with AcOH 0.05%). The purified fractions were combined, frozen and lyophilized to afford the product. LC (method B): 6.215 min. (>95%). MS: 1778.4  (M+2H)/2 ⁺ and 1185.5 (M+3H)/3 ⁺ . Step 2. Compound 6 A solution of the compound of Step 1 (39 mg, 0.011 mmol) and (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-  tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(8-(2,5-dioxo-2,5-dihydro-1H-pyrrol- 1-yl)octyl)-2,5-dioxopyrrolidin-3-yl)thio)-4-methylpentanoyl )-N-methyl-L-alaninate (DM4, 17.1 mg, 0.022 mmol) in DMF (0.22 mL) was treated with aqueous sodium bicarbonate (1.14 M, 0.039 mL, 0.044 mmol). The mixture was applied to a reverse phase RediSep C18 AQ  cartridge, and the column was eluted with acetonitrile (5% step to 35% gradient to 55%) in water (solvents buffered with NH4OAc 10mM). The purified fractions were combined, frozen and lyophilized, to afford the product. LC (method B): 6.412 min. (97%); MS: 2168.4 (M+2H)/2 ⁺ and 1446.3 (M+3H)/3 ⁺ .   Example 7. Preparation of Compound 7 Step 1. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)-   benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2,5-dioxopyrrolidin-1-yl)oxy)-2- oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate 250 mg of hydroxysuccinimide ester (0.34 mmol) were dissolved in DMF (8.0 mL) and cooled in an ice-water bath.48 µL of  DBU (0.34 mmol) was added at once and the mixture was allowed to warm to RT. At that moment LC/MS indicated nearly 76% conversion and 23% of dimer by-product. The reaction was quenched with the addition of ca.0.1 mL AcOH. The crude reaction mixture solution was concentrated by high vacuum (to 1/3 volume) and was directly loaded onto 100 g C18Aq column and purified via standard 10-95% B gradient (A: water w.0.05% AcOH; B: MeCN w.0.05% AcOH). Product containing fractions were lyophilized to afford 200 mg of product (67% yield). HPLC purity at 254 nm: 97%. Retention time: 1.48 min (Method C). LCMS: 934.3 M+H =935.6.   Step 2. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2-(2,5-dioxo-2,5-dihydro-1H-pyrrol- 1-yl)ethyl)amino)-2-oxoethyl)thio)-4-methylpentanoyl)-N-meth yl-L-alaninate   22.0 hloro-1 ⁴ - hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)- oxirana-8(1,3)-benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2,5-dioxopyrrolidin- 1-yl)oxy)-2-oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-ala ninate (from Step 1) and 5.0  mg of 2-maleimido-ethyl-1-amine hydrochloride (0.0282 mmol) were cooled to 0 °C in an ice bath, under Ar atmosphere. Anhydrous DMF (1.0 mL) was added and the mixture was allowed to stir for 5 minutes, then Et3N (0.0470 mmol) was added. The ice bath was removed, and the reaction was stirred for an additional 10 min when the reaction was judged complete by LCMS. The crude reaction mixture was directly loaded onto 30 g C18Aq  column and purified via standard 15-95% B gradient (A: water w.0.05% AcOH; B: MeCN w.0.05% AcOH). The fractions were lyophilized to afford 18.3 mg of product (white solid, 81% yield). HPLC purity at 254 nm: 98%. Retention time: 2.65 min (Method A). LCMS: 942.4; [M-H2O] = 942.5.   Step 3. Compound 7 The product of Step 2 (18.3 mg, 0.0191 mmol) and peptide Pv1 (63.3 mg, 0.0187 mmol) were dissolved in anhydrous DMF (380 µL), at room temperature, under Ar atmosphere. Et3N (8.0 µL, 0.0573 mmol) was added. The reaction mixture was left to stir at room temperature for 70 min. LC/MS (method A) showed ~5% residual starting material. The crude reaction mixture was diluted with ~1 mL of DMSO and directly loaded onto EZPrep 150x30 mm C8 Kinetex column and purified via standard 10-95% B gradient (A:  water w.10 mM NH4OAc; B: MeCN w.10 mM NH4OAc). The product containing fractions were lyophilized. The obtained product was re-lyophilized from 1:1 H ₂ O/MeCN (containing 0.1%TFA) to afford 63.3 mg of product (white solid, 74% yield). HPLC purity at 254 nm: 98.2%. Retention time: 6.64 min (Method B). LCMS: 2120.6; [(M+1)/2] = 2120.3.   Example 8. Preparation of Compound 8 Step 1.1 ⁴ S,1 ⁶ S,3 ² S,3 , , , , , - -c oro- - y roxy- ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2-aminoethyl)amino)-2-  oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate 1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -Chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2,5-dioxopyrrolidin-1-yl)oxy)-2- oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate (40 mg, 0.043 mmol) and N1-((4-  methoxyphenyl)diphenylmethyl)ethane-1,2-diamine (57 mg, 0.17 mmol, 4 eq) were dissolved in dioxane (1.5 mL). After 3 h the reaction appeared to be complete by LC/MS. The mixture was concentrated to dryness and dissolved in 80% AcOH in water (2 mL). LC/MS showed complete deprotection of the intermediate. The mixture was directly freeze-dried. The residue was dissolved in DMSO (1 mL) and loaded onto 30 g C18Aq column and purified via  standard 5-95% B gradient (A: water w.0.05% AcOH; B: water w.0.05% AcOH). Product containing fractions were lyophilized to afford 38mg (92%) of the product as a white solid. HPLC purity at 254 nm: 99%. Retention time: 2.08 min (Method A). LCMS: 879.4 M+H = 880.3.   Step 2. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl (S)-1-bromo-10,10,14,15-tetramethyl-2,7,13- trioxo-9-thia-3,6,14-triazahexadecan-16-oate   2-B -b]pyridin-3- yl)oxy)tri(pyrrolidin-1-yl)phosphonium (PyAOP, 0.068 mmol, 36 mg) was treated with anhydrous DMF (2 mL) at room temperature under nitrogen followed by addition of DIEA (15 µL) via micro syringe. To this solution was added dropwise a 1 mL solution of 30 mg of 1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1+-hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-  tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2-aminoethyl)amino)-2- oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate (from Step 1, 0.034 mmol) in DMF. After 1 h, the reaction was complete by LC/MS. The crude residue was concentrated under high vacuum and dissolved in DMSO (1 mL) and loaded onto 30 g C18Aq column and purified via standard 5-95% B gradient (A: water w.0.05% AcOH; B: water w.0.05% AcOH). Product containing fractions were lyophilized to afford 27 mg (79%) of product as a  white solid. HPLC purity at 254 nm: 99%. Retention time: 1.30 min (Method C). LCMS: 999.3 M+H = 1022.3 and 1024.6, Br isotope). Step 3. Compound 8 (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-  3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl (S)-1-bromo-10,10,14,15-tetramethyl-2,7,13- trioxo-9-thia-3,6,14-triazahexadecan-16-oate (12.3 mg, 0.0123 mmol) was treated with a solution of 44.7 mg (0.0132 mmol) of Pv1 in anhydrous DMF (1.10 mL) at room temperature. Tris buffer (1.1 mL) was added followed by the addition of NaHCO3 (17.2 mg,  0.205 mmol). The reaction mixture was sonicated for 1 minute and then allowed to stir at room temperature for 45 min. TFA (80 µL, 1.04 mmol) was added and the solution was loaded onto a 150x30 mm C8 Kinetex column and purified via a standard 10-100% B gradient (A: water w.0.1% TFA; B: MeCN w.0.1% TFA). Product containing fractions were lyophilized to afford 30.3 mg of product (white solid, 56% yield). HPLC purity at 254 nm:  99.3%. Retention time: 6.62 min (Method B). LC/MS: 2100.4; [(M+H)/2] = 2100.3 Example 9. Preparation of Compound 9 Step 1. (1 ⁴ S,1 ⁶ , , , , , , , - -c oro- - y roxy-8 ⁵ ,14-dimethoxy-  3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(2-aminoethyl)-2,5-dioxopyrrolidin-3- yl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate Solid 1-(2-aminoeth n chloride (17.7 mg, 0.100   mmol) was added to a solution of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ - hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)- oxirana-8(1,3)-benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-mercapto-4- methylpentanoyl)-N-methyl-L-alaninate (DM4, 52.2 mg, 0.0669 mmol). Sodium bicarbonate (27 mg, 0.032 mmol) and water (0.1 mL) were added and stirred at ambient temperature for 3  hours. Acetic acid (0.025 mL) was added. The solution was applied to a medium pressure reverse phase RediSep C18 AQ cartridge (50 g). Acetonitrile (gradient 10% to 95%) in water (solvents buffered with AcOH 0.05%) was used as the eluent. The fractions were combined, frozen and lyophilized to afford the product, 45.6 mg (70%) as a white solid. LC (method A): 2.087 min. (>95%). MS: 920.4 (M+H) ⁺ .   Step 2. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(2-(2-bromoacetamido)ethyl)-2- oxopyrrolidin-3-yl)thio)-4-methylpentanoyl)-N-methyl-L-alani nate (Intermediate 9-2a)   Intermediate 9-2a Intermediate 9-2b Sol (7-Azabenzotriazol-1- yloxy)tripyrrolidinophosphonium hexafluorophosphate (“PyAOP,” 39.6 mg, 0.0760 mmol) was dissolved in DMF (1 mL) and treated with DIEA (0.020 mL, 0.114 mmol). The resultant  solution was added to a vial with solid (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ - hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)- oxirana-8(1,3)-benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((1-(2-aminoethyl)-2,5- dioxopyrrolidin-3-yl)thio)-4-methylpentanoyl)-N-methyl-L-ala ninate (from Step 1, 45.6 mg, 0.0465 mmol) and stirred at ambient temperature for 2 hours. Acetic acid (0.020 mL) was  added, and the resultant solution was applied to a medium pressure reverse phase RediSep C18 AQ cartridge (15.5 g). Acetonitrile (gradient 10% to 95%) in water (solvents buffered with AcOH 0.05%) was used as the eluent. The fractions were combined, frozen and lyophilized to afford the desired product, 26 mg (a mixture of Intermediate 9-2a and Intermediate 9-2b, about 1:3).   Step 3. Compound 9 Solid peptide, Pv1 (59.4 mg, 0.0169 mmol) and (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)- 8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)- oxazinana-3(2,3)-oxirana-8(1,3)-benzenacyclotetradecaphane-1 0,12-dien-4-yl N-(4-((1-(2-(2-  bromoacetamido)ethyl)-2-oxopyrrolidin-3-yl)thio)-4-methylpen tanoyl)-N-methyl-L-alaninate (Intermediate 9-2a with Intermediate 9-2b, 1:3, 26 mg) was treated with Tris-Buffer (pH: 8.5, 50 mM, 2 mL) and DMF (1 mL), then solid sodium bicarbonate (32 mg, 0.381 mmol), and stirred at ambient temperature for 20 hours. The mixture was applied to a medium pressure reverse phase cartridge Biotage C18300Å (25 g) and eluted with acetonitrile (10%  step to 30% gradient to 95%) in water (solvents buffered with AcOH 0.05%). The purified fractions were combined, frozen and lyophilized to afford the crude product (30 mg). The product was further purified by pHPLC, Kinetex C8, 5 micron, 100Å, 150 x 30 mm, using acetonitrile (10% step to 35% gradient to 95%) in water (solvents buffered with NH ₄ OAc, 10 mM). The purified fractions were combined, frozen and lyophilized to afford impure product. The product was further purified by pHPLC, Kinetex C8, 5 micron, 100Å, 150 x 30 mm, using acetonitrile (10% step to 35% gradient to 95%) in water (solvents buffered with TFA, 0.05%). The purified fractions were combined, frozen and lyophilized, to afford the  product (15.6 mg) as the bis-TFA salt in 15% yield. LC (method B): 6.0756.119 min. (diastereomeric doublet, 99%); MS: 2120.2 (M+2H)/2 ⁺ , 1413.8 (M+3H)/3 ⁺ and 1407.7 (M- H2O+3H)/3 ⁺ . Example 10. Preparation of Compound 10 O O NH   3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4--((2-((2,5-dioxopyrrolidin-1-yl)oxy)-2- oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate   A solution 0.0.720 mmol) in DMF (2 mL) was added to a solution of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ - hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)- oxirana-8(1,3)-benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-mercapto-4-  methylpentanoyl)-N-methyl-L-alaninate (DM4, 487 mg, 0.624 mmol) in DMF (3 mL) and cooled in an ice-bath. DBU (0.110 mL, 0.724 mmol) was added to the cooled solution dropwise over 1 min. The ice-bath was removed, and the solution was stirred at ambient temperature for 2 hours. Acetic acid (0.050 mL) was added. The solution was applied to a medium pressure reverse phase RediSep C18 AQ cartridge (100 g). Acetonitrile (10% step to 30% gradient to 95%) in water (solvents buffered with AcOH 0.05%) was used as the eluent.  The product elutes at 62% acetonitrile. The fractions were combined, frozen and lyophilized to afford the product, 377 mg (65%) as a white solid. LC (method A): 2.816 min. (~90%). MS: 917.3 (M+H-H2O) ⁺ , 935 (M+H) ⁺ . Step 2. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-  3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2-aminoethyl)amino)-2- oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate. A soluti iamine (442 mg,  1.33 mmol) in dioxane (4 mL) was added to a solution of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10- tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4--((2-((2,5-dioxopyrrolidin-1-yl)oxy)-2- oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate (from Step 1, 298 mg, 0.319 mmol)  in dioxane, and stirred at ambient temperature for 2 hours. The solvent was evaporated in vacuo, and the residue was treated with acetic acid (8 mL) and water (2 mL) for 1 hour. The solution was diluted with water (3 mL), frozen and lyophilized to a red oil. The oil was dissolved in DMSO, applied to a RediSep C18 reverse phase cartridge (100 g), and eluted with acetonitrile (gradient 10% to 95%) in water (solvents buffered with AcOH 0.05%). The  product elutes at 39% acetonitrile. Fractions were combined, frozen and lyophilized to afford the product (165 mg) as the AcOH salt in 59% yield. LC (method A): 1.994 (99%); MS: 880.2 (M+H) ⁺ , 441.7 (M+2H)/2 ⁺ . Step 3. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl (S)-2,3,7,7-tetramethyl-4,10,15-trioxo-8-thia-  3,11,14-triazaheptadec-16-ynoate A soluti ⁵ ydroxy-8 ,14- dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((2-((2-aminoethyl)amino)-2-  oxoethyl)thio)-4-methylpentanoyl)-N-methyl-L-alaninate (from Step 2, 10.4 mg, 0.0111 mmol) in DMF (0.3 mL) was treated with propiolic acid (0.003, 0.0484 mmol) and EEDQ (3.3 mg, 0.013 mmol) overnight. The solution was applied to a RediSep cartridge, C18 AQ (5.5 g), and the column was eluted with acetonitrile (gradient 20% to 95%) in water (solvent buffered with NH ₄ OAc, 10 mM). The product eluted at 45% acetonitrile. The fractions were  combined, frozen and lyophilized to afford the product (10.8 mg) as a white solid. NMR(CDCl ₃ ); LC (method A): 2.907 (>95%); MS: 914.1 (M+H-H ₂ O) ⁺ and 930.2 (M-H)-. Step 4. Compound 10 Solid peptide Pv1 (40 mg, 0.0114 mmol) was added to a solution of   (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-3 ³ ,2,7,10- tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl (S)-2,3,7,7-tetramethyl-4,10,15-trioxo-8-thia- 3,11,14-triazaheptadec-16-ynoate (from Step 3, 10.8 mg, 0.0116 mmol) in DMF (3 mL). Saturated aqueous sodium bicarbonate (1 mL) was added and the resulting mixture was  stirred at ambient temperature for 2 hours, then treated with acetic acid (0.1 mL). The mixture was applied to a Biotage reverse phase C18300Å cartridge (25 G ). The column was eluted with acetonitrile (gradient 20% to 95%) in water (solvents buffered with NH ₄ OAc, 10mM). The product eluted at 50% acetonitrile. The purified fractions were combined, frozen and lyophilized, to afford the product (24.1 mg) as the bis-AcOH salt in 47% yield. LC (method B): 6.355 min. (99%); MS: 2106.6 (M+2H)/2 ⁺ and 1404.2 (M+3H)/3 ⁺ .   Example 11. Preparation of Compound 11 Step 1. (1 ⁴ S,1 ⁶ S,3 , , , , , , )- -c oro- - y roxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((4-(bromomethyl)benzyl)thio)-4-  methylpentanoyl)-N-methyl-L-alaninate A solution ⁴ -hydr ⁵ oxy-8 ,14- dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-mercapto-4-methylpentanoyl)-N-methyl-  L-alaninate (DM4, 151 mg, 0.193 mmol) in DMF (3 mL) was treated with solid α,α’- dibromo-p-xylene (338 mg, 1.28 mmol.) and diluted with additional DMF (3 mL). The resultant solution was treated with saturated aqueous sodium bicarbonate (1.0 mL). Within two minutes a heavy precipitate developed. The resultant mixture was stirred at room temperature for two hours. The precipitate was removed by filtration, and the mother liquor was applied to a medium pressure reverse phase RediSep C18 Gold cartridge (50 g). The product was eluted with acetonitrile (10% step to 40% and a gradient to 90%) in water (solvents buffered with acetic acid 0.05%). The product eluted at 71% acetonitrile. Purified fractions were combined, frozen and lyophilized to afford the product as a colorless glass  (116 mg) in 62% yield. LC (method A): 3.599 min. (99%). MS: 944.3 and 946.3 (MH- H ₂ O) ⁺ , 962 and 964.3 MH ⁺ , 984 and 986.2 (M+Na) ⁺ . Step 2. Compound 11 Solid (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-  3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(4-((4-(bromomethyl)benzyl)thio)-4- methylpentanoyl)-N-methyl-L-alaninate (from Step 1, 116 mg, 0.120 mmol) was treated with a solution of peptide Pv1 (422 mg, 0.120 mmol) in DMF (4 mL), and the resultant solution was treated with saturated aqueous sodium bicarbonate (1 mL). The mixture was stirred at  room temperature until the starting materials were consumed (3 hours). The mixture was made acidic with acetic acid (0.3 mL) and applied to a medium pressure reverse phase cartridge RediSep Aq C18 (100 g) and eluted with acetonitrile (10% step to 30% and a gradient to 90%) in water (solvents buffered with TFA 0.05%). The product eluted at 59% acetonitrile. The purified fractions were combined, frozen and lyophilized to afford the  product as a white solid (321 mg) as the bis-TFA salt in 61% yield. LC (Method B): 7.076 min. (>95%); MS: 2181.4 (M+2H)/2 ⁺ , 1387.4 (M+3H)/3 ⁺ and 1381 (M-H ₂ O + 3H)/3 ⁺ . Example 12. Preparation of Compound 12 Step 1.2-((3-(((S)-1-(((1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14- dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl)oxy)-1-oxopropan- 2-yl)(methyl)amino)-3- oxopropyl)thio)acetic acid   Mertansine ( mL of dry THF at room temperature.300 µL of a solution of bromoacetic acid (3.4 M in THF, 1.02 mmol) and 2.7 mL of saturated NaHCO3 were added sequentially. The reaction mixture was left to stir at room temperature for 24 hours. The reaction was quenched with AcOH and diluted with  EtOAc. The mixture was washed with brine and the organic layer was dried with Na ₂ SO ₄ , filtered, and concentrated. The crude material was purified on a 100 g C18 Aq column via a standard 10-95% B gradient (A: water w.0.05% AcOH; B: MeCN w.0.05% AcOH). Product containing fractions were lyophilized to afford 54 mg of product (50% yield). HPLC purity at 254 nm: 99.2%. Retention time: 1.24 min (Method C). LCMS: 796.4; [M+H] = 796.3.   Step 2. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(3-((2-((2-(2,5-dioxo-2,5-dihydro-1H-pyrrol- 1-yl)ethyl)amino)-2-oxoethyl)thio)propanoyl)-N-methyl-L-alan inate   2-((3-(((S)-1-(((1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14- dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl)oxy)-1-oxopropan- 2-yl)(methyl)amino)-3- oxopropyl)thio)acetic acid (11 mg, 0.014 mmol) was dissolved in DMF (500 µL), at room  temperature, under Argon atmosphere.2-Maleimido ethanamine (2.9 mg, 0.021 mmol), HATU (10.5 mg, 0.028 mmol) and NMM (3.1 µL, 0.028 mmol) were added sequentially. The reaction mixture was left to stir at room temperature. After 1.5 h, the reaction was complete. The solution was loaded on 15.5 g C18 Aq column and purified via standard 10- 95% B gradient (A: water w.0.05% AcOH; B: CH3CN w.0.05% AcOH). Product containing  fractions were lyophilized to afford 10 mg of product (79% yield). HPLC purity at 254 nm: 97.7%. Retention time: 2.45 min (Method A). LCMS: 900.3 (M-H2O) Step 3. Compound 12 (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy-  3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(3-((2-((2-(2,5-dioxo-2,5-dihydro-1H-pyrrol- 1-yl)ethyl)amino)-2-oxoethyl)thio)propanoyl)-N-methyl-L-alan inate (10 mg, 0.01089 mmol) and 40.6 mg peptide Pv1 (0.01198 mmol) were dissolved in dry DMF (300 µL), at room temperature, under Argon atmosphere. Et ₃ N (4.5 µL) was added. The reaction mixture was  left to stir at room temperature for 2 h. LCMS (method B) showed <5% residual starting material. The reaction mixture was diluted with DMF (700 µL) and loaded on EZPrep 150x30 mm C8 Kinetex column. It was purified via standard 5-95% B gradient (A: water, 10 mM NH4OAc; B: CH ₃ CN, 10 mM NH ₄ OAc). Product containing fractions were lyophilized to afford product contaminated with 3% payload. The white solid was dissolved in DMF (1  mL) and loaded on EZPrep 150x30 mm C8 Kinetex column. It was purified via standard 5- 95% B gradient (A: water w.0.05% TFA; B: CH3CN w.0.05% TFA). The product containing fractions were lyophilized to afford the desired product (20 mg) as a white solid in 44% yield. HPLC purity at 254 nm: 98.8%. Retention time: 6.56 min (Method B). LCMS: 2099.5 [(M+2)/2].   Example 13. Preparation of Compound 13

Step 1. (1 ⁴ S,1 ⁶ , , , , , , , )- -c oro- - y roxy- , -dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(3-((2-((2-aminoethyl)amino)-2-  oxoethyl)thio)propanoyl)-N-methyl-L-alaninate 2-((3-(( hydroxy-8 ⁵ ,14- dimethoxy-3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl)oxy)-1-oxopropan- 2-yl)(methyl)amino)-3-  oxopropyl)thio)acetic acid (from Example 1, Step 1; 25 mg, 0.0314 mmol) was dissolved in dry DMF (350 µL) at room temperature. HATU (23.9 mg) and NMM (7.0 µL) were added sequentially. The reaction mixture was left to stir for 5 minutes and then 100 µL of a solution of N ¹ -((4-methoxyphenyl)diphenylmethyl)ethane-1,2-diamine (0.8 M in 2:1 DMF/THF) was added. The reaction mixture was left to stir at room temperature for 4 hours. The solution was  loaded on a 30 g C18 Aq column. It was purified via a standard 10-95% B gradient (A: water w.0.05% AcOH; B: MeCN w.0.05% AcOH). Product containing fractions were lyophilized. The resulting product (3:2 MMT protected/deprotected material) was dissolved in 2 mL of 80% AcOH in water and left to stir for 1.5 hours. The solution was then frozen and lyophilized. The crude material was purified on a 15.5 g C18 Aq column via a standard 10- 95% B gradient (A: water w.0.05% AcOH; B: MeCN w.0.05% AcOH). Product containing fractions were lyophilized to afford the product (11.5 mg) in 45% yield. HPLC purity at 254 nm: 98.6%. Retention time: 2.16 min (Method A). LCMS: 838.3; [M+H] = 838.4   Step 2. (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl (S)-1-bromo-13,14-dimethyl-2,7,12-trioxo-9- thia-3,6,13-triazapentadecan-15-oate   3.8 m om temperature under Ar atmosphere.10.4 mg of HATU and 3.8 µL of NMM were added sequentially. The reaction mixture was left to stir for 5 minutes then 11.5 mg (0.0137 mmol) of (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-85,14-dimethoxy-3 ³ ,2,7,10-  tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl N-(3-((2-((2-aminoethyl)amino)-2- oxoethyl)thio)propanoyl)-N-methyl-L-alaninate (MV-0747-011) in 150 µL of dry DMF were added. The reaction mixture was left to stir at room temperature under Ar atmosphere for 1.5 hours. The solution was loaded on a 15.5 g C18 Aq column. It was purified via a standard 10-  95% B gradient (A: water w.0.05% AcOH; B: MeCN w.0.05% AcOH). via a standard 10- 95% B gradient (A: water w.0.05% AcOH; B: MeCN w.0.05% AcOH). Product containing fractions were lyophilized to afford 5.9 mg of product (45% yield). HPLC purity at 254 nm: 96.7%. Retention time: 2.50 min (Method A). LCMS: 942.2; [M-OH] = 942.3   Step 3. Compound 13 (1 ⁴ S,1 ⁶ S,3 ² S,3 ³ S,2R,4S,10E,12E,14R)-8 ⁶ -chloro-1 ⁴ -hydroxy-8 ⁵ ,14-dimethoxy- 3 ³ ,2,7,10-tetramethyl-1 ² ,6-dioxo-7-aza-1(6,4)-oxazinana-3(2,3)-oxirana-8(1,3)- benzenacyclotetradecaphane-10,12-dien-4-yl (S)-1-bromo-13,14-dimethyl-2,7,12-trioxo-9- thia-3,6,13-triazapentadecan-15-oate (5.9 mg, 0.00615 mmol) was dissolved in dry DMF (615 µL) at room temperature. Pv1 (24.2 mg ) and Tris buffer (615 µL) were added sequentially. The reaction mixture was sonicated for 2 minutes and then allowed to stir at  room temperature for 2.5 hours. NaHCO3 (8.0 mg) was added. The reaction mixture was sonicated for 2 minutes and allowed to stir for 21 hours. TFA (50 µL) was added and the solution was loaded on a 150x30 mm C8 Kinetex column. It was purified via a standard 10- 95% B gradient (A: water w.0.1% TFA; B: MeCN w.0.1% TFA). Fractions containing product were lyophilized to afford the desired product (12.2 mg ) as a white solid in 48%  yield. HPLC purity at 254 nm: 97.8%. Retention time: 6.49 min (Method B). LCMS: 2079.4; [(M+H)/2] = 2079.0 Example A. Growth Delay Assay Cells were plated in 96 well black walled-clear bottom plates (Griener), HCT116 at  3000 cells per well, in growth media containing 10% FBS. Cells were allowed to adhere at room temperature for 60 minutes before returning to a 37 °C, 5% CO2 incubator. After 24 hours, media was removed and replaced with fresh growth media containing various drug concentrations. Each drug concentration was added in triplicate. Non-drug treated controls contained growth media only. Cells were returned to the incubator. Ninety-six hours after  addition of drug, cells were fixed with 4% paraformaldehyde for 20 minutes and stained with Hoechst at 1 µg/mL. The plates were imaged on a Cytation 5 auto imager (BioTek) and cells were counted using CellProfiler (http://cellprofiler.org). The percent cell growth delay was calculated and data plotted using GraphPad Prism. The results of the Growth Delay Assay are shown in Table 1. Data is displayed as  follows: * is IC ₅₀ ≤ 20 nM; ** is 20 nM < IC ₅₀ ≤ 200 nM; and ** is 200 nM < IC ₅₀ ≤ 2000 nM. Table 1: Growth Delay Assay data Compound HCT116 Potency (IC50) ** 5 *** *** Example B: Effic acy o Compound and Compound n a C 6 Colorectal Cancer Model Six-week-old female athymic nude Foxn ^nu mice were obtained from Taconic Labs  (Cat# NCRNU-F) and were housed 5 per cage on Alpha-Dri bedding in a disposable caging system. Human HCT116 cells derived from colorectal carcinoma were diluted 1:1 in Phenol Red-free Matrigel and subcutaneously implanted into the left flank of each mouse at a density of 2.5x10 ⁶ cells in 100 µL. When xenografts reached a mean volume of 100-200 mm ³ , mice were randomized into groups and were administered intraperitoneal (IP) doses of vehicle or  either 10 mg/kg or 40 mg/kg of Compound 2, or 2.5 mg/kg of Compound 11. Doses were prepared by diluting 0.1 mg/µL DMSO stocks in 5% mannitol in citrate buffer and were administered to the mice. Xenograft tumors were measured by calipers and volume was calculated using the equation for ellipsoid volume: Volume = π/6 x (length) x (width) ² . Animals were removed from the study due to death, tumor size exceeding 2000mm ³ or loss  of >20% body weight. FIG.1A shows efficacy (in terms of mean tumor volume) of nude mice bearing HCT116 colorectal carcinoma flank tumors after the indicated intraperitoneal doses of Compound 2 dosed for four total doses. FIG.1B shows the percent change in body weight of nude mice bearing HCT116  colorectal carcinoma flank tumors after the indicated intraperitoneal doses of Compound 2 dosed for four total doses. FIG.2A shows efficacy (in terms of mean tumor volume) of nude mice bearing HCT116 colorectal carcinoma flank tumors after the indicated intraperitoneal doses of Compound 11 dosed for four total doses. FIG.2B shows the percent change in body weight of nude mice bearing HCT116 colorectal carcinoma flank tumors after the indicated intraperitoneal doses of Compound 11 dosed for four total doses.   Example C: Efficacy of Compound 1 in a MKN45 HER2 Negative Gastric Cancer Model Six-week-old female athymic nude Foxn ^nu mice were obtained from Taconic Labs (Cat# NCRNU-F) and were housed 5 per cage on Alpha-Dri bedding in a disposable caging system. Human MKN45 cells derived from gastric carcinoma were diluted 1:1 in Phenol  Red-free Matrigel and subcutaneously implanted into the left flank of each mouse at a density of 2x10 ⁶ cells in 100 µL. When xenografts reached a mean volume of 100-200 mm ³ , mice were randomized into groups and were administered intraperitoneal (IP) doses of vehicle or 2.5 or 5.0 mg/kg of Compound 1. Doses were prepared by diluting 0.1 mg/µL DMSO stocks in 5% mannitol in citrate buffer and were administered to the mice. Xenograft tumors were  measured by calipers and volume was calculated using the equation for ellipsoid volume: Volume = π/6 x (length) x (width) ² . Animals were removed from the study due to death, tumor size exceeding 2000 mm ³ , or loss of >20% body weight. FIG.3A shows a plot of efficacy (in terms of mean tumor volume) of nude mice bearing MKN45 gastric cancer tumors after the indicated intraperitoneal doses of Compound  1 dosed for four total doses. FIG.3B shows a plot of the percent change in body weight of nude mice bearing MKN45 gastric cancer tumors after the indicated intraperitoneal doses of Compound 1 dosed for four total doses.   Various modifications of the invention, in addition to those described herein, will be apparent to those skilled in the art from the foregoing description. Such modifications are also intended to fall within the scope of the appended claims. Each reference, including without limitation all patent, patent applications, and publications, cited in the present application is incorporated herein by reference in its entirety.